The DOI matches its Crossref record; 294 of the 310 references it cites were found in a registry or an index; 82 of the 506 sources its claims cite were checked for support.
Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach
Open accessAbstract
Traumatic brain injury (TBI) is a growing public health problem worldwide and is a leading cause of death and disability. The causes of TBI include motor vehicle accidents, which are the most common cause, falls, acts of violence, sports-related head traumas, and war accidents including blast-related brain injuries. Recently, pituitary dysfunction has also been described in boxers and kickboxers. Neuroendocrine dysfunction due to TBI was described for the first time in 1918. Only case reports and small case series were reported until 2000, but since then pituitary function in TBI victims has been investigated in more detail. The frequency of hypopituitarism after TBI varies widely among different studies (15-50% of the patients with TBI in most studies). The estimates of persistent hypopituitarism decrease to 12% if repeated testing is applied. GH is the most common hormone lost after TBI, followed by ACTH, gonadotropins (FSH and LH), and TSH. The underlying mechanisms responsible for pituitary dysfunction after TBI are not entirely clear; however, recent studies have shown that genetic predisposition and autoimmunity may have a role. Hypopituitarism after TBI may have a negative impact on the pace or degree of functional recovery and cognition. What is not clear is whether treatment of hypopituitarism has a beneficial effect on specific function. In this review, the current data related to anterior pituitary dysfunction after TBI in adult patients are updated, and guidelines…
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Written from the paper’s full text.
TL;DR
This review updates adult anterior pituitary dysfunction after traumatic brain injury, covering prevalence, sports- and blast-related injury, cognition, metabolism, pathophysiology, diagnosis, screening, and treatment. It reports that GH is the most frequently affected axis, that prevalence estimates vary with testing strategy, and that vascular, autoimmune, and genetic mechanisms are proposed but not fully established.
Key findings
- In the authors’ systematic review of 16 studies and 1,291 TBI patients, pooled prevalence of any hormone deficiency without confirmatory testing was 28% and multiple deficiencies 6%; after confirmatory testing in 313 patients, these fell to 15% and 4%, with GH deficiency at 9%, ACTH at 6%, LH/FSH at 5%, and TSH at 1%.
- A 5-year prospective study found persistent deficiencies at year five of 28% for GH, 4% for gonadotropin, and 4% for ACTH; GH was generally the most common deficit after TBI.
- Sports-related repetitive head trauma was linked to pituitary dysfunction: 45% of amateur boxers had isolated GH deficiency in one study, kickboxers showed 22.7% GH and 9.1% ACTH deficiency with 27.3% having at least one anterior deficiency, and retired professional football players had 23.5% hypopituitarism, 50% metabolic syndrome, 19.1% GH deficiency, and 8.8% hypogonadism.
- Proposed mechanisms include vascular injury, autoimmunity, and genetic susceptibility; APO E3/E3 genotype was associated with lower pituitary dysfunction (17.7% vs 41.9%, OR 0.29), and antipituitary/antihypothalamus antibodies were associated with persistent hypopituitarism in prospective follow-up.
Methods
- This is a narrative review that also includes a systematic literature search of Medline through March 21, 2014, using terms for brain injury/TBI and hypopituitarism/pituitary, limited to human studies, with additional reference-list searches.
- For prevalence, the authors included adult studies with stimulatory testing of GH and/or ACTH axes and more than three anterior pituitary deficiencies, excluded case reports/series under 10 patients, posterior pituitary or acute-phase-only studies, and analyzed 16 studies; 1,203 patients remained for chronic-phase prevalence and 313 were in the confirmatory-testing subset.
- The review also synthesizes autopsy, radiological, experimental animal, sports, cognitive, metabolic, diagnostic, screening, and treatment literature.
Limitations
- The authors state that included prevalence studies were heterogeneous in TBI severity, diagnostic tests, cutoffs, and preselection; most lacked control groups, only three had matched controls, and six studies reporting response rates had a 41% participation rate.
- They note that long-term prospective studies had small samples, especially for moderate and severe TBI, and that autopsy findings came from fatal severe injuries, making generalization to nonfatal survivors difficult.
- The text makes evident that many pathophysiological mechanisms and treatment benefits remain uncertain: confirmatory testing was available in only three studies, no large placebo-controlled trials establish GH replacement effects on rehabilitation or cognition after TBI, and recommendations for screening beyond 12 months need further confirmation.
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Claims the paper makes
176 No full text of the sources · 56 Own interpretation · 33 Own result · 32 Partly supported · 20 Supported · 19 No basis given · 18 Supported so far · 13 Not checked yet · 4 Sources not found · 4 Own method · 2 Not supported · 1 Couldn’t confirm · accuracy not yet measured
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“CT and conventional magnetic resonance imaging (MRI) do not allow discrimination of DAI (107).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Disputedcites [107] Kim, 2011, Imaging for the diagnosis and management of traumatic brain injury, Neurotherapeutics sourceExperimental — accuracy not yet measured
The “Traumatic axonal injury” section says CT can show characteristic findings in some patients and that MRI is far more sensitive, detecting both hemorrhagic and nonhemorrhagic lesions. Although the “Advanced MRI techniques” section notes that conventional CT or MR images can be normal despite injury, the paper does not say these methods cannot detect or distinguish axonal injury. (LLM, conf=0.87)
Checked by a reasoning model — may be wrong.
plain- Asserted: passes — The authors put it forward as true.
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- Disputed
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“It is important to note that, in these studies, pituitary hormone evaluations were performed only at one time point during the acute phase of TBI (15, 149, 150).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Disputedcites [149] Agha, 2005, The natural history of post-traumatic hypopituitarism: implications for assessment and treatment, Am J Med sourceExperimental — accuracy not yet measured
The Abstract describes pituitary-function evaluations during the acute phase and again at 6 and 12 months after injury. Table 2 (section 1416.e6) reports results at all three time points, contrary to the claim that evaluations in this study occurred only once during the acute phase. (LLM, conf=0.91)
Checked by a reasoning model — may be wrong.
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Every source the paper cites for this claim was checked and supports it.
In the paper
“GH assessment by Immulite or Isys assay caused no significant diagnostic differences.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > Severity
What the sources say
- Supportedcites [21] Klose, 2014, Prevalence of posttraumatic growth hormone deficiency is highly dependent on the diagnostic set-up: results from The Danish National Study on Posttraumatic Hypopituitarism, J Clin Endocrinol Metab source
The Impact of GH assay section reports concordant diagnostic test outcomes for Immulite and iSYS in 546 of 555 tests (98%). The Diagnostic thresholds section explicitly states that the assays showed excellent agreement with no significant diagnostic difference. (LLM, conf=0.95)
plainn = 439- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“and by ITT than by PD-GHRH/GHRHϩARG (P ϭ .006[local cutoffs]; P Ͻ .001[guideline cutoffs]).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > Severity
What the sources say
- Supportedcites [21] Klose, 2014, Prevalence of posttraumatic growth hormone deficiency is highly dependent on the diagnostic set-up: results from The Danish National Study on Posttraumatic Hypopituitarism, J Clin Endocrinol Metab source
The Abstract reports lower GHD prevalence by ITT than by PD-GHRH/GHRH-arg, with P = .006 using local cutoffs and P < .001 using guideline cutoffs. The “Impact of diagnostic test” section likewise reports higher prevalence with the combined tests than with ITT in patients. (LLM, conf=0.95)
plainn = 439 ·- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Moreover, they showed that a substantial number of false-positive results were found in the control group.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > Severity
What the sources say
- Supportedcites [21] Klose, 2014, Prevalence of posttraumatic growth hormone deficiency is highly dependent on the diagnostic set-up: results from The Danish National Study on Posttraumatic Hypopituitarism, J Clin Endocrinol Metab source
The Figure 2 caption (Conclusion section; page not provided) explicitly describes a high false-positive rate in healthy controls when guideline-derived GH test cutoffs were applied. The Single vs confirmatory testing section also reports that some controls had an insufficient result on one test, but none did on both. (LLM, conf=0.92)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Only 1% of patients had GHD according to two tests.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > Severity
What the sources say
- Supportedcites [21] Klose, 2014, Prevalence of posttraumatic growth hormone deficiency is highly dependent on the diagnostic set-up: results from The Danish National Study on Posttraumatic Hypopituitarism, J Clin Endocrinol Metab source
The Abstract states that only 1% of patients had GHD according to two tests. The ‘Single vs confirmatory testing’ section specifies that this result applies to the 169 patients who underwent both tests. (LLM, conf=0.95)
plainn = 439- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The prevalence of GHD was found to be lower by local than by guideline cutoffs (12 vs 19% [PD-GHRH/GHRHϩARG, P Ͻ .001];4.5 vs 5% [ITT, P ϭ .9])”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > Severity
What the sources say
- Supportedcites [21] Klose, 2014, Prevalence of posttraumatic growth hormone deficiency is highly dependent on the diagnostic set-up: results from The Danish National Study on Posttraumatic Hypopituitarism, J Clin Endocrinol Metab source
The Abstract reports lower GHD prevalence with local than guideline cutoffs: 12% versus 19% for PD-GHRH/GHRH-arginine and 4.5% versus 5% for ITT, with the same P values as the citing sentence. The ‘Impact of local vs guideline-derived cutoff values’ section gives the corresponding unrounded figures and notes that the ITT difference was not statistically significant (P = .9). (LLM, conf=0.95)
plainn = 439 ·- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Of the individuals who have sustained TBI, those with lower T levels also appear to have an increased risk for Alzheimer's disease, which makes the connection between sex hormones and brain injury even more intriguing (65).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Gonadotropins
What the sources say
- Partly supportedcites [65] Jellinger, 2001, Traumatic brain injury as a risk factor for Alzheimer disease. Comparison of two retrospective autopsy cohorts with evaluation of ApoE genotype, BMC Neurol sourceExperimental — accuracy not yet measured
The Abstract Conclusions and Discussion report an association between TBI and Alzheimer disease. They do not address whether testosterone levels change that risk among people with TBI; searches for testosterone, lower T levels, and androgens found no such passage. No page numbers are available in our copy. (LLM, conf=0.85)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The results of T supplementation in hypogonadal males, as well as in normal healthy males, have shown some improvement in some domains of memory (61,62);”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Gonadotropins
What the sources say
- Supportedcites [61] Cherrier, 2003, Cognitive changes associated with supplementation of testosterone or dihydrotestosterone in mildly hypogonadal men: a preliminary report, J Androl source
The Discussion reports significant improvement in verbal memory after testosterone supplementation in hypogonadal men. It also describes prior findings of improved spatial and verbal memory in eugonadal men receiving testosterone; the paper’s introductory passage identifies these as young and healthy older men. Page numbers are not provided in our copy. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites [62] Cherrier, 2005, The role of aromatization in testosterone supplementation: effects on cognition in older men, Neurology source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“GHD (19.1%) and hypogonadism (8.8%) were found to be the most common pituitary dysfunction after repetitive sports-related concussion in football players (48).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Supportedcites [48] Kelly, 2014, Prevalence of pituitary hormone dysfunction, metabolic syndrome, and impaired quality of life in retired professional football players: a prospective study, J Neurotrauma source
The Results section (page unavailable) reports GHD in 19.1% and hypogonadism in 8.8% of the retired football players studied; no other pituitary deficiencies were found. The paper describes the cohort as having sustained repetitive head impacts and concussions. It does not establish that concussions caused the deficiencies. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Additionally, Klose et al (21) showed that false-positive results after GH testing occurred in 2-8% of controls, depending on the tests and cutoffs used.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > D. Is hypopituitarism more common after brain damage than in the normal population?
What the sources say
- Partly supportedcites [21] Klose, 2014, Prevalence of posttraumatic growth hormone deficiency is highly dependent on the diagnostic set-up: results from The Danish National Study on Posttraumatic Hypopituitarism, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
The 'Impact of local vs guideline-derived cutoff values' section reports false-positive GH-deficiency results in healthy controls that varied by test and cutoff. But it gives 4% for ITT and up to 20% for combined tests under guideline cutoffs, so the claimed 2–8% range is not supported. (LLM, conf=0.88)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
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In the paper
“The pathophysiological mechanism of diabetes and insulin resistance in patients with hypopituitarism is not completely understood; however, available evidence suggests GH as the principal player due to its interaction with many other hormonal and/or peptidic systems (74,91).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Partly supportedcites [74] Luque, 2011, Metabolic impact of adult-onset, isolated, growth hormone deficiency (AOiGHD) due to destruction of pituitary somatotropes, PLoS One sourceExperimental — accuracy not yet measured
The Discussion (section “AOiGHD improves whole body insulin sensitivity”; page not supplied) reports that isolated GH deficiency improved insulin sensitivity in mice and discusses anti-insulin effects of GH in clinical studies. It does not establish GH as the principal cause of diabetes and insulin resistance in patients with hypopituitarism, or attribute that role to interactions with many other hormonal or peptide systems; it says the mechanism by which GH reduces insulin sensitivity remains unclear. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [91] Mersebach, 2003, Comparisons of leptin, incretins and body composition in obese and lean patients with hypopituitarism and healthy individuals, Clin Endocrinol (Oxf) source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Consequently, it is feasible that TBI patients with neuroendocrine dysfunction may have metabolic alterations; however, few studies have evaluated these issues, including changes in body composition and BMI, lipid profile, glucose metabolism, and hypertension (46,48,80,81).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [46] Tanriverdi, 2008, Brief communication: pituitary volume and function in competing and retired male boxers, Ann Intern Med source
- Supportedcites [48] Kelly, 2014, Prevalence of pituitary hormone dysfunction, metabolic syndrome, and impaired quality of life in retired professional football players: a prospective study, J Neurotrauma source
The Discussion (Quality of life, erectile dysfunction, metabolic syndrome, and obesity; page unavailable) says growth hormone deficiency and hypogonadism can contribute to changes in body composition, obesity, and metabolic syndrome. The study evaluated BMI and metabolic-syndrome measures in retired football players, supporting the citing sentence’s cautious statement that neuroendocrine dysfunction after TBI may accompany metabolic alterations; it did not establish a causal link. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [80] Klose, 2007, Posttraumatic hypopituitarism is associated with an unfavorable body composition and lipid profile, and decreased quality of life 12 months after injury, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [81] Prodam, 2013, Metabolic alterations in patients who develop traumatic brain injury (TBI)-induced hypopituitarism, Growth Horm IGF Res source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Low HDL-cholesterol was shown in classical hypopituitarism subjects with respect to controls chosen in obese subjects without hypopituitarism (75).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Partly supportedcites [75] Nyenwe, 2009, Nonalcoholic fatty liver disease and metabolic syndrome in hypopituitary patients, Am J Med Sci sourceExperimental — accuracy not yet measured
The Results section reports a significantly higher prevalence of low HDL cholesterol in hypopituitary patients than in controls. But the Methods say controls were matched for BMI, and the Results distinguish obese from non-obese controls; the comparison was not exclusively with obese subjects without hypopituitarism. Page numbers were not available in our copy. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“DAI is the primary neuropathology of TBI that is caused by the shearing of fragile axons (disruption of axonal fibers and myelin sheaths) by acceleration/deceleration forces from the head trauma (105, 106).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Partly supportedcites [105] Johnson, 2013, Axonal pathology in traumatic brain injury, Exp Neurol sourceExperimental — accuracy not yet measured
The Introduction calls DAI one of the most common neuropathological consequences of TBI and links it to mechanical loading during rapid head acceleration; it does not call DAI the primary neuropathology. The section “Potential Primary Mechanical Damage due to Axonal Trauma” also says immediate shearing apart of axons is relatively rare and that disconnection usually develops secondarily after cytoskeletal damage, so the claim oversimplifies the mechanism. Page numbers were not available in our copy. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites [106] Adams, 1989, Diffuse axonal injury in head injury: definition, diagnosis and grading, Histopathology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These processes induce adhesion molecules and, in order, mobilize immune and glial cells in a parallel and synergistic way (94, 126 -128).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [94] Frattalone, 2013, Moderate and severe traumatic brain injury: pathophysiology and management, Neurosurg Clin N Am source
- Not checked — no full text of the sourcecites [126] Fabricius, 2006, Cortical spreading depression and peri-infarct depolarization in acutely injured human cerebral cortex, Brain source
- Supportedcites [127] Lucas, 2006, The role of inflammation in CNS injury and disease, Br J Pharmacol source
The section “Expression of inflammatory mediators in the CNS” says that proinflammatory cytokines and other mediators induce adhesion molecules, recruit immune cells, and activate immune and glial cells. It also describes related cytokine pathways in which mediators potentiate one another, supporting the claim’s broad description of parallel and synergistic activity. No page number is available in our copy. (LLM, conf=0.86)
- Partly supportedcites [128] Potts, 2006, Traumatic injury to the immature brain: inflammation, oxidative injury, and iron-mediated damage as potential therapeutic targets, NeuroRx sourceExperimental — accuracy not yet measured
The “Inflammation and brain injury” section (pp. 2–3) describes integrated inflammatory activity, adhesion-molecule upregulation after traumatic brain injury, and leukocyte recruitment. It also identifies activated microglia as a feature of early inflammation, but does not say that these processes mobilize glial cells or that immune and glial cells act in a parallel, synergistic way. (LLM, conf=0.83)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Every source the paper cites for this claim was checked and supports it.
In the paper
“In this investigation, all patients with large-or medium-sized pituitary infarctions had increased ICP at some point.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Supportedcites [141] Harper, 1986, Analysis of abnormalities in pituitary gland in non-missile head injury: study of 100 consecutive cases, J Clin Pathol source
The Discussion states that every patient with a large or medium-sized infarct had raised intracranial pressure at some stage. Table 2 is consistent with this: it records evidence of raised intracranial pressure in all 13 large-infarct and all five medium-infarct cases. (LLM, conf=0.95)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Antibodies may form after TBI due to the disruption of the blood-brain barrier, which allows brain proteins (especially the release of sequestered pituitary and hypothalamic antigens from injured/ necrotic tissue) to leak into the circulation, evoking an immune response (164, 165).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [164] Tanriverdi, 2010, Investigation of antihypothalamus and antipituitary antibodies in amateur boxers: is chronic repetitive head trauma-induced pituitary dysfunction associated with autoimmunity?, Eur J Endocrinol source
- Partly supportedcites [165] Papa, 2012, Elevated levels of serum glial fibrillary acidic protein breakdown products in mild and moderate traumatic brain injury are associated with intracranial lesions and neurosurgical intervention, Ann Emerg Med sourceExperimental — accuracy not yet measured
The Results report that GFAP breakdown products appeared rapidly in serum after TBI, and the Discussion describes their release from injured glial cells. The paper does not attribute that appearance to blood–brain barrier disruption or discuss antibody formation, an immune response, or pituitary and hypothalamic antigens. No page numbers were provided for these passages. (LLM, conf=0.84)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Every source the paper cites for this claim was checked and supports it.
In the paper
“In that study, the authors did not evaluate the effects of TBI on pituitary function, but they clearly demonstrated that serum levels of glial fibrillary acidic protein autoantibodies increased up to 7 days after the injury.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Supportedcites [166] Zhang, 2014, Human traumatic brain injury induces autoantibody response against glial fibrillary acidic protein and its breakdown products, PLoS One source
The Discussion states that GFAP autoantibody levels in TBI patient sera increased by 7 days after injury. The Results also report that these autoantibodies were detectable by day 7 in nine of twelve patients examined. (LLM, conf=0.94)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Based on the prospective clinical studies, significant percentages of the acute pituitary hormonal deficiencies are transient and recover after 3 to 12 months of injury (15, 25, 149 -151).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
- Supportedcites [149] Agha, 2005, The natural history of post-traumatic hypopituitarism: implications for assessment and treatment, Am J Med source
The Discussion reports that some acute pituitary hormone abnormalities were transient and that most recovery occurred by six months. The Somatotropic axis section documents recovery at both six and twelve months, supporting the claimed 3-to-12-month post-injury period. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [151] Krahulik, 2010, Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults, J Neurosurg source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Kasturi and Stein (176) reported that cortical contusion injury in young adult male rats leads to the suppression of GH in the serum and in the anterior pituitary 2 months after injury.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Supportedcites [176] Kasturi, 2009, Traumatic brain injury causes long-term reduction in serum growth hormone and persistent astrocytosis in the cortico-hypothalamo-pituitary axis of adult male rats, J Neurotrauma source
The Discussion states that bilateral medial frontal cortical contusions in young adult male rats suppressed GH in both serum and anterior pituitary at 2 months post-injury. The Abstract also reports significantly lower GH levels in both compared with sham-operated rats. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Based on these findings, the authors concluded that the chronic change seen in the post-TBI GH level is probably the result of systemic and persistent inflammatory changes in the hypothalamus and anterior pituitary (176).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Supportedcites [176] Kasturi, 2009, Traumatic brain injury causes long-term reduction in serum growth hormone and persistent astrocytosis in the cortico-hypothalamo-pituitary axis of adult male rats, J Neurotrauma source
The Abstract (page not provided) explicitly concludes that the chronic post-TBI change in GH is probably due to persistent inflammatory changes in the hypothalamus and anterior pituitary. The conclusion is based on the study’s adult male rat model. (LLM, conf=0.95)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Significant reductions in the levels of GH in both serum and anterior pituitary at 2 months after injury were observed.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Supportedcites [176] Kasturi, 2009, Traumatic brain injury causes long-term reduction in serum growth hormone and persistent astrocytosis in the cortico-hypothalamo-pituitary axis of adult male rats, J Neurotrauma source
The Results report significantly lower serum GH at 2 months after injury than in sham-operated rats. The anterior-pituitary Results report significant suppression of the 22 kDa GH isoform at the same time point; the Discussion summarizes the finding as suppression of GH in both serum and anterior pituitary. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Moreover, they demonstrated the up-regulation of IL-1b and glial fibrillary acidic protein levels in the cerebral cortex, hypothalamus, and anterior pituitary.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Partly supportedcites [176] Kasturi, 2009, Traumatic brain injury causes long-term reduction in serum growth hormone and persistent astrocytosis in the cortico-hypothalamo-pituitary axis of adult male rats, J Neurotrauma sourceExperimental — accuracy not yet measured
The sections on IL-1β production and astrocytosis report increased IL-1β in the cerebral cortex and hypothalamus, and increased GFAP in all three regions. But the IL-1β section explicitly says there was no alteration in the anterior pituitary, so the claim overstates where both markers were up-regulated. Page numbers were not provided in the supplied passages. (LLM, conf=0.94)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“They are critical in understanding the links between the clinical outcomes of TBI and some cellular/ molecular dysfunction resulting in neuroendocrine dysfunction (193).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Partly supportedcites [193] Cernak, 2005, Animal models of head trauma, NeuroRx sourceExperimental — accuracy not yet measured
The Introduction and Conclusion describe animal TBI models as important for relating injury outcomes to cellular and molecular mechanisms. Neither passage establishes that those mechanisms result in neuroendocrine dysfunction; searches for neuroendocrine and endocrine terms did not find support for that part of the claim. (LLM, conf=0.85)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“To date, a significant number of different TBI experimental models have been defined to understand the pathophysiology of brain damage; however, only four experimental model studies investigating the effects of head trauma on the hypothalamo-pituitary region and function have been published recently (175-178).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [175] Greco, 2013, The effects of repeat traumatic brain injury on the pituitary in adolescent rats, J Neurotrauma source
- Supportedcites [176] Kasturi, 2009, Traumatic brain injury causes long-term reduction in serum growth hormone and persistent astrocytosis in the cortico-hypothalamo-pituitary axis of adult male rats, J Neurotrauma source
This citation identifies one of the experimental model studies in the cited group. The Abstract describes a rat cortical-contusion experiment measuring growth hormone and changes in the hypothalamus and anterior pituitary; the Discussion reports persistent changes in the hypothalamo-pituitary axis. The paper need not establish the collective count of four to support its role as one example. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites [177] Osterstock, 2014, Sustained alterations of hypothalamic tanycytes during posttraumatic hypopituitarism in male mice, Endocrinology source
- Not checked — no full text of the sourcecites [178] Ozdemir, 2012, Relationship between circulating IGF-1 levels and traumatic brain injury-induced hippocampal damage and cognitive dysfunction in immature rats, Neurosci Lett source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, the GH response to GHRHϩARG, and to all known GH provocative stimuli, significantly declines with increasing BMI in adults (221, 222); thus, the use of a non-BMI-related cutoff in obese subjects causes a high percentage of false-positive results (203).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Somatotroph axis
What the sources say
- Partly supportedcites [221] Bonert, 2004, Body mass index determines evoked growth hormone (GH) responsiveness in normal healthy male subjects: diagnostic caveat for adult GH deficiency, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
The Results (p. 2) report a significant inverse correlation between BMI and GH response to arginine-GHRH in 59 healthy men. The Discussion (p. 3) also says BMI relates inversely to responses to insulin tolerance testing, but the paper does not establish a decline for all known GH provocative stimuli or for adults generally. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [222] Qu, 2005, Influence of body mass index and gender on growth hormone (GH) responses to GH-releasing hormone plus arginine and insulin tolerance tests, J Clin Endocrinol Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Differences in the reported frequency of TBI-induced hypopituitarism may be due to more stringent diagnostic criteria being applied by some studies but not by others (21,194).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Introduction
What the sources say
- Supportedcites [21] Klose, 2014, Prevalence of posttraumatic growth hormone deficiency is highly dependent on the diagnostic set-up: results from The Danish National Study on Posttraumatic Hypopituitarism, J Clin Endocrinol Metab source
The Abstract reports that estimated post-TBI growth hormone deficiency varied with diagnostic cutoffs, test choice, and whether testing was repeated. The Conclusion states that stringent criteria, including confirmatory testing, yielded a low prevalence of posttraumatic hypopituitarism. These passages support the proposed explanation for differences in reported frequency. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [194] Schneider, 2007, Hypopituitarism, Lancet source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“In most studies, no significant associations between TBI severity according to postresuscitation GCS and hypopituitarism in the chronic phase have been reported (15, 23, 24, 27, 29, 181, 231-233), whereas others have demonstrated that hypopituitarism was more frequent in patients with more severe TBI (18,30,154).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [23] Herrmann, 2006, Hypopituitarism following severe traumatic brain injury, Exp Clin Endocrinol Diabetes source
- Not checked — no full text of the sourcecites [24] Leal-Cerro, 2005, Prevalence of hypopituitarism and growth hormone deficiency in adults long-term after severe traumatic brain injury, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [27] Schneider, 2006, Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury, Eur J Endocrinol source
- Supportedcites [29] Agha, 2004, Anterior pituitary dysfunction in survivors of traumatic brain injury, J Clin Endocrinol Metab source
The Discussion reports no association between hormone abnormalities and TBI severity measured by GCS. The Abstract specifies that GCS was recorded after resuscitation and before sedation, and that survivors were assessed a median of 17 months after injury. This paper supports its cited role as one study reporting no association; it need not establish the claim about most studies on its own. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [181] Aimaretti, 2005, Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [231] Kozlowski Moreau, 2012, Lasting pituitary hormone deficiency after traumatic brain injury, J Neurotrauma source
- Not checked — no full text of the sourcecites [232] Popovic, 2004, Hypopituitarism as a consequence of traumatic brain injury (TBI) and its possible relation with cognitive disabilities and mental distress, J Endocrinol Invest source
- Not checked — no full text of the sourcecites [233] Schneider, 2011, Structured assessment of hypopituitarism after traumatic brain injury and aneurysmal subarachnoid hemorrhage in 1242 patients: the German interdisciplinary database, J Neurotrauma source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“However, in the acute phase of TBI, the diagnosis of glucocorticoid deficiency should not be missed because it is life-threatening (14, 238, 241, 257, 258).”
- Also stated in: § 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase · plain
“However, in the acute phase of TBI, the diagnosis of glucocorticoid deficiency, due to central ACTH insufficiency, should not be missed because it is life-threatening (14, 238, 241, 257).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Acute phase
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
- Not checked — no full text of the sourcecites [238] Cohan, 2005, Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study, Crit Care Med source
- Not checked — no full text of the sourcecites [241] Hannon, 2013, Acute glucocorticoid deficiency and diabetes insipidus are common after acute traumatic brain injury and predict mortality, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [257] Cooper, 2007, Adrenal insufficiency in critical illness, J Intensive Care Med source
- Supportedcites [258] Tanriverdi, 2013, Hypopituitarism due to head trauma: new insights into an old story, Erciyes Med J source
The discussion on p. 1 urges clinicians managing critically ill TBI patients to watch for ACTH deficiency and says steroid replacement in affected patients during the acute phase of head trauma would be lifesaving. This supports the warning that acute glucocorticoid deficiency should not be missed. (LLM, conf=0.93)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase · plain
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“published investigating pituitary function during the first 3 months of TBI and 12 months later (15, 27, 149 -151, 181).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [27] Schneider, 2006, Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury, Eur J Endocrinol source
- Supportedcites [149] Agha, 2005, The natural history of post-traumatic hypopituitarism: implications for assessment and treatment, Am J Med source
The Abstract describes this as a prospective study of pituitary function after traumatic brain injury, with assessments in the acute phase and at 12 months. The Method specifies that the acute assessment occurred 7–20 days after injury, within the first three months. This supports citing the paper as one of the prospective studies described; it does not need to establish the total count of six. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [151] Krahulik, 2010, Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults, J Neurosurg source
- Not checked — no full text of the sourcecites [181] Aimaretti, 2005, Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study, J Clin Endocrinol Metab source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Based on the prospective studies evaluating pituitary function, most pituitary hormonal changes (especially FSH/LH, GH, and TSH deficiencies) are transient and recover within 3 to 12 months after injury (15, 25, 149 -151).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Acute phase
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
- Supportedcites [149] Agha, 2005, The natural history of post-traumatic hypopituitarism: implications for assessment and treatment, Am J Med source
The Discussion says that early anterior pituitary abnormalities were transient in some patients and that recovery occurred by 6 months in the majority. The Abstract and Table 2 (p. 1416.e6) show recovery of most acute gonadotropin deficiencies by 12 months, six of nine acute GH deficiencies by 12 months, and the one acute TSH deficiency by 6 months. The paper also reports new or persistent deficiencies, so the claim is supported as a statement about most changes, not all. (LLM, conf=0.87)
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [151] Krahulik, 2010, Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults, J Neurosurg source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“These prospective studies showed the dynamic properties of hypopituitarism in isolated and multiple pituitary deficiencies as well as in the improvement (recovery) or worsening (new-onset hormonal deficiencies) of pituitary function.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [27] Schneider, 2006, Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury, Eur J Endocrinol source
- Supportedcites [149] Agha, 2005, The natural history of post-traumatic hypopituitarism: implications for assessment and treatment, Am J Med source
The prospective study followed pituitary function after traumatic brain injury at the acute phase, 6 months, and 12 months (Abstract). The Discussion describes time-dependent changes: some deficiencies recovered, while some patients with initially normal responses developed new deficiencies. The paper assesses several hormone axes and considers whether deficiencies occur alongside other pituitary abnormalities. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [151] Krahulik, 2010, Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults, J Neurosurg source
- Not checked — no full text of the sourcecites [181] Aimaretti, 2005, Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study, J Clin Endocrinol Metab source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Her hormonal profile was compatible with the recovery from gonadotropin deficiency.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Supportedcites [260] Ruggeri, 2010, Spontaneous recovery from isolated post-traumatic central hypogonadism in a woman, Hormones (Athens) source
In PATIENT'S DESCRIPTION, the paper reports normal FSH, LH and oestradiol values at the later evaluation, alongside the return of spontaneous menstrual cycles. It states that her subsequent pregnancy proved spontaneous recovery of gonadal function, supporting the interpretation of her hormonal profile. (LLM, conf=0.94)
plaincorrelationalSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Although this is a single case report, the findings suggest that pituitary function may recover as long as 12 years after head trauma.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Supportedcites [260] Ruggeri, 2010, Spontaneous recovery from isolated post-traumatic central hypogonadism in a woman, Hormones (Athens) source
The discussion states that spontaneous recovery of ovulation occurred 12 years after the head trauma in this woman with post-traumatic central hypogonadism. The Abstract also reports normalized hormone levels and a pregnancy 12 years after the trauma. (LLM, conf=0.94)
hedgedconditionalSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, until now, only five clinical studies and two case reports have been published regarding the effects of GH replacement due to TBI (272-278).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Not checked — no full text of the sourcecites [272] Bhagia, 2010, Effect of recombinant growth hormone replacement in a growth hormone deficient subject recovering from mild traumatic brain injury: a case report, Brain Inj source
- Partly supportedcites [273] High, 2010, Effect of growth hormone replacement therapy on cognition after traumatic brain injury, J Neurotrauma sourceExperimental — accuracy not yet measured
The Methods describe this paper's randomized trial of GH replacement after TBI, so it is an example of a clinical study cited in the sentence. The Introduction calls the literature scant, and the Discussion mentions other studies and a case report, but neither section establishes the claimed total of five clinical studies and two case reports. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites [274] Kreitschmann-Andermahr, 2008, Growth hormone deficient patients after traumatic brain injury–baseline characteristics and benefits after growth hormone replacement–an analysis of the German KIMS database, Growth Horm IGF Res source
- Not checked — no full text of the sourcecites [275] Maric, 2010, Psychiatric and neuropsychological changes in growth hormone-deficient patients after traumatic brain injury in response to growth hormone therapy, J Endocrinol Invest source
- Not checked — no full text of the sourcecites [276] Moreau, 2013, Growth hormone replacement therapy in patients with traumatic brain injury, J Neurotrauma source
- Not checked — no full text of the sourcecites [277] Reimunde, 2011, Effects of growth hormone (GH) replacement and cognitive rehabilitation in patients with cognitive disorders after traumatic brain injury, Brain Inj source
- Not checked — no full text of the sourcecites [278] Tanriverdi, 2010, Hypopituitarism due to sports related head trauma and the effects of growth hormone replacement in retired amateur boxers, Pituitary source
plainn = 2- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Current data show that GH replacement seems to have beneficial effects in TBI patients as in those with other causes of GHD in adults.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Supportedcites [273] High, 2010, Effect of growth hormone replacement therapy on cognition after traumatic brain injury, J Neurotrauma source
The Discussion reports improvements in cognitive measures after GH replacement in people with GHD following TBI and says the findings are consistent with literature on GHD from other causes. It also describes cognitive improvements with replacement therapy in adults whose GHD was not caused by TBI. The claim’s cautious wording fits the paper’s preliminary, small-sample findings. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [274] Kreitschmann-Andermahr, 2008, Growth hormone deficient patients after traumatic brain injury–baseline characteristics and benefits after growth hormone replacement–an analysis of the German KIMS database, Growth Horm IGF Res source
- Not checked — no full text of the sourcecites [275] Maric, 2010, Psychiatric and neuropsychological changes in growth hormone-deficient patients after traumatic brain injury in response to growth hormone therapy, J Endocrinol Invest source
- Not checked — no full text of the sourcecites [276] Moreau, 2013, Growth hormone replacement therapy in patients with traumatic brain injury, J Neurotrauma source
- Not checked — no full text of the sourcecites [277] Reimunde, 2011, Effects of growth hormone (GH) replacement and cognitive rehabilitation in patients with cognitive disorders after traumatic brain injury, Brain Inj source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Furthermore, the GH replacement literature suggests that at least some of these deficits may be amenable to treatment.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Supportedcites [273] High, 2010, Effect of growth hormone replacement therapy on cognition after traumatic brain injury, J Neurotrauma source
The Conclusion says that some cognitive impairments after moderate to severe TBI may result from GH deficiency and could potentially be partially reversible with GH replacement therapy. The Discussion also reports improvements in several cognitive domains following GH replacement. This supports the citing sentence’s cautious claim. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites [274] Kreitschmann-Andermahr, 2008, Growth hormone deficient patients after traumatic brain injury–baseline characteristics and benefits after growth hormone replacement–an analysis of the German KIMS database, Growth Horm IGF Res source
- Not checked — no full text of the sourcecites [275] Maric, 2010, Psychiatric and neuropsychological changes in growth hormone-deficient patients after traumatic brain injury in response to growth hormone therapy, J Endocrinol Invest source
- Not checked — no full text of the sourcecites [276] Moreau, 2013, Growth hormone replacement therapy in patients with traumatic brain injury, J Neurotrauma source
- Not checked — no full text of the sourcecites [277] Reimunde, 2011, Effects of growth hormone (GH) replacement and cognitive rehabilitation in patients with cognitive disorders after traumatic brain injury, Brain Inj source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Although the gains are modest, the findings from studies on the effects of GH replacement on neurocogni-tive/neuropsychological functions and quality of life provide promise as a treatment for cognitive impairment after brain injury (273-277).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Supportedcites [273] High, 2010, Effect of growth hormone replacement therapy on cognition after traumatic brain injury, J Neurotrauma source
The Conclusion says cognitive impairments after moderate-to-severe TBI could potentially be partially reversible with GH replacement, and the Discussion reports improvements in several cognitive domains. The Discussion also reports improved quality of life in other post-TBI studies, while noting that this study did not find an improvement on its own quality-of-life measure. Together, these passages support the citing sentence’s cautious, collective claim of promise. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [274] Kreitschmann-Andermahr, 2008, Growth hormone deficient patients after traumatic brain injury–baseline characteristics and benefits after growth hormone replacement–an analysis of the German KIMS database, Growth Horm IGF Res source
- Not checked — no full text of the sourcecites [275] Maric, 2010, Psychiatric and neuropsychological changes in growth hormone-deficient patients after traumatic brain injury in response to growth hormone therapy, J Endocrinol Invest source
- Not checked — no full text of the sourcecites [276] Moreau, 2013, Growth hormone replacement therapy in patients with traumatic brain injury, J Neurotrauma source
- Not checked — no full text of the sourcecites [277] Reimunde, 2011, Effects of growth hormone (GH) replacement and cognitive rehabilitation in patients with cognitive disorders after traumatic brain injury, Brain Inj source
hedgedconditionaln = 11- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Thus, 1203 patients remained (Table 3).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > C. Prevalence and incidence of hypopituitarism after brain injury
plainn = 1,203- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Most studies used only one simulation test for the GH and/or ACTH axes;”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Results
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Within the 16 studies, there was heterogeneity regarding TBI severity.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Results
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There was also heterogeneity regarding the tests used and preselection procedures for testing.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Results
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In these six studies, a total of 1563 eligible patients were invited to participate.From these eligible patients, 645 patients participated, representing a response rate of 41%.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Results
plainn = 645- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“According to the combined tests, the pooled prevalence of GHD was 11.1 and 1.3% in patients and controls, respectively (P Ͻ .001).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > D. Is hypopituitarism more common after brain damage than in the normal population?
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“The pooled prevalence of abnormal results suggesting ACTH deficiency was 14.1 and 6.6% in patients and controls, respectively (P ϭ .12).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > D. Is hypopituitarism more common after brain damage than in the normal population?
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Moreover, in very recent data from our clinic including 129 patients, we have shown that by using appropriate cutoff values, the reliability and efficacy of GST and ITT are similar (229).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Somatotroph axis
What the sources say
- Not checked — no full text of the sourcecites [229] Simsek, 2015, A comparison of low-dose ACTH, glucagon stimulation and insulin tolerance test in patients with pituitary disorders, Clin Endocrinol (Oxf) source
plainn = 129- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total N | 313 | 37 | 21 | 34 | 4 | 62 | 12 |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total % | 100.0 | 11.8 | 6.7 | 10.9 | 1.3 | 19.8 | 3.8 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 313- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § X. Summary and Future Directions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total TBI, n | 1203 | 156 | 123 | 142 | 51 | 315 | 70 | |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total TBI, % | 100.0% 13.0% 10.2% 11.8% 4.2% 27.8% | 6.2% | | | | | | |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 1,203- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § X. Summary and Future Directions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total TBI, n | 1203 | 156 | 123 | 142 | 51 | 315 | 70 | |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total TBI, % | 100.0% 13.0% 10.2% 11.8% 4.2% 27.8% | 6.2% | | | | | | |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 1,203- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § X. Summary and Future Directions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total TBI, n | 1203 | 156 | 123 | 142 | 51 | 315 | 70 | |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total TBI, % | 100.0% 13.0% 10.2% 11.8% 4.2% 27.8% | 6.2% | | | | | | |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 1,203- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § X. Summary and Future Directions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total N | 313 | 27 | 14 | 19 | 3 | 46 | 12 |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total % | 100.0 | 8.6 | 4.5 | 6.1 | 1.0 | 14.7 | 3.8 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 313- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § X. Summary and Future Directions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total TBI all GCS, n | 957 | 144 | 81 | 129 | 39 | 255 | 50 | |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total TBI all GCS, % | 100.0% 15.0% 8.5% | 13.5% 4.1% 28.8% | 5.6% | | | | | |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 957- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § X. Summary and Future Directions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total N | 313 | 37 | 21 | 34 | 4 | 62 | 12 |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total % | 100.0 | 11.8 | 6.7 | 10.9 | 1.3 | 19.8 | 3.8 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 313- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § X. Summary and Future Directions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Days of coma | 14.0 Ϯ 2.7 | 1.8 Ϯ 0.8 | Ͻ.003 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Dyslipidemia, % (n) | 12.8 (6) | 46.7 (7) | Ͻ.01 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Altered glucose, % (n) | 2.6 (1) | 33.3 (5) | Ͻ.005 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Age, y | 37.1 Ϯ 2.5 | 46.4 Ϯ 3.7 | Ͻ.02 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total TBI GCS Յ 8, n | 246 | 12 | 42 | 13 | 12 | 60 | 20 | |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 246- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total N | 313 | 27 | 14 | 19 | 3 | 46 | 12 |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total % | 100.0 | 8.6 | 4.5 | 6.1 | 1.0 | 14.7 | 3.8 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 313- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § X. Summary and Future Directions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total TBI, n | 1203 | 156 | 123 | 142 | 51 | 315 | 70 | |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total TBI, % | 100.0% 13.0% 10.2% 11.8% 4.2% 27.8% | 6.2% | | | | | | |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 1,203- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § X. Summary and Future Directions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Gender (M/F), n | 24/15 | 14/1 | Ͻ.01 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Epilepsy, % (n) | 23.7 (9) | 6.7 (1) | Ͻ.03 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| HOMA-IR | 3.4 Ϯ 0.2 | 4.8 Ϯ 0.8 | Ͻ.02 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Triglycerides, mg/dL | 98.0 Ϯ 16.8 | 161.3 Ϯ 29.3 | Ͻ.05 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In addition, two preliminary studies reported a high prevalence of hypopituitarism after TBI (13,18).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > II. Prevalence of Chronic Posttraumatic Anterior Pituitary Dysfunction in Adults
What the sources say
- Not checked — no full text of the sourcecites [13] Lieberman, 2001, Prevalence of neuroendocrine dysfunction in patients recovering from traumatic brain injury, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [18] Kelly, 2000, Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report, J Neurosurg source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“TBI was recognized as a potential cause of hypopituitarism after a review summarized the literature on 367 cases of posttraumatic hypopituitarism (12).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > II. Prevalence of Chronic Posttraumatic Anterior Pituitary Dysfunction in Adults
What the sources say
- Not checked — no full text of the sourcecites [12] Benvenga, 2000, Clinical review 113: hypopituitarism secondary to head trauma, J Clin Endocrinol Metab source
plaindirectn = 367- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The frequency of hypopituitarism after TBI varies widely among different studies (15-50% of the patients with TBI in most studies).”
- Also stated in: § I. Introduction · plain
“Although the frequency of hypopituitarism after TBI varies widely in published reports, this finding at most reports a range of 15-50% of the patients with TBI (14,15).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > Abstract
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § I. Introduction · plain
In the paper
“In 2007, a systematic review was performed to summarize the literature, suggesting that neuroendocrine dysfunction was common after TBI (14).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > II. Prevalence of Chronic Posttraumatic Anterior Pituitary Dysfunction in Adults
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Other studies questioned these results by reporting a lower prevalence of hypopituitarism after brain damage (28 vs 5% [19] to 30% [20]).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > II. Prevalence of Chronic Posttraumatic Anterior Pituitary Dysfunction in Adults
What the sources say
- Not checked — no full text of the sourcecites [19] Kokshoorn, 2010, Hypopituitarism following traumatic brain injury: prevalence is affected by the use of different dynamic tests and different normal values, Eur J Endocrinol source
- Not checked — no full text of the sourcecites [20] Bavisetty, 2008, Chronic hypopituitarism after traumatic brain injury: risk assessment and relationship to outcome, Neurosurgery source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Of the patients, 27.3% had at least one anterior pituitary hormone deficiency.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked — no full text of the sourcecites [38] Tanriverdi, 2007, Kickboxing sport as a new cause of traumatic brain injury-mediated hypopituitarism, Clin Endocrinol (Oxf) source
plainn = 22- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These two studies suggest that blast injury may cause hypopituitarism at least 12 months after the event.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > E. Hypopituitarism after blast-related TBI
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Tanriverdi et al (59) measured pituitary functions within 24 hours of trauma in a sample of 104 patients with TBI.They found that there was a positive relationship between cortisol levels and the GCS: the less severe injuries were associated with higher cortisol levels.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Cortisol
What the sources say
- Not checked — no full text of the sourcecites [59] Tanriverdi, 2007, Pituitary functions in the acute phase of traumatic brain injury: are they related to severity of the injury or mortality?, Brain Inj source
plaincorrelationaln = 104- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In other words, eight of the 17 retired boxers (47%) had GHD.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked — no full text of the sourcecites [46] Tanriverdi, 2008, Brief communication: pituitary volume and function in competing and retired male boxers, Ann Intern Med source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, boxers and kickboxers are at risk of hypopituitarism.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > C. Prevention of sports-related neuroendocrine dysfunction
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Sustained, increased levels of neuron-specific enolase in amateur boxers suggest subacute brain injury due to repetitive head blows.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Definition of sports-related traumatic brain injury
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Body composition variables, including fat ratio, fat mass, abdominal fat ratio, abdominal fat mass, body mass index (BMI), and waist circumference, were significantly higher in boxers with GHD when compared with GH-normal boxers.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked — no full text of the sourcecites [46] Tanriverdi, 2008, Brief communication: pituitary volume and function in competing and retired male boxers, Ann Intern Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, boxing and kickboxing are novel causes of hypopituitarism.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > C. Prevention of sports-related neuroendocrine dysfunction
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Interestingly, pituitary volume in GH-deficient boxers was significantly lower than pituitary volume in GH-normal boxers.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked — no full text of the sourcecites [46] Tanriverdi, 2008, Brief communication: pituitary volume and function in competing and retired male boxers, Ann Intern Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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In the paper
“Presently, the issue of cognitive changes with sex hormone supplementation or replacement remains unresolved (66).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Gonadotropins
What the sources say
- Not checked — no full text of the sourcecites [66] Moffat, 2005, Effects of testosterone on cognitive and brain aging in elderly men, Ann NY Acad Sci source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“however, studies on cognitive improvement after estrogen supplementation in females have yielded conflicting results (63,64).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Gonadotropins
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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In the paper
“For example, in a study by Zetterberg et al (43), neuron-specific enolase (NSE), a glycolytic enzyme expressed selectively in neurons, was significantly increased after boxing when compared to normal controls.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Definition of sports-related traumatic brain injury
What the sources say
- Not checked — no full text of the sourcecites [43] Zetterberg, 2009, Sustained release of neuron-specific enolase to serum in amateur boxers, Brain Inj source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Hypothyroid patients typically demonstrate the types of deficits so commonly seen after TBI, such as in executive functioning, speed of information processing, and aspects of memory, predominantly short-term memory (55).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Thyroid hormone
What the sources say
- Not checked — no full text of the sourcecites [55] Denicoff, 1990, Neuropsychiatric manifestations of altered thyroid state, Am J Psychiatry source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Similarly, peak GH levels after GHRHϩ GHRP-6 stimulation correlated negatively with boxing duration and number of bouts.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked — no full text of the sourcecites [37] Kelestimur, 2004, Boxing as a sport activity associated with isolated GH deficiency, J Endocrinol Invest source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, the results of these two studies suggest that factors associated with injury severity are antagonistic to an elevated cortisol response.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Cortisol
hedgeddirectn = 104- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The diagnosis and treatment of posttraumatic hypopituitarism may, therefore, play a significant role in the cognitive recovery from a brain injury.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Cognitive impairment after TBI: what is the contribution of pituitary dysfunction?
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Clearly, the common cognitive symptoms after a TBI are quite similar to the cognitive symptoms of hypothyroidism.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Thyroid hormone
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“however, there are no clear data regarding thyroid hormone replacement and cognitive outcomes in TBI patients.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Thyroid hormone
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“IGF-1 levels were found to be significantly lower in retired boxers than in actively competing young and adult competitors.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked yetcites [47] Tanriverdi, 2008, Body composition, serum IGF-1 and leptin level changes in amateur boxers: retired boxers have risk factors for cardiovascular disorders, Obes Metab
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“This study clearly shows that the low IGF-1 levels, which were negatively correlated with body composition variables in retired boxers, could be responsible for abnormal anthropometric and body composition parameters (47).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked yetcites [47] Tanriverdi, 2008, Body composition, serum IGF-1 and leptin level changes in amateur boxers: retired boxers have risk factors for cardiovascular disorders, Obes Metab
boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“GH appears to affect cognitive functioning by enhancing excitatory synaptic transmission through the N-methyl-D-aspartate receptors in the hippocampus (67).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [67] Le Grevès, 2006, Growth hormone replacement in hypophysectomized rats affects spatial performance and hippocampal levels of NMDA receptor subunit and PSD-95 gene transcript levels, Exp Brain Res source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“These results must be interpreted cautiously, however, because there was no indication that injury severity was similar across groups.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [73] León-Carrión, 2007, Cognitive deterioration due to GH deficiency in patients with traumatic brain injury: a preliminary report, Brain Inj source
plainn = 22- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Greater cognitive dysfunction has been reported in patients with TBI who have GHD compared to those with normal GH levels (71).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [71] Kelly, 2006, Neurobehavioral and quality of life changes associated with growth hormone insufficiency after complicated mild, moderate, or severe traumatic brain injury, J Neurotrauma source
hedgedcorrelationaln = 44- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“These data are supported by evidence that GHD is the most common pituitary defect in TBI, either isolated or associated with other deficiencies.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“GH also modulates brain neurotransmitters (68) and may play a role in recovery from TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [68] Burman, 1996, Growth hormone treatment affects brain neurotransmitters and thyroxine, Clin Endocrinol (Oxf) source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, there is a rapidly growing body of literature suggesting that hypopituitarism after TBI indeed has a negative impact on cognition.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
In the paper
“In fact, GHD has been demonstrated to interfere with cognitive functioning in individuals with nontraumatic conditions (70).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [70] Falleti, 2006, The effects of growth hormone (GH) deficiency and GH replacement on cognitive performance in adults: a meta-analysis of the current literature, Psychoneuroendocrinology source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In view of the risk for premature cardiovascular death in patients with hypopituitarism (77,88), major attention should be paid to those who encounter TBI because they suffer from the same comorbidities and may present other deterioration factors due to pharmacological treatments and restriction in participation in life activities and a healthy lifestyle.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [77] Tomlinson, 2001, Association between premature mortality and hypopituitarism. West Midlands Prospective Hypopituitary Study Group, Lancet source
- Not checked — no full text of the sourcecites [88] Rosén, 1990, Premature mortality due to cardiovascular disease in hypopituitarism, Lancet source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although growing at a more moderate pace, the body of literature suggests that treatment of posttraumatic hypopituitarism has a positive effect on the cognitive problems associated with TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
In the paper
“GH also modulates brain neurotransmitters (68) and may play a role in recovery from TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [68] Burman, 1996, Growth hormone treatment affects brain neurotransmitters and thyroxine, Clin Endocrinol (Oxf) source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“More recently, Prodam et al (81), in a cross-sectional retrospective study in a tertiary care endocrinology center, confirmed that TBI patients who developed hypopituitarism had a worse metabolic profile than TBI patients who did not, particularly in terms of altered glucose levels, insulin resistance, and dyslipidemia, independent of the BMI of the patients (Table 6).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [81] Prodam, 2013, Metabolic alterations in patients who develop traumatic brain injury (TBI)-induced hypopituitarism, Growth Horm IGF Res source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“It should be taken into account that HDL cholesterol is mainly influenced by physical activity (89), and physical limitations and prolonged recovery are specific for TBI patients.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [89] Barter, 2011, Raising HDL-C can be achieved by both lifestyle changes and pharmacological means. Introduction, Atheroscler Suppl source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Consistent with impaired cognitive performance, P300 amplitudes were found to be significantly lower in GH-deficient boxers and kickboxers when compared with GH-sufficient boxers and kickboxers and healthy controls (72).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [72] Tanriverdi, 2013, Growth hormone deficiency due to sports-related head trauma is associated with impaired cognitive performance in amateur boxers and kickboxers as revealed by P300 auditory event-related potentials, Clin Endocrinol (Oxf) source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, TBI patients with hypopituitarism frequently present metabolic alterations, particularly in terms of altered glucose levels, insulin resistance, and hypertriglyceridemia.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The second finding is the high prevalence of fasting or postchallenge glucose alterations.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [81] Prodam, 2013, Metabolic alterations in patients who develop traumatic brain injury (TBI)-induced hypopituitarism, Growth Horm IGF Res source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In fact, the cardiovascular risk in patients with hypopituitarism without any GH treatment was the main reason that prompted researchers also to propose this substitutive therapy in adults (88).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [88] Rosén, 1990, Premature mortality due to cardiovascular disease in hypopituitarism, Lancet source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“After an injury to the brain, IGF-1 has also been found to increase progenitor cell proliferation and new neurons, oligodendrocytes, and blood vessels in the dentate gyrus of the hippocampus (69).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [69] Aberg, 2006, Aspects of growth hormone and insulin-like growth factor-I related to neuroprotection, regeneration, and functional plasticity in the adult brain, Scientific World J source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Furthermore, the above-mentioned events lead to membrane degradation of the cellular and vascular structures and eventually to necrosis or apoptosis of neurons (97,129,130).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [97] Werner, 2007, Pathophysiology of traumatic brain injury, Br J Anaesth source
- Not checked — no full text of the sourcecites [129] Nathoo, 2004, Influence of apoptosis on neurological outcome following traumatic cerebral contusion, J Neurosurg source
- Not checked — no full text of the sourcecites [130] Uzan, 2006, Evaluation of apoptosis in cerebrospinal fluid of patients with severe head injury, Acta Neurochir (Wien) source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Moreover, TBI induces inflammatory/immunological tissue responses (neuroinflammation) similar to ischemic reperfusion injury.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In another histopathological study that included 42 patients who died after a motor vehicle accident, acute infarction was confirmed as the underlying adenohypophyseal pathology in those patients with TBI who did not die promptly after the trauma.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [144] Salehi, 2007, Histologic study of the human pituitary gland in acute traumatic brain injury, Brain Inj source
plaindirectn = 42- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Several autopsy studies demonstrated that anterior pituitary necrosis is more frequent in patients who died within 1 week after head trauma (139, 142, 144).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [139] Ceballos, 1966, Pituitary changes in head trauma (analysis of 102 consecutive cases of head injury), Ala J Med Sci
- Not checked — no full text of the sourcecites [142] Kornblum, 1969, Pituitary lesions in craniocerebral injuries, Arch Pathol
- Not checked — no full text of the sourcecites [144] Salehi, 2007, Histologic study of the human pituitary gland in acute traumatic brain injury, Brain Inj source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These histopathological findings suggest that in patients who survived for a couple of days after TBI, secondary insults, including increased ICP and ischemic/hypoxic damage may account for a portion of pituitary and hypothalamic lesions.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
hedgedconditionaln = 30- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Both primary and secondary insults may activate the release of proinflammatory mediators (cytokines or chemokines), prostaglandins, free radicals, and complement.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Previous neuropathological studies, including a total of 638 cases after TBI have demonstrated a high frequency of 26 to 86% hypothalamo-pituitary damage in patients who died after head trauma.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
boostedcorrelationaln = 638- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The brain injury outcome of TBI is determined by two significantly different stages/pathophysiological mechanisms.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In the chronic phase after TBI, Schneider et al (159) demonstrated that 80% of patients with TBI-induced hypopituitarism had at least one radiological anomaly, including decreased pituitary volume or empty sella, abnormal pituitary gland signal heterogeneity, and perfusion deficits.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [159] Schneider, 2007, Pituitary imaging abnormalities in patients with and without hypopituitarism after traumatic brain injury, J Endocrinol Invest source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Autoimmunity may also explain the late appearance of pituitary dysfunction in some TBI patients in whom pituitary function was normal at the beginning but who developed pituitary dysfunction some years after TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Nevertheless, pituitary hormone levels were not reported.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Interestingly, in all patients who had persistent pituitary hormone deficiency from the third year to the fifth year, strong positivity of APA and/or AHA was present in the third year (16).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Moreover, in clinical studies including patients who survived after TBI, acute radiological findings (specifically DAI, basal skull fracture, diffuse brain swelling, evacuated intracerebral hematoma, or multiple contusions on cranial CT or MRI) were shown to be associated with hypopituitarism at least 6 months after the head trauma (18, 20, 154 -156).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [18] Kelly, 2000, Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report, J Neurosurg source
- Not checked — no full text of the sourcecites [20] Bavisetty, 2008, Chronic hypopituitarism after traumatic brain injury: risk assessment and relationship to outcome, Neurosurgery source
- Not checked — no full text of the sourcecites [154] Bondanelli, 2004, Occurrence of pituitary dysfunction following traumatic brain injury, J Neurotrauma source
- Not checked — no full text of the sourcecites [155] Jeong, 2010, Negative effect of hypopituitarism following brain trauma in patients with diffuse axonal injury, J Neurosurg source
- Not checked — no full text of the sourcecites [156] Schneider, 2008, Predictors of anterior pituitary insufficiency after traumatic brain injury, Clin Endocrinol (Oxf) source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“However, despite abnormal pituitary functions in patients with TBI, MRI may fail to reveal any abnormalities (157).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [157] Makulski, 2008, Neuroimaging in posttraumatic hypopituitarism, J Comput Assist Tomogr source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Regarding the pathophysiology of TBI-induced chronic hypopituitarism, the vascular hypothesis is supported by some clinical and radiological studies.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
plaincorrelational- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Most of the acute phase pituitary hormonal changes, such as decreased gonadotropins (FSH and/or LH) and TSH, but increased hypothalamic-pituitary-adrenal (HPA) axis activity, may simply represent adaptive physiological responses to critical illness.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The second line of evidence that supports a vascular etiology for chronic hypopituitarism after TBI is related to the pattern of hormonal loss.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
plaincorrelational- Asserted: passes — The authors put it forward as true.
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, the relation between pathological findings and hormonal consequences was unknown.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, it is difficult to generalize about these histopathological findings for nonfatal TBI to explain the chronic hypopituitarism in survivors.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
plainn = 30- Asserted: passes — The authors put it forward as true.
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In the paper
“First, recent radiological imaging studies of the hypothalamo-pituitary region after TBI have demonstrated several pathological changes consistent with vascular injury (136).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [136] Maiya, 2008, Magnetic resonance imaging changes in the pituitary gland following acute traumatic brain injury, Intensive Care Med source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“There were significant associations between the presence of strongly positive APA and/or AHA and hypopituitarism in the fifth year of TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
plaincorrelationaln = 25- Asserted: passes — The authors put it forward as true.
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In the paper
“Additionally, higher APA titers were shown to be associated with lower GH response to the GHRHϩGHRP-6 test (161).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plaincorrelationaln = 29- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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In the paper
“In an early histopathological study, it was demonstrated that the injured portal vessels can regenerate (mitotic figures among the surviving cells have been documented) and grow down into the surviving areas of the anterior lobe (132).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [132] Daniel, 1959, Traumatic infarction of the anterior lobe of the pituitary gland, Lancet source
boosted- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These studies are in favor of the role of autoimmunity in the development of chronic hypopituitarism after TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
plainconditionaln = 25- Asserted: passes — The authors put it forward as true.
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In the paper
“Activation of the IGF-1 receptor antiapoptotic pathway by mild TBI could be a part of a neuroprotective process for maintaining normal brain function (184).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [184] Rubovitch, 2010, The intricate involvement of the insulin-like growth factor receptor signaling in mild traumatic brain injury in mice, Neurobiol Dis source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“APO E has also been shown to reduce the neuroinflammatory response in vitro and in vivo in an isoform-specific fashion (171).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [171] Laskowitz, 1997, Apolipoprotein E suppresses glial cell secretion of TNF α, J Neuroimmunol source
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In addition, microvascular and microstructural changes have also been documented, especially in mild TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
In the paper
“The APO E4 isoform has been shown to be less effective than the APO E3 isoform in inhibiting inflammatory cytokines, both in the peripheral circulation and in the brain (172).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [172] Laskowitz, 2001, Downregulation of microglial activation by apolipoprotein E and apoE-mimetic peptides, Exp Neurol source
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Recent clinical and experimental data have indicated the possible role of autoimmunity and genetic predisposition in the development of TBI-induced hypopituitarism.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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- Based: unclear — It is unclear why the paper says it holds.
In the paper
“Several pathological alterations were detected in the median eminence as follows: 1) the barrier properties of tanycytes were compromised by the disruption of tight junctions; 2) endogenous IgG was increased near the third ventricle; and 3) increased permeability of the third ventricle.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [177] Osterstock, 2014, Sustained alterations of hypothalamic tanycytes during posttraumatic hypopituitarism in male mice, Endocrinology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, due to the anatomical localization of the pituitary gland, stalk, and hypothalamus, and because the long hypophyseal portal vessels pass through the diaphragma sellae, they are particularly vulnerable to direct mechanical trauma, ischemic changes, and edema compression.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“An increase in Evans Blue dye extravasation in the pituitary gland was observed, which implies that a vascular event occurred, supporting the vascular hypothesis in the pathogenesis (175).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [175] Greco, 2013, The effects of repeat traumatic brain injury on the pituitary in adolescent rats, J Neurotrauma source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“Early pathological changes in the cellular and microvascular structures of the brain may be detected by diffusion tensor imaging in boxers (40).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [40] Zhang, 2003, Increased diffusion in the brain of professional boxers: a preclinical sign of traumatic brain injury?, AJNR Am J Neuroradiol
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Extensive experimental data in animal models indicate that repetitive minor head trauma with axonal damage increases the brain's vulnerability for additional concussive impacts (173, 174).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [173] Barkhoudarian, 2011, The molecular pathophysiology of concussive brain injury, Clin Sports Med source
- Not checked — no full text of the sourcecites [174] Laurer, 2001, Mild head injury increasing the brain's vulnerability to a second concussive impact, J Neurosurg source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This model of repetitive mild TBI documented significant acute and chronic suppression of GH and IGF-1 levels, suggesting that a cumulative effect may occur that results in the disruption of the GH/IGF-1 axis.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The diagnosis of TBI-induced hypopituitarism, defined as the deficient hormone secretion of one or more pituitary hormones because of TBI, is made similarly to the diagnosis of classical hypopituitarism because of hypothalamic or pituitary diseases.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Introduction
What the sources say
- Not checked — no full text of the sourcecites [194] Schneider, 2007, Hypopituitarism, Lancet source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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In the paper
“Therefore, GH and IGF-1 may play a crucial role in brain repair mechanisms or neuronal recovery after trauma by regulating factors including neuronal plasticity, myelin formation, and vascular tone (69,(185)(186)(187)(188)(189).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not matchedcites 69,(185)(186)(187)(188)(189)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
In the paper
“The ratio of pituitary dysfunction was significantly lower in subjects with APO E3/E3 (17.7%) than in subjects without the APO E3/E3 genotype (41.9%) (P ϭ .01;odds ratio ϭ 0.29) (163).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [163] Tanriverdi, 2008, Apolipoprotein E3/E3 genotype decreases the risk of pituitary dysfunction after traumatic brain injury due to various causes: preliminary data, J Neurotrauma source
plaincorrelationaln = 3 ·- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, the vascular hypothesis is currently one of the strong hypotheses for the pathogenesis of chronic hypopituitarism after TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“GH levels were impaired at 1 month after head trauma, suggesting a similarity between new-onset hormone deficiencies (delayed pituitary hormone deficiency long term after TBI) in human studies (16,161,181).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [177] Osterstock, 2014, Sustained alterations of hypothalamic tanycytes during posttraumatic hypopituitarism in male mice, Endocrinology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Several pathological alterations were detected in the median eminence as follows: 1) the barrier properties of tanycytes were compromised by the disruption of tight junctions; 2) endogenous IgG was increased near the third ventricle; and 3) increased permeability of the third ventricle.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [177] Osterstock, 2014, Sustained alterations of hypothalamic tanycytes during posttraumatic hypopituitarism in male mice, Endocrinology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“It was reported that the IGF-1 levels were significantly decreased at both 7 days and 3 weeks after TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [178] Ozdemir, 2012, Relationship between circulating IGF-1 levels and traumatic brain injury-induced hippocampal damage and cognitive dysfunction in immature rats, Neurosci Lett source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Despite exposure to a similar severity of head trauma, some people develop pituitary dysfunction whereas others do not, suggesting individual susceptibility.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, this novel mechanism may partially explain the development of autoantibodies after head trauma and TBI-induced hypopituitarism with normal pituitary gland and pituitary stalk.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Head trauma may trigger an ongoing cascade of vascular and histopathological alterations involving mediators of inflammation (persistent neuroinflammation), particularly in individuals who have a genetic predisposition.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
In the paper
“Several pathological alterations were detected in the median eminence as follows: 1) the barrier properties of tanycytes were compromised by the disruption of tight junctions; 2) endogenous IgG was increased near the third ventricle; and 3) increased permeability of the third ventricle.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [177] Osterstock, 2014, Sustained alterations of hypothalamic tanycytes during posttraumatic hypopituitarism in male mice, Endocrinology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The authors showed that the somatotropes were considerably regenerated during the months after injury, suggesting recovery of somatotropes from stem/progenitor cells (190).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [190] Fu, 2012, The adult pituitary shows stem/progenitor cell activation in response to injury and is capable of regeneration, Endocrinology source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, the dynamic hormonal changes (new-onset hormonal deficiencies or recovery, especially in mild TBI) during the long-term prospective follow-up of TBI patients cannot be completely explained by the vascular hypothesis.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In mild TBI and sports-related repetitive head trauma, concussion resulting in DAI, due to rotational and shearing forces, can also affect hypothalamo-pituitary functions.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“GH levels were impaired at 1 month after head trauma, suggesting a similarity between new-onset hormone deficiencies (delayed pituitary hormone deficiency long term after TBI) in human studies (16,161,181).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [181] Aimaretti, 2005, Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study, J Clin Endocrinol Metab source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Moreover, it was demonstrated that decreased IGF-1 levels were closely associated with hippocampal neuronal loss and spatial memory deficits (178).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [178] Ozdemir, 2012, Relationship between circulating IGF-1 levels and traumatic brain injury-induced hippocampal damage and cognitive dysfunction in immature rats, Neurosci Lett source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In a recent meta-analysis including 27 studies evaluating at least one potential predictor of TBI-induced hypopituitarism, the injury severity according to postresuscitation GCS was significantly associated with an increased risk of long-term hypopituitarism (Ն12 mo after TBI).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [234] Lauzier, 2014, Clinical outcomes, predictors, and prevalence of anterior pituitary disorders following traumatic brain injury: a systematic review, Crit Care Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In conclusion, acute phase radiological findings (specifically DAI, basal skull fracture, diffuse brain swelling, evacuated intracerebral hematoma, or multiple contusions on cranial CT or MRI) seem to be valuable for predicting hypopituitarism during the chronic phase of TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“It has to be borne in mind that no test, including the ITT, can classify all subjects correctly (194, 199, 206 -209).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. HPA axis
What the sources say
- Not checked — no full text of the sourcecites [194] Schneider, 2007, Hypopituitarism, Lancet source
- Not checked — no full text of the sourcecites [199] Arlt, 2003, Adrenal insufficiency, Lancet source
- Not checked — no full text of the sourcecites [206] Mayenknecht, 1998, Comparison of low and high dose corticotropin stimulation tests in patients with pituitary disease, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [207] Nye, 2001, Adrenocorticotropin stimulation tests in patients with hypothalamic-pituitary disease: low dose, standard high dose and 8-h infusion tests, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [208] Soule, 2000, The low dose ACTH stimulation test is less sensitive than the overnight metyrapone test for the diagnosis of secondary hypoadrenalism, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [209] Suliman, 2002, The low-dose ACTH test does not provide a useful assessment of the hypothalamic-pituitary-adrenal axis in secondary adrenal insufficiency, Clin Endocrinol (Oxf) source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In conclusion, for the diagnosis of GHD in TBI patients, we need to consider that none of the tests for the assessment of GHD are totally reliable.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Somatotroph axis
plainn = 129- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In most studies, no significant associations between TBI severity according to postresuscitation GCS and hypopituitarism in the chronic phase have been reported (15, 23, 24, 27, 29, 181, 231-233), whereas others have demonstrated that hypopituitarism was more frequent in patients with more severe TBI (18,30,154).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [18] Kelly, 2000, Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report, J Neurosurg source
- Not checked — no full text of the sourcecites [30] Klose, 2007, Prevalence and predictive factors of post-traumatic hypopituitarism, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [154] Bondanelli, 2004, Occurrence of pituitary dysfunction following traumatic brain injury, J Neurotrauma source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, the GH response to GHRHϩARG, and to all known GH provocative stimuli, significantly declines with increasing BMI in adults (221, 222); thus, the use of a non-BMI-related cutoff in obese subjects causes a high percentage of false-positive results (203).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Somatotroph axis
What the sources say
- Not checked — no full text of the sourcecites [203] Schneider, 2006, Discrepant results in the diagnosis of GH deficiency with the insulin-tolerance test and the GHRH plus arginine test in patients with traumatic brain injury, Eur J Endocrinol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“For the diagnosis of TBI-induced GHD, the ITT and the GHRHϩARG test are now considered as the tests of choice with similar accuracy (194,215).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Somatotroph axis
What the sources say
- Not checked — no full text of the sourcecites [194] Schneider, 2007, Hypopituitarism, Lancet source
- Not checked — no full text of the sourcecites [215] Molitch, 2011, Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society clinical practice guideline, J Clin Endocrinol Metab source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In a small retrospective study, the MRI or CT scans of 22 patients were evaluated long term after TBI (mean time, nearly 17 Ϯ 15 y); abnormalities (the most common abnormality was loss of volume or empty sella) in the pituitary region were found in 80% of patients with TBI, and hypopituitarism compared with only 29% of patients without hypopituitarism (159).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [159] Schneider, 2007, Pituitary imaging abnormalities in patients with and without hypopituitarism after traumatic brain injury, J Endocrinol Invest source
plaincorrelationaln = 22- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The glucagon stimulation test (GST) (1 mg glucagon im, GH measurements every 30 min until 240 min after administration) has been proposed as an alternative diagnostic because it is able to differentiate between GH-deficient and healthy subjects with a sensitivity and specificity of 100% if a peak GH of 3 g/L is considered (215, 226).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Somatotroph axis
What the sources say
- Not checked — no full text of the sourcecites [215] Molitch, 2011, Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society clinical practice guideline, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [226] Gómez, 2002, Growth hormone release after glucagon as a reliable test of growth hormone assessment in adults, Clin Endocrinol (Oxf) source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In an article analyzing MRI as a neuroimaging method in posttraumatic pituitary region evaluation, the authors reported that despite abnormal pituitary functions in patients with TBI, MRI during the chronic phase of TBI may be normal (157).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [157] Makulski, 2008, Neuroimaging in posttraumatic hypopituitarism, J Comput Assist Tomogr source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“For the ITT, peak GH response levels lower than 3 g/L indicate severe GHD in adults (if hypoglycemia is adequately reached) (194,215).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Somatotroph axis
What the sources say
- Not checked — no full text of the sourcecites [194] Schneider, 2007, Hypopituitarism, Lancet source
- Not checked — no full text of the sourcecites [215] Molitch, 2011, Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society clinical practice guideline, J Clin Endocrinol Metab source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, older age does not seem to be a strong predictor, and during daily clinical practice a patient cannot be excluded from pituitary testing based only on age.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In a systematic review by Schneider et al (14) including 1015 TBI patients, the pooled prevalence of hypopituitarism in the chronic phase was significantly higher in severe TBI patients (according to postresuscitation GCS) when compared with mild and moderate TBI patients.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
plaincorrelationaln = 1,015- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The likelihood of GHD in TBI patients increases with additional pituitary axes deficiencies (230).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Somatotroph axis
What the sources say
- Not checked — no full text of the sourcecites [230] Gasco, 2012, Hypopituitarism following brain injury: when does it occur and how best to test?, Pituitary source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, at the chronic phase after TBI, normal radiological findings of the pituitary region do not exclude the presence of posttraumatic hypopituitarism.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, panhypopituitarism in the acute phase may be a predictor of chronic hypopituitarism (181).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [181] Aimaretti, 2005, Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study, J Clin Endocrinol Metab source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Moreover, 15 of 18 mild TBI patients (including the three patients with pituitary dysfunction) had abnormal initial CT findings (mainly epidural/subdural hematoma and cranial vault fractures), clearly showing that complicated mild TBI patients have a substantial risk of hypopituitarism (161).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
boostedcorrelationaln = 18- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The pooled prevalences of hypopituitarism in mild, moderate, and severe TBI were estimated as 16.8, 10.9, and 35.3%, respectively (14).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
hedgedcorrelationaln = 1,015- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“However, previous studies revealed that nearly 10 -39% of patients with mild TBI have day-ofinjury intracranial abnormalities (eg, edema, hematoma, or contusion) detected on CT (250 -252).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [250] Borg, 2004, Non-surgical intervention and cost for mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury, J Rehabil Med source
- Not checked — no full text of the sourcecites [251] French, 1977, The value of computerized tomography in the management of 1000 consecutive head injuries, Surg Neurol
- Not checked — no full text of the sourcecites [252] Iverson, 2000, Prevalence of abnormal CT-scans following mild head injury, Brain Inj source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The authors clearly demonstrated that lower mean plasma cortisol during the first 10 days of TBI was significantly associated with the development of chronic hypopituitarism of any axis.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [241] Hannon, 2013, Acute glucocorticoid deficiency and diabetes insipidus are common after acute traumatic brain injury and predict mortality, J Clin Endocrinol Metab source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Moreover, 15 of 18 mild TBI patients (including the three patients with pituitary dysfunction) had abnormal initial CT findings (mainly epidural/subdural hematoma and cranial vault fractures), clearly showing that complicated mild TBI patients have a substantial risk of hypopituitarism (161).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
boostedcorrelationaln = 18- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“There was also a trend toward significant association for acute central DI to predict hypopituitarism other than GHD (241).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [241] Hannon, 2013, Acute glucocorticoid deficiency and diabetes insipidus are common after acute traumatic brain injury and predict mortality, J Clin Endocrinol Metab source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Moreover, in a retrospective clinical review, loss of consciousness and increased duration of coma were reported to be associated with chronic hypopituitarism (12).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [12] Benvenga, 2000, Clinical review 113: hypopituitarism secondary to head trauma, J Clin Endocrinol Metab source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In a previous study, it was clearly demonstrated that neuropsychological functioning in complicated mild TBI is significantly worse than in uncomplicated TBI (254).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [254] Lange, 2009, Neuropsychological functioning following complicated vs. uncomplicated mild traumatic brain injury, Brain Inj source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the acute phase, most of the pituitary hormonal changes, such as decreased gonadotropins (FSH and/or LH) and TSH, and increased HPA axis activity may simply represent adaptive physiological responses to critical illness.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“This approach seems logical and practical because the severity of head trauma is a strong predictor (Table 8) of hypopituitarism in patients with moderate and severe TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not matchedcites Table 8
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Gender and BMI, which have also been examined, have not been uniformly identified as predictors (15, 24, 30, 154, 232).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [24] Leal-Cerro, 2005, Prevalence of hypopituitarism and growth hormone deficiency in adults long-term after severe traumatic brain injury, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [30] Klose, 2007, Prevalence and predictive factors of post-traumatic hypopituitarism, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [154] Bondanelli, 2004, Occurrence of pituitary dysfunction following traumatic brain injury, J Neurotrauma source
- Not checked — no full text of the sourcecites [232] Popovic, 2004, Hypopituitarism as a consequence of traumatic brain injury (TBI) and its possible relation with cognitive disabilities and mental distress, J Endocrinol Invest source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, in a meta-analysis including 1015 TBI patients, from 10 crosssectional and four prospective studies, the pooled prevalence of anterior hypopituitarism was reported as 27.5% (95% confidence interval, 22.8 -28.9).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
plainn = 1,015- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Currently, there is no clear evidence that the replacement of GH, FSH/LH, and TSH deficiencies in critically ill TBI patients during the acute phase is beneficial (14,244,256).”
- Also stated in: § 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase · plain
“In summary, there is no clear evidence that the replacement of GH, FSH/LH, and TSH deficiencies in critically ill TBI patients during the acute phase is beneficial (14,244,256).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Acute phase
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
- Not checked — no full text of the sourcecites [244] Glynn, 2013, Which patient requires neuroendocrine assessment following traumatic brain injury, when and how?, Clin Endocrinol (Oxf) source
- Not checked yetcites [256] Tanriverdi, 2013, Endocrinology of acute brain injury
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase · plain
In the paper
“Moreover, the low cortisol levels were significantly associated with lower blood pressure and higher vasopressor use (238).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Acute phase
What the sources say
- Not checked — no full text of the sourcecites [238] Cohan, 2005, Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study, Crit Care Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moreover, a 6-month period is generally too short to see the clinical features of GHD, and currently there is no clear evidence that early GH replacement could be beneficial for the recovery of pituitary function or for the rehabilitation of TBI; this is discussed in the pathophysiology and treatment sections in detail (Sections VI and IX).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moreover, a 6-month period is generally too short to see the clinical features of GHD, and currently there is no clear evidence that early GH replacement could be beneficial for the recovery of pituitary function or for the rehabilitation of TBI; this is discussed in the pathophysiology and treatment sections in detail (Sections VI and IX).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“To date, there have been only 11 major studies evaluating pituitary function in the first 2 weeks after TBI; these have reported an incidence of ACTH deficiency of between 4 and 78% (15, 25, 59, 150, 151, 236 -241).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Acute phase
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
- Not checked — no full text of the sourcecites [59] Tanriverdi, 2007, Pituitary functions in the acute phase of traumatic brain injury: are they related to severity of the injury or mortality?, Brain Inj source
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [151] Krahulik, 2010, Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults, J Neurosurg source
- Not checked — no full text of the sourcecites [236] Agha, 2004, Neuroendocrine dysfunction in the acute phase of traumatic brain injury, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [237] Cernak, 1999, Neuroendocrine responses following graded traumatic brain injury in male adults, Brain Inj source
- Not checked — no full text of the sourcecites [238] Cohan, 2005, Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study, Crit Care Med source
- Not checked — no full text of the sourcecites [239] Della Corte, 1998, Provocative hypothalamopituitary axis tests in severe head injury: correlations with severity and prognosis, Crit Care Med source
- Not checked — no full text of the sourcecites [240] Hackl, 1991, Endocrine abnormalities in severe traumatic brain injury–a cue to prognosis in severe craniocerebral trauma?, Intensive Care Med source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Only three long-term prospective studies have reported screening pituitary functions for longer than 12 months (16,25,161).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This study, which included mainly uncomplicated mild TBI patients, suggests that global pituitary screening of all TBI patients admitted to emergency units is not necessary due to the low risk of hypopituitarism.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The main limitation of these three long-term studies (16,25,161) is the low number of patients, especially in the moderate and severe TBI groups.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“All of the patients with TSH and FSH/LH deficiencies recovered completely in the chronic phase.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
plainn = 23- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“A large multicenter study by Takala et al (264) showed that the administration of high doses of GH (0.1 mg/kg/d) in critically ill patients (TBI patients were not included), instead of improving outcome, actually doubled mortality.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase
What the sources say
- Not checked — no full text of the sourcecites [264] Takala, 1999, Increased mortality associated with growth hormone treatment in critically ill adults, N Engl J Med source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In critically ill burn or medical patients, acute thyroid hormone replacement therapy was not shown to produce short-term improvement (262).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase
What the sources say
- Not checked — no full text of the sourcecites [262] Vanhorebeek, 2004, Hormonal and metabolic strategies to attenuate catabolism in critically ill patients, Curr Opin Pharmacol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Overall, the percentage of patients with GHD decreased from 43.3% at 1 year to 23.3% at 3 years.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plaindirectn = 30- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Prospective studies demonstrated that TSH deficiency (central hypothyroidism) generally recovers during or after the acute phase (14,261).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
- Not checked — no full text of the sourcecites [261] Sundaram, 2013, The impact of traumatic brain injury on pituitary function, Endocrinol Metab Clin North Am source
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Adequate replacement with glucocorticoids, L-thyroxine, and sex steroids generally reverses the symptoms and signs of relevant pituitary hormone deficiencies and normalizes the risks associated with it (14).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Treatment of TSH, FSH/LH, and ACTH deficiencies
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“As we discussed in the pathophysiology section (Section VI.B), experimental studies revealed that GH and IGF-1 may play a crucial role in brain repair mechanisms or neuronal recovery after trauma by regulating the factors including neuronal plasticity, myelin formation, and vascular tone (69,(185)(186)(187)(188)(189).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase
What the sources say
- Not matchedcites 69,(185)(186)(187)(188)(189)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“As another limitation of the long-term prospective studies, the number of patients with TSH and gonadotropin deficiencies was significantly lower, causing difficulties in understanding the natural history of these axes (16,25,161).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, the GH status of TBI patients in this particular study was not defined.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase
What the sources say
- Not checked — no full text of the sourcecites [263] Hatton, 2006, Systemic metabolic effects of combined insulin-like growth factor-I and growth hormone therapy in patients who have sustained acute traumatic brain injury, J Neurosurg source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Furthermore, in the 3-and 5-year TBI studies, dynamic hormonal changes in moderate TBI patients were similar to either mild or severe TBI patients.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, in severe TBI, the ACTH and GH status of the patients at the first-year evaluation persisted at the fifth year.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“It is important to note that in both the ACTH and GH axes, a significant number of dynamic hormonal changes (recovery and new-onset deficiencies) have been reported (25).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
plainn = 23- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We think that it is still too early to draw such a conclusion based on the current experimental data and some clinical case experiences because placebo-controlled human studies have not been conducted demonstrating the effects of GH replacement on neuronal/pituitary recovery.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Although the number of patients is insufficient, the study clearly suggests that dynamic hormonal changes could be seen between 24 and 36 months after injury.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
hedgedcorrelationaln = 23- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In a previous randomized, prospective, double-blind, placebo-controlled study by Hatton et al (263), IGF-1 and GH (0.05 mg/kg/d) therapy within 72 hours of TBI produced sustained improvement in metabolic and nutritional endpoints.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase
What the sources say
- Not checked — no full text of the sourcecites [263] Hatton, 2006, Systemic metabolic effects of combined insulin-like growth factor-I and growth hormone therapy in patients who have sustained acute traumatic brain injury, J Neurosurg source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Patients with hypopituitarism, independent of the etiology, require the replacement of deficient hormones as part of their standard clinical care.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Treatment of TSH, FSH/LH, and ACTH deficiencies
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The percentage of patients with ACTH deficiency decreased from 20.0 to 6.6%.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plaindirectn = 30- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“They also found a moderate improvement in memory (especially immediate memory) and information processing speed.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Not checked — no full text of the sourcecites [276] Moreau, 2013, Growth hormone replacement therapy in patients with traumatic brain injury, J Neurotrauma source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“If GH replacement therapy is commenced in GH-deficient patients with mild TBI, it is important to keep in mind that GHD may recover over a 5-year period after TBI, and a yearly evaluation of the GH status is necessary (Figure 2).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Additionally, the results from nontraumatically injured patients suggest that some of the deficits observed after TBI may in fact be the direct result of GHD.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Those individuals with more significant deficits showed the greatest improvements.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Not checked — no full text of the sourcecites [276] Moreau, 2013, Growth hormone replacement therapy in patients with traumatic brain injury, J Neurotrauma source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Probably not a substantial claim. 49
- It may state two separate claims as one. 124
- The quote only partly states this claim. 7
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“however, in three studies, confirmatory testing was applied if a screening test was positive (29,30,255; Table 2).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Results
What the sources say
- Supportedcites [29] Agha, 2004, Anterior pituitary dysfunction in survivors of traumatic brain injury, J Clin Endocrinol Metab source
The Assessment of somatotrophic and corticotrophic function section says the GST was used as an initial screening test and that patients with subnormal responses received further testing. The Discussion describes the second provocative test as a way to make the results more reliable. This supports the claim for this cited study; the paper does not need to establish what the other two studies did. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [30] Klose, 2007, Prevalence and predictive factors of post-traumatic hypopituitarism, Clin Endocrinol (Oxf) source
- Supportedcites [255] van der Eerden, 2010, Should anterior pituitary function be tested during follow-up of all patients presenting at the emergency department because of traumatic brain injury?, Eur J Endocrinol source
The Study design section (p. 3) says patients with abnormal screening results were referred for extensive evaluation. The evaluation section (p. 4) describes the follow-up tests used to confirm pituitary dysfunction. This supports the cited paper as one of the studies using confirmatory testing after a positive screen; it does not need to establish the total of three studies cited in the sentence. (LLM, conf=0.93)
plainn = 3- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The limitations of this study were that the PD-GHRH stimulation test is not a commonly used test in the diagnosis of adult GHD (21), and it is not well-standardized (22).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > Severity
What the sources say
- Partly supportedcites [21] Klose, 2014, Prevalence of posttraumatic growth hormone deficiency is highly dependent on the diagnostic set-up: results from The Danish National Study on Posttraumatic Hypopituitarism, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
The Diagnostic thresholds section (page unavailable) says definite BMI-related cutoffs for the PD-GHRH test are unavailable and that adapting cutoffs from another test was inappropriate, supporting the concern about standardization. The Methods section describes its use in this study, but the paper does not establish that PD-GHRH is uncommon in adult GHD diagnosis generally. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [22] Hazem, 2011, The accuracy of diagnostic tests for GH deficiency in adults: a systematic review and meta-analysis, Eur J Endocrinol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Additionally, most studies did not include a control group.Only three studies included matched control groups (27,29,30; Table 2).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Results
What the sources say
- Not checked — no full text of the sourcecites [27] Schneider, 2006, Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury, Eur J Endocrinol source
- Supportedcites [29] Agha, 2004, Anterior pituitary dysfunction in survivors of traumatic brain injury, J Clin Endocrinol Metab source
The Definition of abnormalities section reports that the study tested 31 healthy subjects matched to the patient population for age, sex, and BMI. This supports citing the paper as an example of a study with a matched control group. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites [30] Klose, 2007, Prevalence and predictive factors of post-traumatic hypopituitarism, Clin Endocrinol (Oxf) source
plainn = 3- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Most sports-related injuries were classified as mild TBI (46%) with a high risk of complications, including mainly cognitive dysfunction (34).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Definition of sports-related traumatic brain injury
What the sources say
- Partly supportedcites [34] Theadom, 2014, Sports-related brain injury in the general population: an epidemiological study, J Sci Med Sport sourceExperimental — accuracy not yet measured
The Discussion (p. 10) says 98% of sports-related TBIs were classified as mild, while 46% of injuries were identified as having a high risk of further complications. The claim conflates those figures and adds that complications were mainly cognitive dysfunction; the Discussion instead gives intracranial lesions as an example and does not establish cognitive dysfunction as the main complication. (LLM, conf=0.91)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The second study included 19 male soldiers who had moderate to severe blast TBI and 39 male controls who had moderate to severe non-blast-related TBI.The authors demonstrated that 32% of the soldiers had anterior pituitary dysfunction that was significantly more frequent than in the non-blast TBI group (32).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > E. Hypopituitarism after blast-related TBI
What the sources say
- Supportedcites [32] Baxter, 2013, Pituitary dysfunction after blast traumatic brain injury: The UK BIOSAP study, Ann Neurol source
The Abstract Methods describes 19 male soldiers with moderate to severe blast TBI and 39 male controls with moderate to severe nonblast TBI. The Results report anterior pituitary dysfunction in 6 of 19 soldiers (31.6%, rounded to 32%) versus 1 of 39 controls (2.6%), a significant difference (p = 0.004). (LLM, conf=0.95)
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The prevalence of hypopituitarism and metabolic syndrome was relatively common (23.5 and 50%, respectively) and could have contributed to their poor quality of life.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Supportedcites [48] Kelly, 2014, Prevalence of pituitary hormone dysfunction, metabolic syndrome, and impaired quality of life in retired professional football players: a prospective study, J Neurotrauma source
The Conclusions report hypopituitarism in 23.5% and metabolic syndrome in 50% of the studied retired professional football players, and say these conditions may contribute to poor quality of life. The Summary of findings specifies that this was a selected cohort of NFL retirees with poor quality of life, not a prevalence estimate for all retirees. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The first study included 26 male soldiers whose blast exposure (blast-related mild TBI) was at least 1 year before the evaluation.In 42% of the participants with blast injury, deficiencies in one or more pituitary axis were reported.The most common pituitary hormone deficits were GH and FSH/LH deficiencies (31).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > E. Hypopituitarism after blast-related TBI
What the sources say
- Partly supportedcites [31] Wilkinson, 2012, High prevalence of chronic pituitary and target-organ hormone abnormalities after blast-related mild traumatic brain injury, Front Neurol sourceExperimental — accuracy not yet measured
The Abstract reports 26 male veterans with blast-related mild TBI whose last blast exposure was at least one year earlier; 11 of 26 (42%) had abnormal hormone levels. It identifies probable growth hormone deficiency in five and findings consistent with hypogonadism in three. The claim overstates the 42% result as deficiencies: the Discussion says that total includes posterior pituitary abnormalities, some of which were elevated hormone levels. (LLM, conf=0.88)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“According to the ITT results with local cutoffs used by Klose et al (21) and standard cutoffs used in the other studies, the pooled prevalence of GHD was 7.7 and 1.4% in patients and controls, respectively (two-sided P with 2 test Ͻ.001).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > D. Is hypopituitarism more common after brain damage than in the normal population?
What the sources say
- Supportedcites [21] Klose, 2014, Prevalence of posttraumatic growth hormone deficiency is highly dependent on the diagnostic set-up: results from The Danish National Study on Posttraumatic Hypopituitarism, J Clin Endocrinol Metab source
The ‘Impact of local vs guideline-derived cutoff values’ section reports ITT results using local cutoffs, as the citing sentence attributes to Klose et al. The 7.7% and 1.4% figures are presented as the citing authors’ pooled estimates across studies, not as estimates from Klose et al. alone. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Cerebral concussion may develop after only one simple punch or as accumulated damage from multiple punches; cognitive dysfunction is reported in most boxers (36).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Definition of sports-related traumatic brain injury
What the sources say
- Partly supportedcites [36] Ohhashi, 2002, Problems in health management of professional boxers in Japan, Br J Sports Med sourceExperimental — accuracy not yet measured
The Abstract says a single punch can cause cerebral concussion, and Damage during a fight reports that 21.2% of boxers who had been knocked out said they collapsed after several punches. It does not establish accumulated damage as the cause of those concussions. The same section reports memory disturbances in 27.7% of boxers who had been knocked out, not cognitive dysfunction in most boxers. (LLM, conf=0.88)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Altered body composition, insulin resistance, hypertension, unfavorable lipid profile, endothelial dysfunction and atherosclerosis have been found in several studies on patients with long-term GHD (74,76,77,(82)(83)(84)(85)(86)(87).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Partly supportedcites [74] Luque, 2011, Metabolic impact of adult-onset, isolated, growth hormone deficiency (AOiGHD) due to destruction of pituitary somatotropes, PLoS One sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports that most clinical studies find adults with GHD insulin resistant and says humans with adult-onset GHD have relatively more fat. It does not establish hypertension, an unfavorable lipid profile, endothelial dysfunction, or atherosclerosis in patients with long-term GHD; the paper’s own experiments concern mice. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites [76] Srinivasan, 2004, Features of the metabolic syndrome after childhood craniopharyngioma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [77] Tomlinson, 2001, Association between premature mortality and hypopituitarism. West Midlands Prospective Hypopituitary Study Group, Lancet source
- Partly supportedcites [82] Evans, 1999, Endothelial dysfunction in hypopituitary adults with growth hormone deficiency, Clin Endocrinol (Oxf) sourceExperimental — accuracy not yet measured
The Discussion (p. 461) reports impaired endothelial function in GHD adults and discusses insulin resistance, altered body composition, and reports of unfavorable lipid profiles. But its own study found no quantitative lipid-profile difference; the Subjects section says all participants were normotensive, and the paper describes endothelial dysfunction as preceding overt atherosclerotic disease rather than finding atherosclerosis in them. Thus this source supports only part of the list. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites [83] Leonsson, 2002, Intima-media thickness in cardiovascularly asymptomatic hypopituitary adults with growth hormone deficiency: relation to body mass index, gender, and other cardiovascular risk factors, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [84] Lombardi, 2012, The cardiovascular system in growth hormone excess and growth hormone deficiency, J Endocrinol Invest source
- Not checked — no full text of the sourcecites [85] Markussis, 1992, Detection of premature atherosclerosis by high-resolution ultrasonography in symptom-free hypopituitary adults, Lancet source
- Not checked — no full text of the sourcecites [86] Murray, 2010, Partial growth hormone deficiency is associated with an adverse cardiovascular risk profile and increased carotid intima-medial thickness, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [87] Sesmilo, 2001, Inflammatory cardiovascular risk markers in women with hypopituitarism, J Clin Endocrinol Metab source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Hypopituitarism, in general, and GHD, in particular, are associated with a number of metabolic alterations (74 -79).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Partly supportedcites [74] Luque, 2011, Metabolic impact of adult-onset, isolated, growth hormone deficiency (AOiGHD) due to destruction of pituitary somatotropes, PLoS One sourceExperimental — accuracy not yet measured
The Discussion (page not provided) reports several metabolic effects of adult-onset isolated GHD, including changes in insulin sensitivity and, under a high-fat diet, impaired glucose clearance. The Introduction (page not provided) says adult-onset GHD often occurs alongside other pituitary defects, but the paper does not establish the broader claim about hypopituitarism in general. (LLM, conf=0.84)
- Supportedcites [75] Nyenwe, 2009, Nonalcoholic fatty liver disease and metabolic syndrome in hypopituitary patients, Am J Med Sci source
The Abstract’s Conclusions state that patients with hypopituitarism, especially growth hormone deficiency, have an increased incidence of an insulin-resistant syndrome with several metabolic features. The Discussion likewise describes hypertension, hyperglycemia, dyslipidemia, and insulin resistance in hypopituitary patients. These passages support the broad association claimed. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites [76] Srinivasan, 2004, Features of the metabolic syndrome after childhood craniopharyngioma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [77] Tomlinson, 2001, Association between premature mortality and hypopituitarism. West Midlands Prospective Hypopituitary Study Group, Lancet source
- Not checked — no full text of the sourcecites [78] Verhelst, 2009, Cardiovascular risk factors in hypopituitary GH-deficient adults, Eur J Endocrinol source
- Not checked — no full text of the sourcecites [79] Verhelst, 2011, Prevalence and characteristics of the metabolic syndrome in 2479 hypopituitary patients with adult-onset GH deficiency before GH replacement: a KIMS analysis, Eur J Endocrinol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“As a neuropathological definition, concussion is thought to be a type of DAI because axons may be injured due to stretching (104, 105).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Partly supportedcites [104] Browne, 2011, Mild traumatic brain injury and diffuse axonal injury in swine, J Neurotrauma sourceExperimental — accuracy not yet measured
The Discussion describes DAI as an important pathological feature of mild TBI or concussion and says axonal deformation may mechanically damage axons. It does not define concussion itself as a type of DAI; the Discussion cautions that the scope of the DAI designation in mild TBI remains uncertain. (LLM, conf=0.84)
- Partly supportedcites [105] Johnson, 2013, Axonal pathology in traumatic brain injury, Exp Neurol sourceExperimental — accuracy not yet measured
The Introduction describes DAI as occurring across severities of closed-head injury, and the Conclusions say axonal damage may contribute to dysfunction in mild TBI. The section on primary mechanical damage explains how rapid stretch can injure axons. These passages support a possible role for stretch-related axonal injury in concussion, but they do not define concussion itself as a type of DAI. Page numbers were not available in our copy. (LLM, conf=0.83)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The exact pathophysiology of pituitary dysfunction after TBI is not well understood, but multiple pathological mechanisms have been proposed, including compression of the pituitary gland, hypothalamic nuclei, or interruption of the long hypophyseal portal vessels by edema; direct mechanical trauma to the pituitary gland, stalk, and/or hypothalamus; increased ICP; hemorrhage; skull fracture; or any”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [18] Kelly, 2000, Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report, J Neurosurg source
- Not checked — no full text of the sourcecites [131] Behan, 2008, Neuroendocrine disorders after traumatic brain injury, J Neurol Neurosurg Psychiatry source
- Not checked — no full text of the sourcecites [132] Daniel, 1959, Traumatic infarction of the anterior lobe of the pituitary gland, Lancet source
- Supportedcites [133] Dusick, 2012, Pathophysiology of hypopituitarism in the setting of brain injury, Pituitary source
The Overview states that the cause of post-TBI pituitary dysfunction remains incompletely understood and identifies multiple contributing factors. The Primary and secondary brain injury section discusses mechanical injury, skull fractures, hemorrhage, brain swelling, raised intracranial pressure, and vulnerability of the long portal vessels—mechanisms reflected in the citing sentence. Page numbers are unavailable in our copy. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites [134] Edwards, 1986, Post-traumatic hypopituitarism. Six cases and a review of the literature, Medicine (Baltimore) source
- Not checked — no full text of the sourcecites [135] Iglesias, 1996, Spontaneous recovery from post-traumatic hypopituitarism, J Endocrinol Invest source
- Not checked — no full text of the sourcecites [136] Maiya, 2008, Magnetic resonance imaging changes in the pituitary gland following acute traumatic brain injury, Intensive Care Med source
- Not checked — no full text of the sourcecites [137] Wachter, 2009, Pituitary insufficiency after traumatic brain injury, J Clin Neurosci source
- Not checked — no full text of the sourcecites [138] Yuan, 1991, Neuroendocrine abnormalities in patients with traumatic brain injury, Front Neuroendocrinol
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The oxidative stress occurring after TBI contributes both to microvascular damage and to neuronal damage (97, 124, 125).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [97] Werner, 2007, Pathophysiology of traumatic brain injury, Br J Anaesth source
- Partly supportedcites [124] Bayir, 2005, Enhanced oxidative stress in iNOS-deficient mice after traumatic brain injury: support for a neuroprotective role of iNOS, J Cereb Blood Flow Metab sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) says oxidative stress is detrimental after TBI, supporting the general claim of damage. The paper does not say that this stress contributes to microvascular damage, and its Assessment of Neuropathology (page unavailable) does not establish a direct link to neuronal damage. (LLM, conf=0.83)
- Not checked — no full text of the sourcecites [125] Shao, 2006, Oxidative stress in head trauma in aging, Free Radic Biol Med source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Autopsy results have revealed different types of lesions including damage to the pituitary capsule (most common form of pituitary injury after TBI, observed in 23-59% of cases), to the pituitary stalk, and to the anterior and posterior lobes in the forms of hemorrhage, necrosis, and fibrosis (139 -144).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked yetcites [139] Ceballos, 1966, Pituitary changes in head trauma (analysis of 102 consecutive cases of head injury), Ala J Med Sci
- Not checked — no full text of the sourcecites [140] Crompton, 1971, Hypothalamic lesions following closed head injury, Brain source
- Partly supportedcites [141] Harper, 1986, Analysis of abnormalities in pituitary gland in non-missile head injury: study of 100 consecutive cases, J Clin Pathol sourceExperimental — accuracy not yet measured
The Haemorrhage and Infarction sections report lesions of the pituitary stalk and both lobes; the Anterior Lobe section describes necrosis followed by a fibrous scar. But the paper does not report capsule damage in 23–59% of cases. Its Discussion instead identifies anterior-lobe infarction as the most common important abnormality. Page numbers were not available in our copy. (LLM, conf=0.88)
- Not checked yetcites [142] Kornblum, 1969, Pituitary lesions in craniocerebral injuries, Arch Pathol
- Not checked — no full text of the sourcecites [143] Pierucci, 1971, Pituitary changes especially necrotic–following cranio-cerebral injuries [in Italian], Pathologica
- Not checked — no full text of the sourcecites [144] Salehi, 2007, Histologic study of the human pituitary gland in acute traumatic brain injury, Brain Inj source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“By using histopathological techniques, DAI can be identified within hours after head trauma and is characterized by sequential changes with an initial shearing of axons that causes disrupted axonal transport, secondary axonal disconnection, and eventually, Wallerian degeneration (105, 110).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Partly supportedcites [105] Johnson, 2013, Axonal pathology in traumatic brain injury, Exp Neurol sourceExperimental — accuracy not yet measured
The paper’s “DAI: Pathological Features and Identification” section says APP staining can detect damaged axons within two hours of injury. “Potential Primary Mechanical Damage due to Axonal Trauma” describes cytoskeletal damage, interrupted transport, secondary disconnection and Wallerian degeneration, but says immediate severing of axons is relatively rare—not the usual initial step implied by “initial shearing of axons.” (LLM, conf=0.87)
- Not checked — no full text of the sourcecites [110] Erb, 1991, Neuroplasticity following traumatic brain injury: a study of GABAergic terminal loss and recovery in the cat dorsal lateral vestibular nucleus, Exp Brain Res source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Regarding the general pathophysiology of TBI, the first stages of brain injury after head trauma are characterized by direct tissue damage and impaired regulation of cerebral blood flow (hypoperfusion or hyperperfusion) and metabolism (93,97).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Partly supportedcites [93] Bouzat, 2013, Beyond intracranial pressure: optimization of cerebral blood flow, oxygen, and substrate delivery after traumatic brain injury, Ann Intensive Care sourceExperimental — accuracy not yet measured
The Introduction describes primary lesions from the initial trauma followed by early secondary injury involving blood flow and energy dysfunction. The Macrovascular dysfunction and Energy dysfunction sections support impaired blood-flow regulation, hypoperfusion, and altered metabolism. Our copy does not substantiate hyperperfusion as an early post-traumatic disturbance, so that part of the citing sentence remains unsupported. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [97] Werner, 2007, Pathophysiology of traumatic brain injury, Br J Anaesth source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The secondary insult (ie, secondary damage, nonmechanical damage), characterizes consecutive neuropathological processes initiated at the moment of injury with delayed clinical presentation.For example, intracranial hypertension, hypoxia, hyponatremia, and cerebral ischemia refer to secondary insults, and these types of injury are variably sensitive to therapeutic interventions (94,97,111).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [94] Frattalone, 2013, Moderate and severe traumatic brain injury: pathophysiology and management, Neurosurg Clin N Am source
- Not checked — no full text of the sourcecites [97] Werner, 2007, Pathophysiology of traumatic brain injury, Br J Anaesth source
- Partly supportedcites [111] Saatman, 2008, Classification of traumatic brain injury for targeted therapies, J Neurotrauma sourceExperimental — accuracy not yet measured
The paper’s “Classification by Pathophysiology” section says secondary injury can arise from processes set in motion at injury and develop at variable times afterward; it also names hypoxia and hyponatremia as secondary insults. The “Common Pathoanatomical and Pathophysiological Sequelae” section says some such processes might be remediable therapeutic targets, but it does not establish that these injury types are variably sensitive to interventions or that they necessarily have a delayed clinical presentation. The indexed passages provide no page numbers. (LLM, conf=0.82)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Interruption of the hypothalamo-hypophyseal portal blood supply (ie, due to ICP or direct vascular insult) was assumed to be one of the possible mechanisms of anterior lobe infarction (18, 132, 135, 141, 142).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [18] Kelly, 2000, Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report, J Neurosurg source
- Not checked — no full text of the sourcecites [132] Daniel, 1959, Traumatic infarction of the anterior lobe of the pituitary gland, Lancet source
- Not checked — no full text of the sourcecites [135] Iglesias, 1996, Spontaneous recovery from post-traumatic hypopituitarism, J Endocrinol Invest source
- Supportedcites [141] Harper, 1986, Analysis of abnormalities in pituitary gland in non-missile head injury: study of 100 consecutive cases, J Clin Pathol source
The Discussion identifies interference with blood flow through the hypothalamo-hypophysial portal vessels as the presumed mechanism of anterior-lobe necrosis. It also reports that every patient with a large or medium-sized infarct had experienced raised intracranial pressure. Page numbers are not provided in the supplied passages. (LLM, conf=0.93)
- Not checked yetcites [142] Kornblum, 1969, Pituitary lesions in craniocerebral injuries, Arch Pathol
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The somatotrophs and gonadotrophs, which are located in the area of the pituitary perfused by long hypophyseal portal vessels, are the most frequent hormonal deficiencies after TBI (15, 18, 27, 29, 150, 160); however, in some studies ACTH deficiency (corticotrophs are located in the territory supplied by the short portal vessels) is the most common or second most common hormonal deficiency after”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [18] Kelly, 2000, Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report, J Neurosurg source
- Not checked — no full text of the sourcecites [27] Schneider, 2006, Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury, Eur J Endocrinol source
- Partly supportedcites [29] Agha, 2004, Anterior pituitary dysfunction in survivors of traumatic brain injury, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
- Partly supportedcites [160] Aimaretti, 2005, Traumatic brain injury and hypopituitarism, Scientific World J sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
- Partly supportedcites [149] Agha, 2005, The natural history of post-traumatic hypopituitarism: implications for assessment and treatment, Am J Med sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The possible mechanisms of transient acute hypopituitarism could be due to direct mechanical injury (ie, hypothalamus, stalk, pituitary, or long portal vessels injury would do not cause pituitary infarction), hypotension, reversible edema formation, increased ICP, and hypoperfusion due to reversible vasospasm; however, none of these mechanisms have been clearly demonstrated in either clinical or”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
- Partly supportedcites [149] Agha, 2005, The natural history of post-traumatic hypopituitarism: implications for assessment and treatment, Am J Med sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [151] Krahulik, 2010, Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults, J Neurosurg source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Moreover, tanycytes are bipolar cells bridging the cerebrospinal fluid to the portal capillaries and may link the cerebrospinal fluid to neuroendocrine events (182, 183).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Partly supportedcites [182] Langlet, 2013, Tanycyte-like cells form a blood-cerebrospinal fluid barrier in the circumventricular organs of the mouse brain, J Comp Neurol sourceExperimental — accuracy not yet measured
The introductory passage (page not supplied) says tanycytes line the ventricle, extend processes to portal vessels, and link the ventricular and vascular compartments. It does not say that they link CSF to neuroendocrine events; the paper describes their barrier role instead. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [183] Mullier, 2010, Differential distribution of tight junction proteins suggests a role for tanycytes in blood-hypothalamus barrier regulation in the adult mouse brain, J Comp Neurol source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“The major limitation of the study, however, was whether this experimental model truly represents a closed head injury (176).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Could not verifycites [176] Kasturi, 2009, Traumatic brain injury causes long-term reduction in serum growth hormone and persistent astrocytosis in the cortico-hypothalamo-pituitary axis of adult male rats, J Neurotrauma sourceExperimental — accuracy not yet measured
The Surgeries section describes a bilateral craniotomy followed by controlled cortical impact, but does not discuss whether the model represents a closed-head injury. Searches for 'closed head injury limitation' and 'major limitation model truly represents closed head' found no passage identifying that question as the study’s major limitation. (LLM, conf=0.74)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“As we discussed above, concussion is the most frequent type of acute TBI in sports-related head trauma, and DAI, which is caused by the shearing of fragile axons, is the primary pathophysiology of TBI (105).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Partly supportedcites [105] Johnson, 2013, Axonal pathology in traumatic brain injury, Exp Neurol sourceExperimental — accuracy not yet measured
The Introduction describes DAI as one of the most common pathological consequences of closed-head TBI, and the section on DAI genesis describes shear strains as a mechanism. The paper does not establish that concussion is the most frequent acute sports-related TBI or that DAI is the primary pathophysiology of all TBI. The section on primary mechanical damage also says immediate axonal disconnection is relatively rare, so describing DAI simply as shearing of fragile axons oversimplifies the mechanism. Page numbers were not available in our copy. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Another potent and validated provocative test is the GHRHϩGHRP-6 test (224, 225).It has a BMI-dependent cutoff (15 and 5 g/L for lean and obese subjects with BMI Ͼ 35 kg/m 2 , respectively) and possesses great accuracy in distinguishing normal subjects from patients with GHD (224, 225).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Somatotroph axis
What the sources say
- Partly supportedcites [224] Kelestimur, 2006, Effect of obesity and morbid obesity on the growth hormone (GH) secretion elicited by the combined GHRH + GHRP-6 test, Clin Endocrinol (Oxf) sourceExperimental — accuracy not yet measured
The Discussion reports BMI-dependent cutoffs and describes the test as validated; the Results compare its ability to distinguish controls from patients with GHD. But the quoted values are assigned incorrectly: for BMI >35, 15 µg/L indicates normal secretion and 5 µg/L indicates deficiency. For BMI ≤35, the corresponding cutoffs are 20 and 10 µg/L, and intermediate results are inconclusive. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [225] Popovic, 2000, GH-releasing hormone and GH-releasing peptide-6 for diagnostic testing in GH-deficient adults, Lancet source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In the TBI population, this test has been used by some authors (18,29,196,197) without adverse effects, but other authors have used alternative tests, suggesting the possible danger of ITT (195,198).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Introduction
What the sources say
- Not checked — no full text of the sourcecites [18] Kelly, 2000, Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report, J Neurosurg source
- Supportedcites [29] Agha, 2004, Anterior pituitary dysfunction in survivors of traumatic brain injury, J Clin Endocrinol Metab source
The Assessment of somatotrophic and corticotrophic function section says this TBI study used alternatives to the ITT for patients with a history of seizures or heart disease. The Discussion likewise says alternatives were used where the ITT was contraindicated. This supports the cited point about a possible safety concern, not a claim that the ITT caused harm. (LLM, conf=0.88)
- Partly supportedcites [196] Brandt, 2004, Fatigue after aneurysmal subarachnoid hemorrhage evaluated by pituitary function and 3D-CBF, Acta Neurol Scand sourceExperimental — accuracy not yet measured
In “Evaluation of pituitary function” (page unavailable), the authors report withholding insulin-induced hypoglycemia from patients with a history of epileptic seizures or neurological sequelae and using basal hormone measurements. This supports the suggestion of a safety concern, but the study involved patients after aneurysmal subarachnoid hemorrhage, not a TBI population; it does not establish ITT danger in TBI. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [197] Kreitschmann-Andermahr, 2004, Prevalence of pituitary deficiency in patients after aneurysmal subarachnoid hemorrhage, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [195] Ghigo, 2005, Consensus guidelines on screening for hypopituitarism following traumatic brain injury, Brain Inj source
- Not checked — no full text of the sourcecites [198] Aimaretti, 2004, Traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarism: screening study at 3 months after the brain injury, Clin Endocrinol (Oxf) source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Most prospective studies have demonstrated that the presence of acute anterior pituitary deficiencies after head trauma does not typically predict chronic hypopituitarism, and most of the acute changes are transient.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Partly supportedcites [149] Agha, 2005, The natural history of post-traumatic hypopituitarism: implications for assessment and treatment, Am J Med sourceExperimental — accuracy not yet measured
The Discussion (page not provided) says that acute anterior pituitary abnormalities resolved by six months in the majority of patients, supporting the claim that many acute changes are transient. But this paper reports one prospective cohort, not findings from “most prospective studies,” and it notes that more severe acute growth-hormone and cortisol deficiencies were associated with persistent deficiency; predictors could not be established confidently. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“In contrast, it has been reported that hypopituitarism is rare (Ͻ1%; median, 13 mo after TBI) in unselected head trauma patients admitted to emergency departments, and the authors concluded that routine pituitary screening in these patients is unlikely to be cost-effective.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Supportedcites [255] van der Eerden, 2010, Should anterior pituitary function be tested during follow-up of all patients presenting at the emergency department because of traumatic brain injury?, Eur J Endocrinol source
The Discussion (p. 9) reports pituitary dysfunction in fewer than 1% of patients evaluated 3–30 months after presenting to the emergency department with TBI. The Patient characteristics section (p. 6) gives a median of 13 months from TBI to endocrine evaluation for participating patients with mild TBI. The Discussion (p. 10) also concludes that routine screening of unselected patients is unlikely to be cost-effective. (LLM, conf=0.88)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“At the end of 12 months, there were still substantial rates of some pituitary hormone deficiency ranging from 13 to 50%, of which GHD was the most common hormonal deficit.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [27] Schneider, 2006, Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury, Eur J Endocrinol source
- Partly supportedcites [149] Agha, 2005, The natural history of post-traumatic hypopituitarism: implications for assessment and treatment, Am J Med sourceExperimental — accuracy not yet measured
Table 2 (p. 1416.e6) supports the claim that pituitary hormone deficiencies persisted at 12 months: 6 of 48 patients had gonadotropin deficiency (about 13%). It does not support a 12-month rate of 50%, and ACTH deficiency (9 of 48) was more common than growth hormone deficiency (5 of 48). The paper’s statement that hypopituitarism affects up to half of long-term survivors is background, not its 12-month result. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [151] Krahulik, 2010, Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults, J Neurosurg source
- Not checked — no full text of the sourcecites [181] Aimaretti, 2005, Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study, J Clin Endocrinol Metab source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The dynamic hormonal changes were defined mainly in the first 6 months but could be seen after 6 months (15, 27, 149 -151, 181).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [27] Schneider, 2006, Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury, Eur J Endocrinol source
- Supportedcites [149] Agha, 2005, The natural history of post-traumatic hypopituitarism: implications for assessment and treatment, Am J Med source
The Discussion (p. 1416.e6) says pituitary function changed particularly in the first 6 months after head injury. The Somatotropic axis results report another patient recovering between 6 and 12 months, supporting that changes could also occur later. The Discussion clarifies that no new abnormalities were detected after 6 months. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites [150] Klose, 2007, Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective single-centre study, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [151] Krahulik, 2010, Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults, J Neurosurg source
- Not checked — no full text of the sourcecites [181] Aimaretti, 2005, Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study, J Clin Endocrinol Metab source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Moreover, she had a spontaneous pregnancy 6 months after recovery (260).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Supportedcites [260] Ruggeri, 2010, Spontaneous recovery from isolated post-traumatic central hypogonadism in a woman, Hormones (Athens) source
The Patient's Description reports restored spontaneous menstrual cycles and normal hormone values at the second evaluation, followed by pregnancy six months later. The Abstract gives the same timing. Page numbers are not provided in our copy. (LLM, conf=0.92)
plainSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“After 10 years, she was re-evaluated in the same endocrinology clinic, and when she discontinued her drug for 6 months, spontaneous menstrual cycles returned.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Supportedcites [260] Ruggeri, 2010, Spontaneous recovery from isolated post-traumatic central hypogonadism in a woman, Hormones (Athens) source
The Patient’s Description says she returned to the clinic ten years after her initial evaluation. At that visit, she had discontinued oestroprogestins for the preceding six months, and spontaneous menstrual cycles had returned. The ten years are measured from her first clinic visit, not from the injury. (LLM, conf=0.94)
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“They found the active medication cohort improved in the following: information processing speed, verbal learning, executive functioning, and dominant hand finger tapping.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Supportedcites [273] High, 2010, Effect of growth hormone replacement therapy on cognition after traumatic brain injury, J Neurotrauma source
The Discussion (page unavailable) reports improvements in information-processing speed, executive functioning, memory, and simple motor speed, including dominant-hand finger tapping. The Results (page unavailable) specifically report improved verbal learning over time in the active rhGH group. The executive-functioning result was a trend and did not show a significant difference from placebo at 12 months, but the claim does not assert such a difference. (LLM, conf=0.91)
plaindirectn = 12- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Recently impaired cognitive functions and quality of life, impaired metabolic parameters, abnormal body composition, increased cardiovascular risk factors, and decreased muscle force and aerobic capacity have been clearly demonstrated in patients with GHD due to TBI and sports-related head trauma (16, 46 -48, 72, 80, 81, 271).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
- Not checked — no full text of the sourcecites [46] Tanriverdi, 2008, Brief communication: pituitary volume and function in competing and retired male boxers, Ann Intern Med source
- Not matchedcites [47] Tanriverdi, 2008, Body composition, serum IGF-1 and leptin level changes in amateur boxers: retired boxers have risk factors for cardiovascular disorders, Obes Metab
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites [48] Kelly, 2014, Prevalence of pituitary hormone dysfunction, metabolic syndrome, and impaired quality of life in retired professional football players: a prospective study, J Neurotrauma sourceExperimental — accuracy not yet measured
The Abstract and Conclusions report GHD, poor quality of life, and metabolic syndrome in retired football players, but say hormonal deficiencies may contribute to poor quality of life and metabolic disturbances; a causal link to repetitive head injury was not proven. The ‘Quality of life, erectile dysfunction, metabolic syndrome, and obesity’ section discusses body composition, exercise capacity, and cardiovascular risk as possible consequences of GHD, but found obesity and metabolic syndrome rates did not differ significantly by hormonal-deficiency status. The paper does not demonstrate the claimed range of impairments—including decreased muscle force—in patients with GHD due to head trauma. Page numbers were not provided in the indexed passages. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [72] Tanriverdi, 2013, Growth hormone deficiency due to sports-related head trauma is associated with impaired cognitive performance in amateur boxers and kickboxers as revealed by P300 auditory event-related potentials, Clin Endocrinol (Oxf) source
- Not checked — no full text of the sourcecites [80] Klose, 2007, Posttraumatic hypopituitarism is associated with an unfavorable body composition and lipid profile, and decreased quality of life 12 months after injury, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [81] Prodam, 2013, Metabolic alterations in patients who develop traumatic brain injury (TBI)-induced hypopituitarism, Growth Horm IGF Res source
- Partly supportedcites [271] Mossberg, 2008, Aerobic capacity and growth hormone deficiency after traumatic brain injury, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
The Results and Conclusions (page unavailable) show reduced aerobic capacity in patients with traumatic brain injury and GH insufficiency or deficiency; the Results also report an association between GH response and body mass index. The paper does not demonstrate the full list of cognitive, quality-of-life, metabolic, cardiovascular-risk, and muscle-force impairments in these patients, and its study population did not include sports-related head trauma. (LLM, conf=0.88)
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The pooled prevalence rates of any hormone deficiency and multiple pituitary deficiencies without confirmatory testing (Table 4) were 28 and 6%, respectively.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > C. Prevalence and incidence of hypopituitarism after brain injury
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These studies included data on 1291 TBI patients.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Results
plainn = 1,291- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one. The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“GH is the most common hormone lost after TBI, followed by ACTH, gonadotropins (FSH and LH), and TSH.”
- Also stated in: § C. Prevalence and incidence of hypopituitarism after brain injury · plain
“GHD was found to be the most common deficit, with a prevalence of 9%, followed by ACTH (6%), LH/FSH (5%), and TSH (1%) deficiencies.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > Abstract
plainn = 313- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § C. Prevalence and incidence of hypopituitarism after brain injury · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The prevalence rates of any hypopituitarism and multiple pituitary deficiencies were 24 and 8%, respectively, when evaluating those with severe TBI, in comparison to 29 and 6%, respectively, in all other studies (P ϭ .47 and P ϭ .08,respectively, with two-sided 2 test).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > C. Prevalence and incidence of hypopituitarism after brain injury
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“After confirmatory testing, the pooled prevalence rates of any hypopituitarism and multiple pituitary deficiencies were 15 and 4%, respectively.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > C. Prevalence and incidence of hypopituitarism after brain injury
plainn = 313- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“GHD was found to be the most common deficit, with a prevalence of 9%, followed by ACTH (6%), LH/FSH (5%), and TSH (1%) deficiencies.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > C. Prevalence and incidence of hypopituitarism after brain injury
plainn = 313- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If the results of pathological screening tests alone had been used in the same 313 patients, the prevalence rates of any hypopituitarism and multiple pituitary deficiencies would have been 20 and 4%, respectively.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > C. Prevalence and incidence of hypopituitarism after brain injury
hedgedn = 313- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the present review, the prevalence rates of any hypopituitarism and multiple pituitary deficiencies in all TBI patients (including all severities) were analyzed, and we found 29 and 6%, respectively (Table 3).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not matchedcites Table 3
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total TBI, n | 1203 | 156 | 123 | 142 | 51 | 315 | 70 | |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total TBI, % | 100.0% 13.0% 10.2% 11.8% 4.2% 27.8% | 6.2% | | | | | | |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 1,203- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
- Also stated in: § X. Summary and Future Directions · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“| Total TBI, n | 1203 | 156 | 123 | 142 | 51 | 315 | 70 | |”
- Also stated in: § X. Summary and Future Directions · plain
“| Total TBI, % | 100.0% 13.0% 10.2% 11.8% 4.2% 27.8% | 6.2% | | | | | | |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
plainn = 1,203- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
- Also stated in: § X. Summary and Future Directions · plain
In the paper
“Recently, a group of experts reviewed the literature on TBI-induced hypopituitarism and concluded that it is often not appreciated or diagnosed and that the medical community is not adequately informed about the importance of the problem (17).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > I. Introduction
What the sources say
- Not checked yetcites [17] Tanriverdi, 2011, Manifesto for the current understanding and management of traumatic brain injury-induced hypopituitarism, J Endocrinol Invest
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hypopituitarism after TBI may have a negative impact on the pace or degree of functional recovery and cognition.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
In the paper
“Additional studies emphasized the role Table 1.Descriptions of Commonly Used Clinical Terms of TBI”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > II. Prevalence of Chronic Posttraumatic Anterior Pituitary Dysfunction in Adults
What the sources say
- Not checked — no full text of the sourcecites [19] Kokshoorn, 2010, Hypopituitarism following traumatic brain injury: prevalence is affected by the use of different dynamic tests and different normal values, Eur J Endocrinol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The GHRHϩARG test, which has been more commonly used and is widely available (22), was only used in patients who had contraindications to other testing.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > Severity
What the sources say
- Not checked — no full text of the sourcecites [22] Hazem, 2011, The accuracy of diagnostic tests for GH deficiency in adults: a systematic review and meta-analysis, Eur J Endocrinol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“At the fifth year, the prevalence of permanent anterior pituitary hormone deficiency was 28, 4, and 4% for GH, gonadotropin, and ACTH, respectively.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > I. Introduction
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
plainn = 25- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Boxing, a very common combative sport that is practiced worldwide, is associated with chronic, repetitive head trauma and may be responsible for TBI (39,40).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Definition of sports-related traumatic brain injury
What the sources say
- Not checked — no full text of the sourcecites [39] Powell, 2001, Cerebral concussion: causes, effects, and risks in sports, J Athl Train
- Not checked yetcites [40] Zhang, 2003, Increased diffusion in the brain of professional boxers: a preclinical sign of traumatic brain injury?, AJNR Am J Neuroradiol
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Both treatment regimens were found to facilitate the initial learning of the spatial task and to mitigate the deleterious effects of scopolamine.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Thyroid hormone
What the sources say
- Not checked — no full text of the sourcecites [57] Smith, 2001, The effects of induced hypogonadism on arterial stiffness, body composition, and metabolic parameters in males with prostate cancer, J Clin Endocrinol Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Kickboxers had a higher incidence of GH and ACTH deficiencies: 22.7 and 9.1%, respectively.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked — no full text of the sourcecites [38] Tanriverdi, 2007, Kickboxing sport as a new cause of traumatic brain injury-mediated hypopituitarism, Clin Endocrinol (Oxf) source
plaincorrelationaln = 22- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one. The quote only partly states this claim.
In the paper
“The amnesic patients (ie, those who could not identify events shortly before, during, or shortly after the crash) demonstrated lower norepinephrine/cortisol ratios, were less likely to meet criteria for PTSD, and displayed fewer symptoms of PTSD than those who were not amnesic.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Cortisol
What the sources say
- Not checked — no full text of the sourcecites [60] Flesher, 2001, Amnesia, neuroendocrine levels and PTSD in motor vehicle accident victims, Brain Inj source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A study in amateur boxers in 2004 (37) evaluated pituitary function in 11 actively competing or retired male amateur boxers compared with those of healthy nonboxing controls.Based on the GHRHϩGHRP-6 test, isolated GHD was diagnosed in 45% of the boxers, and the mean IGF-1 levels in boxers were significantly lower than in the control group.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked — no full text of the sourcecites [37] Kelestimur, 2004, Boxing as a sport activity associated with isolated GH deficiency, J Endocrinol Invest source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Nine of the 61 boxers (15%; eight retired and one actively competing) had GHD, and five of the 61 boxers (8%) had ACTH deficiency.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked — no full text of the sourcecites [46] Tanriverdi, 2008, Brief communication: pituitary volume and function in competing and retired male boxers, Ann Intern Med source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Applying a very conservative approach, with the arbitrary assumption that relevant neuroendocrine dysfunction is present in only 6% of TBI survivors (for reasons of simplicity, assuming that only those with multiple hormone deficiencies are relevantly affected by pituitary dysfunction), we would expect an incidence of seven cases per 100 000 persons per year in the population.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > C. Prevalence and incidence of hypopituitarism after brain injury
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- The authors state this as an assumption: Relevant neuroendocrine dysfunction is present in only 6% of TBI survivors.
- The authors state this as an assumption: Only those with multiple hormone deficiencies are relevantly affected by pituitary dysfunction.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“It is noteworthy that in these studies, only the results of stimulation tests were analyzed and no additional information, such as clinical signs of ACTH or GH deficiency, was analyzed.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > D. Is hypopituitarism more common after brain damage than in the normal population?
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Therefore, kickboxing is a newly appreciated cause of TBI, and kickboxers are at increased risk of hypopituitarism, particularly isolated GH deficiency (38).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Pituitary dysfunction due to sports-related brain injury
What the sources say
- Not checked — no full text of the sourcecites [38] Tanriverdi, 2007, Kickboxing sport as a new cause of traumatic brain injury-mediated hypopituitarism, Clin Endocrinol (Oxf) source
plaindirectn = 22- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Despite the frequency and well-known health outcomes, trauma due to sports is not generally taken into account as a cause of TBI in most epidemiological studies (7).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Definition of sports-related traumatic brain injury
What the sources say
- Not checked — no full text of the sourcecites [7] Kelestimur, 2005, Chronic trauma in sports as a cause of hypopituitarism, Pituitary source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The data suggest that thyroid hormone regulates neurogenesis in the rat hippocampus, providing a logical role for the thyroid hormone in learning and memory (56).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Thyroid hormone
What the sources say
- Not checked — no full text of the sourcecites [56] Desouza, 2005, Thyroid hormone regulates hippocampal neurogenesis in the adult rat brain, Mol Cell Neurosci source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, these analyses only show the prevalence of abnormal results and do not necessarily reflect true GHD or ACTH deficiency.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > D. Is hypopituitarism more common after brain damage than in the normal population?
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The extent to which thyroid replacement improves cognitive, psychological, and psychiatric symptoms is somewhat unclear and may be dependent upon the severity of hypothyroidism before treatment (eg, subclinical vs pri- mary hypothyroidism) (58).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Thyroid hormone
What the sources say
- Not checked — no full text of the sourcecites [58] Davis, 2007, Exercise adherence in patients with chronic obstructive pulmonary disease: an exploration of motivation and goals, Rehabil Nurs source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Chronic TBI has been reported in 20% of professional boxers (41,42).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Definition of sports-related traumatic brain injury
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Isolated GHD is the most common pituitary dysfunction.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > C. Prevention of sports-related neuroendocrine dysfunction
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“BMI was similar in those with TBI with hypopituitarism and in those without, suggesting that the data were independent of obesity.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The authors noted a weak trend toward the GH-deficient/-insufficient group having a more severe injury as seen on computed tomography (CT) scans.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [71] Kelly, 2006, Neurobehavioral and quality of life changes associated with growth hormone insufficiency after complicated mild, moderate, or severe traumatic brain injury, J Neurotrauma source
hedgedcorrelationaln = 44- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Both studies showed alterations in lipid profile and body composition with an increase in BMI in their subjects.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [80] Klose, 2007, Posttraumatic hypopituitarism is associated with an unfavorable body composition and lipid profile, and decreased quality of life 12 months after injury, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [46] Tanriverdi, 2008, Brief communication: pituitary volume and function in competing and retired male boxers, Ann Intern Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“However, many studies on metabolic impairments in classical hypopituitarism demonstrated that alterations are equally prevalent between isolated GHD or multiple deficits (79,91), suggesting GHD as the principal actor.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [79] Verhelst, 2011, Prevalence and characteristics of the metabolic syndrome in 2479 hypopituitary patients with adult-onset GH deficiency before GH replacement: a KIMS analysis, Eur J Endocrinol source
- Not checked — no full text of the sourcecites [91] Mersebach, 2003, Comparisons of leptin, incretins and body composition in obese and lean patients with hypopituitarism and healthy individuals, Clin Endocrinol (Oxf) source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The authors confirmed previous data on a tendency toward an altered lipid profile in TBI subjects with hypopituitarism with elevated triglycerides, but similar high-density lipoprotein (HDL), low-density lipoprotein, and total cholesterol in both populations.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [81] Prodam, 2013, Metabolic alterations in patients who develop traumatic brain injury (TBI)-induced hypopituitarism, Growth Horm IGF Res source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Others classify TBI into acute and chronic mechanisms: 1) acute brain injury that consists of mild TBI or concus-sion, including its short-term sequel and catastrophic brain injury that may lead to death; or 2) chronic brain injury, called chronic traumatic encephalopathy (CTE), which is a neurodegenerative disorder due to chronic repetitive head trauma in athletes participating in contact sports”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [92] Blennow, 2012, The neuropathology and neurobiology of traumatic brain injury, Neuron source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“An interaction with untreated hypogonadism cannot be ruled out because T replacement is frequently forgotten or underestimated, whereas hypothyroidism and hypocortisolism have always been treated in patients with hypopituitarism due to their fundamental importance for life.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > V. Metabolic Consequences of Posttraumatic Hypopituitarism
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The major biomechanical mechanisms of brain damage after TBI include: 1) focal brain damage due to contact injury types causing fracture of the skull, contusions, lacerations, intracranial hemorrhage, and intracerebral hematomas; or 2) diffuse (multifocal) brain damage due to acceleration/deceleration injury types causing concussion, diffuse axonal injury (DAI), diffuse vascular injury, hypoxic-Is”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [99] Graham, 2000, Recent advances in neurotrauma, J Neuropathol Exp Neurol source
- Not matchedcites [100] Marshall, 2000, Head injury: recent past, present, and future, Neurosurgery
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites [101] Nortje, 2004, Traumatic brain injury: physiology, mechanisms, and outcome, Curr Opin Neurol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“The GH-deficient group showed greater deficits in simple attention, more intrusions and repetitions on a memory task, increased reaction time, and greater emotional disruption.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [73] León-Carrión, 2007, Cognitive deterioration due to GH deficiency in patients with traumatic brain injury: a preliminary report, Brain Inj source
plaincorrelationaln = 22- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Compared to individuals with normal pituitary function, those with deficits of the GH axis had higher rates of at least one marker of depression, as well as reduced quality of life in the domains of general health, physical health, emotional health, pain, energy, and fatigue.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 4. Growth hormone: cognitive impact of posttraumatic GHD
What the sources say
- Not checked — no full text of the sourcecites [71] Kelly, 2006, Neurobehavioral and quality of life changes associated with growth hormone insufficiency after complicated mild, moderate, or severe traumatic brain injury, J Neurotrauma source
plaincorrelationaln = 44- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Brain swelling (edema) after TBI can be induced by primary or secondary insults, and it causes increased intracerebral pressure (ICP) and secondary ischemic events (119, 120).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [119] Marmarou, 2000, Contribution of edema and cerebral blood volume to traumatic brain swelling in head-injured patients, J Neurosurg source
- Not checked — no full text of the sourcecites [120] Marmarou, 2006, Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries, J Neurosurg source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The mechanisms by which cerebral ischemia occurs comprise morphological injury, such as vessel distortion as a result of mechanical displacement, hypotension in the presence of autoregulatory failure, inadequate availability of cholinergic neurotransmitters or nitric oxide, and potentiation of prostaglandin-induced vasoconstriction (112-115).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [112] Armstead, 2006, Differential activation of ERK, p38, and JNK MAPK by nociceptin/orphanin FQ in the potentiation of prostaglandin cerebrovasoconstriction after brain injury, Eur J Pharmacol source
- Not checked — no full text of the sourcecites [113] DeWitt, 2003, Traumatic cerebral vascular injury: the effects of concussive brain injury on the cerebral vasculature, J Neurotrauma source
- Not checked — no full text of the sourcecites [114] McIntosh, 1996, Neuropathological sequelae of traumatic brain injury: relationship to neurochemical and biomechanical mechanisms, Lab Invest
- Not checked — no full text of the sourcecites [115] Scremin, 1997, Cholinergic modulation of cerebral cortical blood flow changes induced by trauma, J Neurotrauma source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Nevertheless, novel MRI techniques, including diffusion tensor imaging, have been found to be useful to evaluate axonal integrity and to identify DAI in patients with mild TBI (108, 109).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [108] Bazarian, 2007, Diffusion tensor imaging detects clinically important axonal damage after mild traumatic brain injury: a pilot study, J Neurotrauma source
- Not checked — no full text of the sourcecites [109] Mayer, 2010, A prospective diffusion tensor imaging study in mild traumatic brain injury, Neurology source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The second stages of the pathophysiological cascade are characterized by terminal membrane depolarization accompanied by excessive release of excitatory neurotransmitters (excitotoxicity) such as glutamate and aspartate, activation of N-methyl-D-aspartate, and voltage-dependent channel opening (Na ϩ , K ϩ , Ca 2ϩ ) (97, 121-123).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [97] Werner, 2007, Pathophysiology of traumatic brain injury, Br J Anaesth source
- Not checked — no full text of the sourcecites [121] Floyd, 2005, Mechanical strain injury increases intracellular sodium and reverses Na+/Ca2+ exchange in cortical astrocytes, Glia source
- Not checked — no full text of the sourcecites [122] Obrenovitch, 1997, Is high extracellular glutamate the key to excitotoxicity in traumatic brain injury?, J Neurotrauma source
- Not checked — no full text of the sourcecites [123] Robertson, 1999, Prevention of secondary ischemic insults after severe head injury, Crit Care Med source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Moreover, posttraumatic vasospasm is an important secondary insult that determines the ultimate outcome and further increases ischemia and hypoxia (116).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [116] Oertel, 2005, Posttraumatic vasospasm: the epidemiology, severity, and time course of an underestimated phenomenon: a prospective study performed in 299 patients, J Neurosurg source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“However, it is important to emphasize that the autopsy studies were focused on fatal injury victims, and these cases probably had severe hypotension, hypoxemia, and/or ischemia due to high ICP and herniation.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The primary insult (ie, primary damage, mechanical damage) happens at the moment of impact.In terms of treatment, this type of injury is entirely sensitive to preventive, but not therapeutic measures.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Because cerebral metabolic dysfunction occurs due to head trauma, cerebral ischemia and hypoxia lead to the accumulation of lactic acid due to anaerobic glycolysis, increased permeability of membranes, and consecutive edema formation (117, 118).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. General terms and hypotheses concerning pathophysiology of brain damage in TBI
What the sources say
- Not checked — no full text of the sourcecites [117] Clark, 1997, Cerebrospinal fluid adenosine concentration and uncoupling of cerebral blood flow and oxidative metabolism after severe head injury in humans, Neurosurgery source
- Not checked — no full text of the sourcecites [118] Glenn, 2003, Energy dysfunction as a predictor of outcome after moderate or severe head injury: indices of oxygen, glucose, and lactate metabolism, J Cereb Blood Flow Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In one study, it was shown that in the acute phase of TBI, the pituitary glands of the patients were significantly enlarged compared to those of the control subjects, and most patients also demonstrated other abnormalities, such as hemorrhage, infarction, signal abnormalities, and/or partial stalk transection (136).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [136] Maiya, 2008, Magnetic resonance imaging changes in the pituitary gland following acute traumatic brain injury, Intensive Care Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Some patients may have a pre-existing susceptibility to TBI-induced pituitary dysfunction.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Genetic polymorphisms may also play a role in the development of some central nervous system disorders.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“The apolipoprotein (APO) E4 allele has been suggested as a risk factor for the development of Alzheimer's disease (167).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [167] Welsh-Bohmer, 1997, Apolipoprotein E genotypes in a neuropathological series from the Consortium to Establish a Registry for Alzheimer's Disease, Ann Neurol source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Conversely, a potential association between the APO E polymorphism, head injury outcome, and traumatic hematoma volume was also reported (168, 169).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [168] Liaquat, 2002, Effect of apolipoprotein E genotype on hematoma volume after trauma, J Neurosurg source
- Not checked — no full text of the sourcecites [169] Nicoll, 1995, Apolipoprotein E ϵ 4 allele is associated with deposition of amyloid β-protein following head injury, Nat Med source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In addition, it is important to keep in mind that some medications (eg, high doses of heparins, phenobarbital, opioids, and etomidate) used in the ICU may adversely impact endocrine function or may alter the accuracy of laboratory testing (152, 153).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [152] Thomas, 2010, Drug-induced endocrine disorders in the intensive care unit, Crit Care Med source
- Not checked — no full text of the sourcecites [153] Vuong, 2010, The effects of opioids and opioid analogs on animal and human endocrine systems, Endocr Rev source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the fifth year, seven of 25 patients (28%) had strongly positive (titers Ն 1/16) AHAs, and five of 25 patients (20%) had strongly positive APAs.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
plainn = 25- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“AHAs and APAs were detected in 21.3 and 22.9% of the boxers, respectively.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [164] Tanriverdi, 2010, Investigation of antihypothalamus and antipituitary antibodies in amateur boxers: is chronic repetitive head trauma-induced pituitary dysfunction associated with autoimmunity?, Eur J Endocrinol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The mean pituitary apparent diffusion coefficient (which reflects mean tissue water diffusivity) was significantly decreased, correlating with the existence of hypopituitarism, suggesting that microstructural damage occurs in the normal-appearing brain of mild TBI patients (158).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [158] Zheng, 2014, Decrease in pituitary apparent diffusion coefficient in normal appearing brain correlates with hypopituitarism following traumatic brain injury, J Endocrinol Invest source
hedgedcorrelationaln = 42- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one. The quote only partly states this claim.
In the paper
“APO E, which is a key protein in enhancing lipid transport and metabolism within the nervous system and has a role in neuronal repair and maintenance, is one of the most abundant proteins in the hypothalamo-pituitary region (170).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [170] Nishida, 2005, The top 10 most abundant transcripts are sufficient to characterize the organs functional specificity: evidences from the cortex, hypothalamus and pituitary gland, Gene source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together these data suggested a possible role of vascular injury.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
In the paper
“Antipituitary antibodies (APAs) were positive in 44.8% of the patients, but none of the control patients had APA positivity, and the pituitary dysfunction development ratio was significantly higher in APA-positive patients when compared with APA-negative patients.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plaincorrelationaln = 29- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Other studies have suggested the possible role of autoimmunity and genetic predisposition in the development of TBI-induced hypopituitarism (16,(162)(163)(164).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
- Not checked — no full text of the sourcecites [162] Tanriverdi, 2008, Antipituitary antibodies after traumatic brain injury: is head trauma-induced pituitary dysfunction associated with autoimmunity?, Eur J Endocrinol source
- Not checked — no full text of the sourcecites [163] Tanriverdi, 2008, Apolipoprotein E3/E3 genotype decreases the risk of pituitary dysfunction after traumatic brain injury due to various causes: preliminary data, J Neurotrauma source
- Not checked — no full text of the sourcecites [164] Tanriverdi, 2010, Investigation of antihypothalamus and antipituitary antibodies in amateur boxers: is chronic repetitive head trauma-induced pituitary dysfunction associated with autoimmunity?, Eur J Endocrinol source
hedgedconditionaln = 29- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Each pituitary hormone must be tested separately because there is a variable pattern of hormone deficiency among patients with TBI-induced hy-popituitarism (194).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Introduction
What the sources say
- Not checked — no full text of the sourcecites [194] Schneider, 2007, Hypopituitarism, Lancet source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Based on the experimental evidence, it was hypothesized that GH may facilitate the proliferation, differentiation, and survival of new neurons in response to brain injury (191,192).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [191] Arce, 2013, Role of growth hormone (GH) in the treatment on neural diseases: from neuroprotection to neural repair, Neurosci Res source
- Not checked — no full text of the sourcecites [192] Devesa, 2013, Growth hormone (GH) and brain trauma, Horm Behav source
hedgedconditional- Asserted: fails — The authors may not put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The authors may not put it forward as true. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Biomechanical properties in sports-related chronic repetitive low-energy head trauma are different from highenergy single head trauma due to traffic accidents.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There are several secondary mechanisms (secondary insult) derived from the primary insult that may contribute to the maintenance of the primary damage and may lead to further vascular and pituitary gland injury.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the largest clinical study regarding pituitary functions in boxers, duration of boxing and retirement age were significantly associated with a decrease in pituitary function, supporting the cumulative effect of sports-related head trauma (46).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [46] Tanriverdi, 2008, Brief communication: pituitary volume and function in competing and retired male boxers, Ann Intern Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“These include an increase in ICP, cytokines, impaired blood flow, high blood pressure, hypotension, edema, hyponatremia, cerebral ischemia and hypoxia, increased free radicals, oxidative stress, neuronal metabolic dysfunction, and increased levels of excitatory amino acids.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“As in classical hypopituitarism, evaluation of the somatotroph and corticotroph axes requires dynamic stimulation testing to clearly separate normal from deficient responses, and the normative cutoff should be defined using healthy volunteers in each local laboratory (18,194,195).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Introduction
What the sources say
- Not checked — no full text of the sourcecites [18] Kelly, 2000, Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report, J Neurosurg source
- Not checked — no full text of the sourcecites [194] Schneider, 2007, Hypopituitarism, Lancet source
- Not checked — no full text of the sourcecites [195] Ghigo, 2005, Consensus guidelines on screening for hypopituitarism following traumatic brain injury, Brain Inj source
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It seems that chronic hypopituitarism after head trauma could be a consequence of the dynamic balance between neurodegenerative and neuroprotective mechanisms.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although a single, mild impact may not yield sufficient force to cause an injury, repeated mild impacts may result in acute vascular injury in the pituitary gland, probably with the presence of increased inflammatory activity.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Experimental animal models of trauma allow control of mechanical procedures, as well as standardization of the injury.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“High titers of APA/AHA formation and damage to the barrier properties of tanycytes may also play a role in long-term pituitary damage and may intensify the deleterious effects of neuroinflammation.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As a result of primary injury (primary insult), direct mechanical damage (via edema, skull fracture, hematoma, rotational and shearing injuries, etc) to the hypothalamo-pituitary region and/or hypophyseal portal vessels may occur.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 3. Summary and proposed mechanisms of TBI-induced hypopituitarism
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“An increase in Evans Blue dye extravasation in the pituitary gland was observed, which implies that a vascular event occurred, supporting the vascular hypothesis in the pathogenesis (175).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Experimental models of posttraumatic hypopituitarism and future directions
What the sources say
- Not checked — no full text of the sourcecites [175] Greco, 2013, The effects of repeat traumatic brain injury on the pituitary in adolescent rats, J Neurotrauma source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Boxers have been shown to have microstructural damage to the brain associated with chronic TBI by using MRI and diffusion-weighted imaging, and interestingly, increased diffusion values were found even when routine MRI results were negative.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Infrequent concussions and DAI, however, seem to be insufficient to cause chronic hypopituitarism a long time after head trauma, suggesting the importance of cumulative effect.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Current hypotheses on TBI-induced hypopituitarism
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“however, the measurement of basal hormones alone may not be distinctive due to the pulsatile, circadian, or situational secretion of some hormones.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Diagnostic tests
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“The authors demonstrated that DAI and/or basal skull fracture during the acute phase and older age are major risk factors of hypopituitarism in the chronic phase (156).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [156] Schneider, 2008, Predictors of anterior pituitary insufficiency after traumatic brain injury, Clin Endocrinol (Oxf) source
boostedcorrelationaln = 78- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In TBI patients, central hypothyroidism is easily diagnosed when levels of free T 4 are decreased and TSH levels are low or more often normal.Dynamic testing is generally not necessary because it does not add to diagnostic reliability.T 3 is still normal in most cases (210 -213).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. TRH-TSH-thyroid axis
What the sources say
- Not checked — no full text of the sourcecites [210] Ferretti, 1999, Evaluation of the adequacy of levothyroxine replacement therapy in patients with central hypothyroidism, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [211] Hartoft-Nielsen, 2004, Thyrotropin-releasing hormone stimulation test in patients with pituitary pathology, Horm Res source
- Not checked — no full text of the sourcecites [212] Mehta, 2003, Is the thyrotropin-releasing hormone test necessary in the diagnosis of central hypothyroidism in children, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [213] Westwood, 2000, The combined pituitary function test in children: an evaluation of the clinical usefulness of TRH and LHRH stimulation tests through a retrospective analysis of one hundred and twenty six cases, Clin Endocrinol (Oxf) source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Moreover, they showed that the presence of skull fractures on the admission CT and increased age were significantly associated with chronic phase hypopituitarism (234).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [234] Lauzier, 2014, Clinical outcomes, predictors, and prevalence of anterior pituitary disorders following traumatic brain injury: a systematic review, Crit Care Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, the literature is insufficient to define precise predictive factors, and there are controversial results among studies.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In TBI patients, secondary adrenal insufficiency can be excluded at morning cortisol levels greater than 500 nmol/L (Ͼ18 g/dL) and is indicated below 83-100 nmol/L (Ͻ3 g/dL).Levels in between require a stimulation test (194, 199 -201).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. HPA axis
What the sources say
- Not checked — no full text of the sourcecites [194] Schneider, 2007, Hypopituitarism, Lancet source
- Not checked — no full text of the sourcecites [199] Arlt, 2003, Adrenal insufficiency, Lancet source
- Not checked — no full text of the sourcecites [200] Lamberts, 1998, Pituitary insufficiency, Lancet source
- Not matchedcites [201] Snyder PJ , CooperDS, MartinKA. Diagnosis of hypopituitarism. UpToDate web site. http://www.uptodate.com/contents/diagnosis-of-hypopituitarism. Updated May 6, 2014.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Preliminary data suggest that APAs and AHAs could be potential predictors and useful clinical markers (162).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [162] Tanriverdi, 2008, Antipituitary antibodies after traumatic brain injury: is head trauma-induced pituitary dysfunction associated with autoimmunity?, Eur J Endocrinol source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These data clearly show that although the risk of developing hypopituitarism is highest in severe TBI, the risk is substantially high in mild TBI and is even comparable with moderate TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
boostedcorrelationaln = 1,015- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Because TBI is an important cause of hypopituitarism, it is tempting to suggest that the first approach should be testing all patients with a history of TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
- Rests on an assumption: TBI is an important cause of hypopituitarism.
In the paper
“The authors showed that TBI-induced DI was not associated with the presence of anterior hypopituitarism but was associated with more severe head trauma and the presence of cerebral edema on CT scan (235).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [235] Agha, 2004, Posterior pituitary dysfunction after traumatic brain injury, J Clin Endocrinol Metab source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The first consensus guideline on screening for hypopituitarism after TBI was published by Ghigo et al (195) in 2005.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [195] Ghigo, 2005, Consensus guidelines on screening for hypopituitarism following traumatic brain injury, Brain Inj source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, this strategy is not cost-effective and would result in unnecessary health resource consumption for a community.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
- Rests on an assumption: Global screening of all patients with a history of TBI is not cost-effective.
In the paper
“However, these data need confirmation because ICP was monitored in only 27 patients, and elevated ICP was present in only three patients (30).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [30] Klose, 2007, Prevalence and predictive factors of post-traumatic hypopituitarism, Clin Endocrinol (Oxf) source
plainn = 3- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In contrast, it has been reported that hypopituitarism is rare (Ͻ1%; median, 13 mo after TBI) in unselected head trauma patients”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“It is important to note that, in the literature, most of the evaluated mild TBI patients had complicated mild TBI, which will be defined below.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, when we consider the high frequency of mild TBI among all TBI patients, it is obvious that pituitary dysfunction is not uncommon in patients with mild TBI and should not be ignored.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Overall, 12 of 32 patients (37.5%, mainly GH or ACTH deficiencies) had at least one pituitary hormone deficit during the chronic phase, and all of the patients with chronic hypopituitarism had suffered from either acute hypocortisolemia or acute central DI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [241] Hannon, 2013, Acute glucocorticoid deficiency and diabetes insipidus are common after acute traumatic brain injury and predict mortality, J Clin Endocrinol Metab source
plaincorrelationaln = 32- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Moreover, some experts in this field also suggest that global screening for hypopituitarism would, from a practical point of view, only focus on patients with moderate or severe head trauma (GCS Ͻ 13) (131, 230, 242-244).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [131] Behan, 2008, Neuroendocrine disorders after traumatic brain injury, J Neurol Neurosurg Psychiatry source
- Not checked — no full text of the sourcecites [230] Gasco, 2012, Hypopituitarism following brain injury: when does it occur and how best to test?, Pituitary source
- Not checked — no full text of the sourcecites [242] Aimaretti, 2007, Should every patient with traumatic brain injury be referred to an endocrinologist?, Nat Clin Pract Endocrinol Metab source
- Not checked — no full text of the sourcecites [243] Corneli, 2007, Managing patients with hypopituitarism after traumatic brain injury, Curr Opin Endocrinol Diabetes Obes source
- Not checked — no full text of the sourcecites [244] Glynn, 2013, Which patient requires neuroendocrine assessment following traumatic brain injury, when and how?, Clin Endocrinol (Oxf) source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Global screening of all mild TBI patients is not practical or costeffective (246).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [246] Tanriverdi, 2010, Pituitary function in subjects with mild traumatic brain injury: a review of literature and proposal of a screening strategy, Pituitary source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Another cross-sectional study including 104 hospitalized TBI patients reported increased ICP to predict posttraumatic hypopituitarism.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > A. Predictive factors for hypopituitarism
What the sources say
- Not checked — no full text of the sourcecites [30] Klose, 2007, Prevalence and predictive factors of post-traumatic hypopituitarism, Clin Endocrinol (Oxf) source
plaincorrelationaln = 3- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“All mild TBI patients included in the study needed hospitalization of more than 24 hours, and most of them were monitored in the ICU.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plainn = 18- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For instance, in one 3-year pro-spective follow-up study, 63% of patients had mild TBI, and three of 18 (17%) mild TBI patients had pituitary dysfunction.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plainn = 18- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“It has been reported that approximately 40% of mild TBI patients have no loss of consciousness (249).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked yetcites [249] Kraus, 2005, Epidemiology
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“It is important to recognize that, by definition, mild TBI is a heterogeneous diagnosis, and selection bias in TBI research is a common problem in this patient group (247).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [247] Luoto, 2013, Who gets recruited in mild traumatic brain injury research?, J Neurotrauma source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The number of TBI cases expected for a hospital covering a population of 500 000 inhabitants was estimated as 500 -1250 patients per year (80% mild, 10% moderate, and 10% severe TBI), which clearly suggests that mild TBI is the most common type of head trauma (245).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
What the sources say
- Not checked — no full text of the sourcecites [245] Lorenzo, 2005, Hypopituitarism and growth hormone deficiency in adult subjects after traumatic brain injury: who and when to test, Pituitary source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Agha et al (235) investigated posttraumatic diabetes insipidus (DI) retrospectively (median, 17 mo after the event) and reported the incidence of permanent central DI as 6.9%, although 26% of the patients were diagnosed as having central DI in the acute phase.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 7. Presence of APAs and AHAs
What the sources say
- Not checked — no full text of the sourcecites [235] Agha, 2004, Posterior pituitary dysfunction after traumatic brain injury, J Clin Endocrinol Metab source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Throughout the first 10 days after TBI, 78 of 100 patients had at least one plasma cortisol measurement of less than 300 nm/L, and most of the patients (63 of 78) had glucocorticoid deficiency on days 1-3.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Acute phase
What the sources say
- Not checked — no full text of the sourcecites [241] Hannon, 2013, Acute glucocorticoid deficiency and diabetes insipidus are common after acute traumatic brain injury and predict mortality, J Clin Endocrinol Metab source
plainn = 100- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In all six studies, pituitary function improved over a 12-month period, but in four of the studies (15, 27, 151, 181), new-onset pituitary abnormalities (reported as lower frequency than recovery) were reported at the 12month evaluation.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked — no full text of the sourcecites [27] Schneider, 2006, Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury, Eur J Endocrinol source
- Not checked — no full text of the sourcecites [151] Krahulik, 2010, Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults, J Neurosurg source
- Not checked — no full text of the sourcecites [181] Aimaretti, 2005, Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study, J Clin Endocrinol Metab source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“This is because isolated GHD was reported in most of the prospec- tive studies, and a significant number of the patients recovered at 12 months after TBI.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked yetcites [17] Tanriverdi, 2011, Manifesto for the current understanding and management of traumatic brain injury-induced hypopituitarism, J Endocrinol Invest
- Not checked — no full text of the sourcecites [246] Tanriverdi, 2010, Pituitary function in subjects with mild traumatic brain injury: a review of literature and proposal of a screening strategy, Pituitary source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“One of the most important findings of this study was the low plasma cortisol, which has been reported to be significantly associated with increased mortality and hyponatremia.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Acute phase
What the sources say
- Not checked — no full text of the sourcecites [241] Hannon, 2013, Acute glucocorticoid deficiency and diabetes insipidus are common after acute traumatic brain injury and predict mortality, J Clin Endocrinol Metab source
plaincorrelationaln = 100- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“ACTH deficiency occurred in 53% of the patients, with 75% of them developing adrenal insufficiency within the first 4 days.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Acute phase
What the sources say
- Not checked — no full text of the sourcecites [238] Cohan, 2005, Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study, Crit Care Med source
plaincorrelationaln = 80- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The wide range in the percentages of ACTH deficiency among different studies could be due to the measurement of morning serum cortisol levels at different time points after TBI or using different diagnostic cutoff levels for adrenal insufficiency.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Acute phase
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When we only screen complicated mild TBI patients and use exclusion criteria, more than 50% of the mild TBI patients will not be screened unnecessarily.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Which patients should be screened?
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Current evidence suggests that HPA axis insufficiency during the acute phase after head trauma is associated with a poor neurological outcome, a greater need for vasoactive drug therapy, hyponatremia, relative or absolute hypoglycemia, hemodynamic instability, and rapidly progressive hypotension, all of which may increase the risk of morbidity and mortality (238 -241).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Acute phase
What the sources say
- Not checked — no full text of the sourcecites [238] Cohan, 2005, Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study, Crit Care Med source
- Not checked — no full text of the sourcecites [239] Della Corte, 1998, Provocative hypothalamopituitary axis tests in severe head injury: correlations with severity and prognosis, Crit Care Med source
- Not checked — no full text of the sourcecites [240] Hackl, 1991, Endocrine abnormalities in severe traumatic brain injury–a cue to prognosis in severe craniocerebral trauma?, Intensive Care Med source
- Not checked — no full text of the sourcecites [241] Hannon, 2013, Acute glucocorticoid deficiency and diabetes insipidus are common after acute traumatic brain injury and predict mortality, J Clin Endocrinol Metab source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The present data suggest that the changes in the gonadotropic axis in the acute phase of TBI are mainly an adap-tive response, and most of the hormone deficiencies are transient (14,15,256).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 1. Treatment of TSH, FSH/LH, and GH deficiencies in the acute phase
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
- Not checked — no full text of the sourcecites [15] Tanriverdi, 2006, High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma, J Clin Endocrinol Metab source
- Not checked yetcites [256] Tanriverdi, 2013, Endocrinology of acute brain injury
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“It is important to note that the dynamic hormonal changes were reported mainly in mild TBI patients, but in severe TBI patients, ACTH and GH deficiencies at the first year persisted at the third-year evaluation (161).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In patients with mild and moderate TBI, ACTH and GH deficiencies may improve over time in a considerable number of patients, but, although rarely, they may also worsen over the 5-year period.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
hedgedconditionaln = 25- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the chronic phase, 48% of the patients had ACTH deficiency, and 39% had GH deficiency.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [25] Kleindienst, 2009, Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation, J Neurotrauma source
plainn = 23- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“However, based on the strong evidence given in retrospective studies, the clinical behavior and neurological and neuroendocrinological consequences of moderate TBI are similar to severe TBI and are generally classified with severe TBI (14,195,244).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [14] Schneider, 2007, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review, JAMA source
- Not checked — no full text of the sourcecites [195] Ghigo, 2005, Consensus guidelines on screening for hypopituitarism following traumatic brain injury, Brain Inj source
- Not checked — no full text of the sourcecites [244] Glynn, 2013, Which patient requires neuroendocrine assessment following traumatic brain injury, when and how?, Clin Endocrinol (Oxf) source
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Nevertheless, it is important to emphasize that GH replacement therapy could be beneficial in aiding rehabilitation of TBI patients, but currently no studies have been performed in this area.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“In addition, five of six (83.3%)ACTH-deficient patients recovered after 1 year, and new-onset ACTH deficiency was detected at 3 years in one patient.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In patients with moderate and severe TBI, if there is any pituitary hormonal deficiency at the 12th month, we suggest appropriate replacement of the deficient hormones, and because the recovery of pituitary dysfunction is extremely rare, we recommend routine follow-up for the titration of replacement therapy.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
In the paper
“Although most of the pituitary hormone deficiencies improved over time, there were substantial percentages of pituitary hormone deficiencies at the fifth year (28% GH, 4% ACTH, and 4% gonadotropin deficiencies).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [16] Tanriverdi, 2013, A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity?, J Neurotrauma source
plainn = 25- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The CRASH trial, which is a large-scale clinical study including 10 000 patients with head trauma, and other literature reviews have clearly shown that routine administration of corticosteroids at high doses or pharmacological doses (30 mg/kg methylprednisolone) to all TBI patients is not indicated or may be harmful (257, 265).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of ACTH deficiency in the acute phase
What the sources say
- Not checked — no full text of the sourcecites [257] Cooper, 2007, Adrenal insufficiency in critical illness, J Intensive Care Med source
- Not checked — no full text of the sourcecites [265] Roberts, 2004, Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial, Lancet source
boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“No patient had TSH or gonadotropin deficiencies after 3 years, compared with 6.6 and 3.3%, respectively, at 1 year.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“After an individual evaluation of GHD from 1 year to 3 years after TBI, seven of 13 (53.8%)GH-deficient patients recovered after 1 year, and new-onset GHD was detected at 3 years in one patient.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Chronic phase
What the sources say
- Not checked — no full text of the sourcecites [161] Tanriverdi, 2008, Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study, Clin Endocrinol (Oxf) source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We believe that awareness of TBI-induced hypopituitarism in the medical community may lead to early diagnosis and, therefore, early treatment of hypopituitarism.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.
In the paper
“After only 3 months of treatment, they found an improvement in the treated group in the domains of vocabulary, verbal IQ, and total IQ.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Not checked — no full text of the sourcecites [277] Reimunde, 2011, Effects of growth hormone (GH) replacement and cognitive rehabilitation in patients with cognitive disorders after traumatic brain injury, Brain Inj source
plaindirectn = 11- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“An understanding of possible neuroprotective mechanisms (the regeneration capacity of portal vessels or the activation of pituitary stem/progenitor cells) in the recovery of pituitary functions is necessary to prevent the development of permanent pituitary dysfunction.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
In the paper
“In an observational uncontrolled study, Kreitschmann-Andermahr et al (274) reported an improved quality of life after 12 months of GH replacement following TBI, similar to that seen in patients with GHD from other causes.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Not checked — no full text of the sourcecites [274] Kreitschmann-Andermahr, 2008, Growth hormone deficient patients after traumatic brain injury–baseline characteristics and benefits after growth hormone replacement–an analysis of the German KIMS database, Growth Horm IGF Res source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“They did not see any change in attention, executive functioning, or language.”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Not checked — no full text of the sourcecites [276] Moreau, 2013, Growth hormone replacement therapy in patients with traumatic brain injury, J Neurotrauma source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Therefore, in the latest Endocrine Society guideline on the evaluation and treatment of adult GHD, as part of their standard clinical care, patients with severe GHD (diagnosed by appropriate dynamic tests and with relevant clinical features) were recommended individualized physiological doses of recombinant GH treatment (215).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Not checked — no full text of the sourcecites [215] Molitch, 2011, Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society clinical practice guideline, J Clin Endocrinol Metab source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“It is important to mention that adult GH-deficient patients, both with isolated GHD and with multiple pituitary hormone deficiencies, have similar baseline clinical characteristics and respond similarly to GH replacement (269, 270).”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > 2. Treatment of GHD
What the sources say
- Not checked — no full text of the sourcecites [269] Abs, 2005, Isolated growth hormone (GH) deficiency in adult patients: baseline clinical characteristics and responses to GH replacement in comparison with hypopituitary patients. A sub-analysis of the KIMS database, Growth Horm IGF Res source
- Not checked — no full text of the sourcecites [270] Klose, 2009, From isolated GH deficiency to multiple pituitary hormone deficiency: an evolving continuum - a KIMS analysis, Eur J Endocrinol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The authors state this as an assumption.
Relevant neuroendocrine dysfunction is present in only 6% of TBI survivors.
“with the arbitrary assumption that relevant neuroendocrine dysfunction is present in only 6% of TBI survivors”
The authors state this as an assumption.
Only those with multiple hormone deficiencies are relevantly affected by pituitary dysfunction.
“for reasons of simplicity, assuming that only those with multiple hormone deficiencies are relevantly affected by pituitary dysfunction”
The authors state this as an assumption.
Posttraumatic hypopituitarism poses a relevant burden to public health worldwide.
“Therefore, we assume that posttraumatic hypopituitarism poses a relevant burden to public health worldwide.”
The paper relies on this without support.
There are no clear data regarding the effects of sex hormone replacement on cognitive outcomes in patients with TBI-induced gonadotropin deficiency.
“Additionally, there are no clear data regarding the effects of sex hormone replacement on cognitive outcomes in patients with TBI-induced gonadotropin deficiency.”
The paper relies on this without support.
There are presently only a small but growing number of reports on the cognitive effects of GHD after TBI.
“There are presently only a small (but growing) number of reports on the cognitive effects of GHD after TBI.”
The paper relies on this without support.
Physical limitations and prolonged recovery are specific for TBI patients.
“It should be taken into account that HDL cholesterol is mainly influenced by physical activity (89), and physical limitations and prolonged recovery are specific for TBI patients.”
The paper relies on this without support.
Concussion is the most common clinical type of TBI.
“Concussion is the most common clinical type of TBI.”
The paper relies on this without support.
Few studies have investigated the pathophysiology of hypopituitarism during the acute phase of TBI.
“Few studies have investigated the pathophysiology of hypopituitarism during the acute phase (generally the first 2 wk) of TBI.”
The paper relies on this without support.
The pathophysiology of the reversibility of pituitary dysfunction is unclear.
“Moreover, the pathophysiology of the reversibility of pituitary dysfunction is also unclear.”
The paper relies on this without support.
Findings from experimental animal models of TBI can be extrapolated to human TBI-induced hypopituitarism.
“This is an important experimental model for sportsrelated chronic repetitive mild TBI, and it supports the previous clinical data (38,46,48,179,180).”
“However, further human studies are needed to understand the clinical relevance of these experimental findings.”
The paper relies on this without support.
TBI is an important cause of hypopituitarism.
“Because TBI is an important cause of hypopituitarism, it is tempting to suggest that the first approach should be testing all patients with a history of TBI.”
The paper relies on this without support.
Global screening of all patients with a history of TBI is not cost-effective.
“However, this strategy is not cost-effective and would result in unnecessary health resource consumption for a community.”
The paper relies on this without support.
The diagnostic criteria and cutoffs for classical hypopituitarism are valid for TBI-induced hypopituitarism.
“The diagnosis of TBI-induced hypopituitarism, defined as the deficient hormone secretion of one or more pituitary hormones because of TBI, is made similarly to the diagnosis of classical hypopituitarism because of hypothalamic or pituitary diseases.”
The paper relies on this without support.
A morning plasma cortisol level ≤11 g/dL (300 nmol/L) is a valid diagnostic cutoff for ACTH deficiency during the acute phase after TBI.
“we suggest a morning plasma cortisol level Յ11 g/dL (300 nmol/L) as the diagnostic cutoff for ACTH deficiency during the acute phase.”
The paper relies on this without support.
Screening and treating hypopituitarism in TBI patients improves clinical outcomes.
“We believe that awareness of TBI-induced hypopituitarism in the medical community may lead to early diagnosis and, therefore, early treatment of hypopituitarism.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In studies of endocrine deficiencies following TBI in adults, patient selection and dissimilar methodologies accounted for variations in overall prevalence and influenced the incidence of abnormality detected [15,22].”
From Update of Endocrine Dysfunction following Pediatric Traumatic Brain Injury (2015) · cites this paper as [22]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Overall, hypothalamic-pituitary dysfunction has been reported in 23% to 69% of adult patients, assessed at 12 months or more after moderate to severe TBI [21,22].”
From Update of Endocrine Dysfunction following Pediatric Traumatic Brain Injury (2015) · cites this paper as [22]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“In adults and children who have suffered TBI, GHD is one of the most common endocrine deficiencies [21,22,56,57,58,59].”
From Update of Endocrine Dysfunction following Pediatric Traumatic Brain Injury (2015) · cites this paper as [22]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“| Dyslipidemia, % (n) | 12.8 (6) | 46.7 (7) | Ͻ.01 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
Reported 12.8 · recomputed 15.384615
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
“| Bondanelli, 2004 (154) | 50 | 4 | 7 | 0 | 5 | 14 |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
“| 14 | 6 | 86% GCS Յ 12 |”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > B. Results
“Although three studies (n ϭ 246 subjects) included only severe cases as defined by a postresuscitation Glasgow Coma Scale (GCS) score of 8 or lower (23,24)”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
“| Leal-Cerro, 2005 (24) | 170 | 6 | 29 | 11 | 10 | 42 | 15 | 100% GCS Յ 8 | | Herrmann, 2006 (23) | 76 | 6 | 13 | 2 | 2 | 18 | 5 | 100% GCS Յ 8 |”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“| GCS 9 -12, % (n) | 11.1 (4) | 33.3 (5) | ns | | GCS (Ͻ9), % (n) | 88.9 (35) | 66.7 (10) | |”
§ Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach > X. Summary and Future Directions
Reported 11.1 · recomputed 10.25641
Citations
Cites
ASSESSMENT OF COMA AND IMPAIRED CONSCIOUSNESS
Teasdale, G., & Jennett, B. (1974) · The Lancet · doi:10.1016/s0140-6736(74)91639-0 · Cited by 13,215
Pathophysiology of traumatic brain injury
Werner, C., & Engelhard, K. (2007) · British Journal of Anaesthesia · doi:10.1093/bja/aem131 · Cited by 1,712
Position statement: definition of traumatic brain injury
Menon, D. K., Schwab, K., Wright, D. W., & Maas, A. I. (2010) · Archives of Physical Medicine and Rehabilitation · doi:10.1016/j.apmr.2010.05.017 · Cited by 1,678
Premature mortality due to cardiovascular disease in hypopituitarism
Rosén, T., & Bengtsson, B.-Å. (1990) · The Lancet · doi:10.1016/0140-6736(90)91812-o · Cited by 1,402
Assessment of executive functions: Review of instruments and identification of critical issues.
CHAN, R., SHUM, D., TOULOPOULOU, T., & CHEN, E. (2008) · Archives of Clinical Neuropsychology · doi:10.1016/j.acn.2007.08.010 · Cited by 1,401
Axonal pathology in traumatic brain injury
Johnson, V. E., Stewart, W., & Smith, D. H. (2013) · Experimental Neurology · doi:10.1016/j.expneurol.2012.01.013 · Cited by 1,273
The role of inflammation in CNS injury and disease
Lucas, S., Rothwell, N. J., & Gibson, R. M. (2006) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0706400 · Cited by 1,272
A systematic review of brain injury epidemiology in Europe
Tagliaferri, F., Compagnone, C., Koršič, M., Servadei, F., & Kraus, J. F. (2005) · Acta Neurochirurgica · doi:10.1007/s00701-005-0651-y · Cited by 1,223
Diffuse axonal injury in head injury: definition, diagnosis and grading
Adams, J. H., Doyle, D., Ford, I., Gennarelli, T. A., Graham, D. I., & Mclellan, D. R. (1989) · Histopathology · doi:10.1111/j.1365-2559.1989.tb03040.x · Cited by 1,176
Classification of traumatic brain injury for targeted therapies
Saatman, K. E., Duhaime, A.-C., Bullock, R., Maas, A. I. R., Valadka, A., & Manley, G. T. (2008) · Journal of Neurotrauma · doi:10.1089/neu.2008.0586 · Cited by 1,141
Research works printed but not linked: 5
- Cryan, 1918, Pituitary damage due to skull base fracture, Deutsche Medizinische Wochenschrift, 44, 1261
- Rouvillois, 1921, Lesions traumatiques de l'hypophyse dans les fractures de la bas du crane, Bull Mem Soc Chirurg Paris, 47, 685
- Schereschewsky, 1927, La symptomatologie et la diagnostic de la maladie de Simmonds (cachexie hypophysaire), Rev Franc Endocr, 5, 275
- Kraus, 2005, Epidemiology, 3
- Tanriverdi, 2013, Endocrinology of acute brain injury, 465
Cited by
Sorted by citations
Hormonal Replacement in Hypopituitarism in Adults: An Endocrine Society Clinical Practice Guideline
Fleseriu, M., Hashim, I. A., Karavitaki, N., Melmed, S., Murad, M. H., Salvatori, R., & Samuels, M. H. (2016) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2016-2118 · Cited by 945
Higham, C., Johannsson, G., & Shalet, S. M. (2016) · The Lancet · doi:10.1016/s0140-6736(16)30053-8 · Cited by 273
Hahner, S., Ross, R. J., Arlt, W., Bancos, I., Burger-Stritt, S., Torpy, D. J., Husebye, E. S., & Quinkler, M. (2021) · Nature Reviews Disease Primers · doi:10.1038/s41572-021-00252-7 · Cited by 223
Dissemination of brain inflammation in traumatic brain injury
Shi, K., Zhang, J., Dong, J., & Shi, F. (2019) · Cellular and Molecular Immunology · doi:10.1038/s41423-019-0213-5 · Cited by 187
Prevalence of Medical and Psychiatric Comorbidities Following Traumatic Brain Injury
Hammond, F. M., Corrigan, J. D., Ketchum, J. M., Malec, J. F., Dams-O’Connor, K., Hart, T., Novack, T. A., Bogner, J. A., Dahdah, M. N., & Whiteneck, G. G. (2019) · Journal of Head Trauma Rehabilitation · doi:10.1097/htr.0000000000000465 · Cited by 145
“6) 25 (20-28) Posttraumatic amnesia,a d 388 31.”
Metadata
- Authors
- Tanriverdi, F., Schneider, H. J., Aimaretti, G., Masel, B. E., Casanueva, F. F., & Kelestimur, F.
- Affiliations
- Erciyes University Medical School (F.T., F.K.), Department of Endocrinology, 38039 Kayseri, Turkey;
- LMU Klinikum (DE)
- Università degli Studi del Piemonte Orientale “Amedeo Avogadro” (IT)
- Transitional Learning Center (US)
- Universidade de Santiago de Compostela (ES)
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 2015-05-07
- Volume
- 36
- Issue
- 3
- Pages
- 305-342
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- OpenAlex
- W2103564728
- Cited by
- 218
- References
- 310
- Citations by year
- 2026: 18 · 2025: 21 · 2024: 20 · 2023: 14 · 2022: 22 · 2021: 15 · 2020: 15 · 2019: 29 · 2018: 21 · 2017: 18 · 2016: 16 · 2015: 9
- FWCI
- 3.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrine Reviews (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- RUNA. Repositorio Institucional del Sergas (Servicio Gallego de Salud (SERGAS)) (submittedVersion, other-oa)
- Funders
- Erciyes Üniversitesi
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Keywords
- traumatic brain injury, hypopituitarism, anterior pituitary dysfunction, neuroendocrine dysfunction, growth hormone deficiency, ACTH deficiency, gonadotropin deficiency, thyroid-stimulating hormone deficiency, boxing, autoimmunity, genetic susceptibility, cognitive impairment, metabolic effects
- MeSH terms
- Brain Injuries, Humans, Pituitary Diseases, Pituitary Gland
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-11, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-11 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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