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.
- 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.
- 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
- 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.
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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.
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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.
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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.
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- 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.
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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.
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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.
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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.
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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.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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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.
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- 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
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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
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Dissemination of brain inflammation in traumatic brain injury
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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.”
Shultz, S. R., McDonald, S. J., Haar, C. V., Meconi, A., Vink, R., van Donkelaar, P., Taneja, C., Iverson, G. L., & Christie, B. R. (2016) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2016.09.014 · Cited by 149
“One major hypothesis of why emotional changes are common in humans following bTBI is that the pituitary is particularly sensitive to damage and thus affects the entire hypothalamic-pituitary-adrenal axis (Tanriverdi et al., 2015; Wilkinson et al., 2012).”
Pertab, J. L., Merkley, T. L., Cramond, A. J., Cramond, K. M. J., Paxton, H., & Wu, T. C. (2018) · Neurorehabilitation · doi:10.3233/nre-172298 · Cited by 161
“Some of the most cited reasons for persistent complaints after concussion include: • Persistent central nervous system neuropathology (Bigler et al., 2016; D’Souza M et al., 2015; Dean, Sato, Vieira, McNamara, & Sterr, 2015; Nordin et al., 2016; Shahim et al., 2017; Zagorchev et al., 2016) • Malingering (Carroll et al…”
Chronic Hyponatremia Causes Neurologic and Psychologic Impairments
Fujisawa, H., Sugimura, Y., Takagi, H., Mizoguchi, H., Takeuchi, H., Izumida, H., Nakashima, K., Ochiai, H., Takeuchi, S., Kiyota, A., et al. (2015) · Journal of the American Society of Nephrology · doi:10.1681/asn.2014121196 · Cited by 115
Kickboxing review: anthropometric, psychophysiological and activity profiles and injury epidemiology
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“Accordingly, Tanriverdi et al. [66] reported that GH is the most common hormone lost after TBI, followed by ACTH, gonadotropins (luteinizing hormone (LH) and follicle-stimulating hor - mone (FSH)), and thyroid-stimulating hormone (TSH).”
BackgroundMolaie, A. M., & Maguire, J. L. (2018) · Frontiers in Endocrinology · doi:10.3389/fendo.2018.00176 · Cited by 69
“Interested readers can refer to thorough reviews by Tanriverdi and colleagues (43) and Tan et al.”
BackgroundDifferential Responses of the HPA Axis to Mild Blast Traumatic Brain Injury in Male and Female Mice
Russell, A. L., Mc, R., Bauman, B. M., Hernandez, I. M., Saperstein, S., Handa, R. J., & Wu, T. J. (2018) · Endocrinology · doi:10.1210/en.2018-00203 · Cited by 74
Pituitary pathology in traumatic brain injury: A review
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DIAGNOSIS OF ENDOCRINE DISEASE: Expanding the cause of hypopituitarism
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Update of Endocrine Dysfunction following Pediatric Traumatic Brain Injury
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“after TBI in adults, including effects on cognitive impairment, metabolic consequences of hypopituitarism, screening and diagnostic methods, and which patients should be screened [22].”
BackgroundInfluentialInsights into non-classic and emerging causes of hypopituitarism
Prodam, F., Caputo, M., Mele, C., Marzullo, P., & Aimaretti, G. (2020) · Nature Reviews Endocrinology · doi:10.1038/s41574-020-00437-2 · Cited by 64
Self-citationClassical and non-classical causes of GH deficiency in the paediatric age
Iorgi, N. D., Morana, G., Allegri, A. E. M., Napoli, F., Gastaldi, R., Calcagno, A., Patti, G., Loche, S., & Maghnie, M. (2016) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2016.11.008 · Cited by 63
Diffuse traumatic brain injury affects chronic corticosterone function in the rat
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Pituitary dysfunction following traumatic brain injury: clinical perspectives
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“The diagnosis and treatment of hypopituitarism are beyond the scope of this review, and the details have been reviewed elsewhere.(22,56,57) However, it is important to note that the clinical manifestations of hypopituitarism, especially isolated hormone deficiencies as in TBI, could be mild or subtle, so most patients…”
Willems, C., Fu, Q., Roose, H., Mertens, F., Cox, B., Chen, J., & Vankelecom, H. E. J. (2015) · Endocrinology · doi:10.1210/en.2015-1741 · Cited by 56
“Recovery of blood hormone levels has been found after mild TBI but not after severe impact (55).”
BackgroundInfluentialNeuroinflammation and Hypothalamo-Pituitary Dysfunction: Focus of Traumatic Brain Injury
Mele, C., Pingue, V., Caputo, M., Zavattaro, M., Pagano, L., Prodam, F., Nardone, A., Aimaretti, G., & Marzullo, P. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22052686 · Cited by 60
“Overall, growth hormone deficiency (GHD), ACTH insufficiency, and gonadotropin deficiency are the most frequent abnormalities observed in post-TBI patients [27,32,38,155].”
BackgroundSelf-citationMaking sense of gut feelings in the traumatic brain injury pathogenesis
Royes, L. F. F., & Gómez‐Pinilla, F. (2019) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2019.05.012 · Cited by 55
“TBI patients with hypopituitarism frequently present metabolic alterations in glucose levels, insulin resistance and hypertriglyceridemia (Tanriverdi et al., 2015).”
BackgroundTraumatic brain injuries induced pituitary dysfunction: a call for algorithms
Gilis‐Januszewska, A., Kluczyński, Ł., & Hubalewska–Dydejczyk, A. (2020) · Endocrine Connections · doi:10.1530/ec-20-0117 · Cited by 61
Garrahy, A., Sherlock, M., & Thompson, C. J. (2017) · European Journal of Endocrinology · doi:10.1530/eje-16-0962 · Cited by 53
Krewer, C., Schneider, M., Schneider, H. J., Kreitschmann-Andermahr, I., Buchfelder, M., Faust, M., Berg, C., Wallaschofski, H., Renner, C., Uhl, E., et al. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2015.4109 · Cited by 47
“36 We assume that the treating physicians classified their patients as insufficient, being aware of an impaired test result despite normal basal hormonal values.”
Self-citationEndocrine Dysfunction After Traumatic Brain Injury: An Ignored Clinical Syndrome?
Mahajan, C., Prabhakar, H., & Bilotta, F. (2023) · Neurocritical Care · doi:10.1007/s12028-022-01672-3 · Cited by 60
“…fracture, epidural/subdural hematomas, cranial vault fracture] on admission, have hypoxia/hypotension, have repetitive injuries [sports related], had polyuria/polydipsia during the acute phase, or have signs of pituitary dysfunction) thereafter should be evaluated for hormonal deficiency [43].”
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Grashow, R. G., Weisskopf, M. G., Miller, K. K., Nathan, D. M., ZAFONTE, R. D., Speizer, F. E., Courtney, T. K., Baggish, A. L., Taylor, H. A., Pascual‐Leone, Á., et al. (2019) · JAMA Neurology · doi:10.1001/jamaneurol.2019.2664 · Cited by 46
Circulating MicroRNAs as Potential Biomarkers for Traumatic Brain Injury-Induced Hypopituitarism
Taheri, S., Tanrıverdi, F., Zararsız, G., Elbüken, G., Ulutabanca, H., Karaca, Z., Selçuklu, A., Ünlühızarcı, K., Tanrıverdi, K., & Keleştimur, F. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2015.4281 · Cited by 46
Self-citationPituitary Medicine From Discovery to Patient-Focused Outcomes
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The frequency and the diagnosis of pituitary dysfunction after traumatic brain injury
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Brain Trauma, Glucocorticoids and Neuroinflammation: Dangerous Liaisons for the Hippocampus
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“In general, signs of mild TBI, including absence of amnesia and a higher Glasgow coma scale score, are associated with higher cortisol levels [38], while the severity of coma positively correlates with acute cortisol level (within 6 h after TBI) [34].”
BackgroundJaved, Z., Qamar, U., & Sathyapalan, T. (2015) · Indian Journal of Endocrinology and Metabolism · doi:10.4103/2230-8210.167561 · Cited by 39
“Also, before confirming diagnosis of central hypogonadism, it is important to exclude hyperprolactinemia as it has been seen to be associated with hypogonadism in some cases that might be due to lesions of pituitary stalk or hypothalamus or drug interference.[5,100]”
BackgroundMethodInfluentialCarosi, G., Brunetti, A., Mangone, A., Baldelli, R., Tresoldi, A. S., Sindaco, G. D., Lavezzi, E., Sala, E., Mungari, R., Fatti, L. M., et al. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.925378 · Cited by 39
Wright, T. J., Urban, R. J., Durham, W., Dillon, E. L., Randolph, K. M., Danesi, C. P., Gilkison, C. R., Karmonik, C., Zgaljardic, D. J., Masel, B. E., et al. (2019) · Journal of Neurotrauma · doi:10.1089/neu.2019.6690 · Cited by 39
Self-citationJohannsson, G., & Ragnarsson, Ó. (2021) · Journal of Internal Medicine · doi:10.1111/joim.13382 · Cited by 39
Santi, A., Genı́s, L., & Torres‐Alemán, I. (2017) · Cerebral Cortex · doi:10.1093/cercor/bhx106 · Cited by 37
Untangling PTSD and TBI: Challenges and Strategies in Clinical Care and Research
Hendrickson, R. C., Schindler, A. G., & Pagulayan, K. F. (2018) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-018-0908-5 · Cited by 39
Zhong, Y., Luo, J., Tang, T., Li, P., Liu, T., Cui, H., Wang, Y., & Huang, Z. (2018) · Evidence-based Complementary and Alternative Medicine · doi:10.1155/2018/8916938 · Cited by 39
“Discussion Traumatic brain injury (TBI) is a growing public health problem worldwide and is a leading cause of death and disability [84].”
BackgroundClinical picture and the treatment of TBI-induced hypopituitarism
Caputo, M., Mele, C., Prodam, F., Marzullo, P., & Aimaretti, G. (2019) · Pituitary · doi:10.1007/s11102-019-00956-w · Cited by 40
Self-citationGiuliano, S., Talarico, S., Bruno, L., Nicoletti, F. B., Ceccotti, C., & Belfiore, A. (2016) · Endocrine · doi:10.1007/s12020-016-1183-3 · Cited by 42
Pituitary dysfunction due to sports-related traumatic brain injury
Hacioglu, A., Kelestimur, F., & Tanriverdi, F. (2019) · Pituitary · doi:10.1007/s11102-019-00937-z · Cited by 36
Pituitary Remodeling Throughout Life: Are Resident Stem Cells Involved?
Laporte, E., Vennekens, A., & Vankelecom, H. E. J. (2021) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.604519 · Cited by 41
Kopczak, A., Krewer, C., Schneider, M., Kreitschmann‐Andermahr, I., Schneider, H., & Stalla, G. K. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms17010002 · Cited by 32
“In fact, treatment guidelines recommend dynamic testing for the evaluation of the corticotropic and somatotropic axes [2,16].”
BackgroundSelf-citationPost-concussive Dizziness: A Review and Clinical Approach to the Patient
Gianoli, G. J. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2021.718318 · Cited by 31
Pituitary function within the first year after traumatic brain injury or subarachnoid haemorrhage
Tölli, A., Borg, J., Bellander, B.-M., Johansson, F., & Höybye, C. (2017) · Journal of Endocrinological Investigation · doi:10.1007/s40618-016-0546-1 · Cited by 30
“These conditions may share some pathophysiological mechanisms such as vascular support of the pituitary [46–48].”
BackgroundTan, H., Yang, W., Wu, C., Liu, B., Lu, H., Wang, H., & Yan, H. (2017) · Scientific Reports · doi:10.1038/s41598-017-04008-w · Cited by 32
Neuroendocrine changes after aneurysmal subarachnoid haemorrhage
Karaca, Z., Hacıoğlu, A., & Keleştimur, F. (2019) · Pituitary · doi:10.1007/s11102-018-00932-w · Cited by 32
Self-citationClassical and non-classical causes of GH deficiency in adults
Tanrıverdi, F., & Keleştimur, F. (2017) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2017.02.001 · Cited by 31
Self-citationPituitary dysfunction after traumatic brain injury: Are there definitive data in children?
Casano-Sancho, P. (2017) · Archives of Disease in Childhood · doi:10.1136/archdischild-2016-311609 · Cited by 30
Minimizing Ischemia Reperfusion Injury in Xenotransplantation
Patel, P. M., Connolly, M. R., Coe, T. M., Calhoun, A., Pollok, F., Markmann, J. F., Burdorf, L., Azimzadeh, A. M., Madsen, J. C., & Pierson, R. N. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.681504 · Cited by 33
Curtò, L., & Trimarchi, F. (2016) · Journal of Endocrinological Investigation · doi:10.1007/s40618-016-0487-8 · Cited by 28
Ntali, G., & Tsagarakis, S. (2019) · Pituitary · doi:10.1007/s11102-019-00944-0 · Cited by 29
Isolated anterior pituitary dysfunction in adulthood
Prencipe, N., Marinelli, L., Varaldo, E., Cuboni, D., Berton, A. M., Bioletto, F., Bona, C., Gasco, V., & Grottoli, S. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1100007 · Cited by 28
Epidemiology of Pediatric Traumatic Brain Injury and Hypothalamic-Pituitary Disorders in Arizona
Ortiz, J. B., Sukhina, A. S., Balkan, B., Harootunian, G., Adelson, P. D., Lewis, K. S., Oatman, O. J., Subbian, V., Rowe, R. K., & Lifshitz, J. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2019.01410 · Cited by 28
“2% of patients having more than one endocrine dysfunction post-TBI (16).”
BackgroundSchneider, K., Emery, C. A., Black, A. M., Yeates, K. O., Debert, C. T., Lun, V. M. Y., & Meeuwisse, W. H. (2019) · Journal of Orthopaedic and Sports Physical Therapy · doi:10.2519/jospt.2019.8926 · Cited by 28
Karamouzis, I., Pagano, L., Prodam, F., Mele, C., Zavattaro, M., Busti, A., Marzullo, P., & Aimaretti, G. (2015) · Endocrine · doi:10.1007/s12020-015-0796-2 · Cited by 27
Self-citationAdvances in understanding hypopituitarism
Stieg, M. R., Renner, U., Stalla, G. K., & Kopczak, A. (2017) · F1000Research · doi:10.12688/f1000research.9436.1 · Cited by 25
Hypoprolactinemia. Does it matter? Redefining the hypopituitarism and return from a mumpsimus
Karaca, Z., Ünlühızarcı, K., & Keleştimur, F. (2023) · Reviews in Endocrine and Metabolic Disorders · doi:10.1007/s11154-023-09847-9 · Cited by 27
“Traumatic brain injury (TBI) is an another cause of hypopi - tuitarism in which the extent of pituitary hormone deficiency ranges from isolated to panhypopituitarism [9 , 21].”
Self-citationHypopituitarism After Traumatic Brain Injury
Gray, S. F.-M., Bilski, T. R., Dieudonne, B. E., & Saeed, S. (2019) · Cureus · doi:10.7759/cureus.4163 · Cited by 27
“suggest that autoimmunity may cause neuroendocrine dysfunction with the presence of anti-pituitary antibodies up to three years after diagnosis [11-12].”
BackgroundYuen, K. C. J., Masel, B. E., Reifschneider, K. L., Sheffield-Moore, M., Urban, R. J., & Pyles, R. B. (2020) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgaa398 · Cited by 24
Self-citationHypothalamitis: A Novel Autoimmune Endocrine Disease. A Literature Review and Case Report
Türe, U., Bellis, A. D., Harput, M. V., Bellastella, G., Topçuoğlu, O. M., Yaltırık, C. K., Cirillo, P., Yola, R. N., Sav, A., & Keleştimur, F. (2020) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgaa771 · Cited by 24
Self-citationA clinical and pathophysiological approach to traumatic brain injury-induced pituitary dysfunction
Temizkan, Ş., & Keleştimur, F. (2019) · Pituitary · doi:10.1007/s11102-019-00941-3 · Cited by 26
Self-citationTaheri, S., Karaca, Z., Mehmetbeyoğlu, E., Hamurcu, Z., Şükranlı, Z. Y., Dal, F., Çınar, V., Ulutabanca, H., Tanrıverdi, F., Ünlühızarcı, K., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232415699 · Cited by 26
“Besides frequently seen neuropsychiatric symptoms including irritability, depression, and anxiety, one of the most 10 important neuroendocrine disorders emerging after TBI is pituitary insufficiency (Tanriverdi et al. 2015; Karaca et al. 2016).”
BackgroundSelf-citationPituitary dysfunction and association with fatigue in stroke and other acute brain injury
Booij, H. A., Gaykema, W. D. C., Kuijpers, K. A. J., Pouwels, M.-J. J., & den Hertog, H. M. (2018) · Endocrine Connections · doi:10.1530/ec-18-0147 · Cited by 24
Long-term neuroendocrine consequences of traumatic brain injury and strategies for management
Hacıoğlu, A., Keleştimur, F., & Tanrıverdi, F. (2020) · Expert Review of Endocrinology & Metabolism · doi:10.1080/17446651.2020.1733411 · Cited by 23
“However, deterioration of pituitary secretion may occur during the chronic phase and new onset deficiencies can be observed even years after the traumatic event [11] For this reason, much effort has been made to develop screening strategies during long term follow up [7].”
BackgroundMethodInfluentialSelf-citationVijapur, S. M., Yang, Z., Barton, D. J., Vaughan, L., Awan, N., Kumar, R. G., Oh, B.-M., Berga, S. L., Wang, K. K., & Wagner, A. K. (2020) · Journal of Neurotrauma · doi:10.1089/neu.2019.6780 · Cited by 20
“Other work suggests that growth hormone may be the most common posttraumatic pituitary deficiency, with gonadotropin, adrenocorticotropic, and thyroid stimulating hormones having lower incidence.(5)”
BackgroundDisease-directed engineering for physiology-driven treatment interventions in neurological disorders
Wood, T. R., & Nance, E. A. (2019) · APL Bioengineering · doi:10.1063/1.5117299 · Cited by 21
Balasubramanian, N., Sagarkar, S., Jadhav, M., Shahi, N., Sirmaur, R., & Sakharkar, A. J. (2020) · Neuroendocrinology · doi:10.1159/000513638 · Cited by 19
Jung, E., Ro, Y. S., Park, J. H., Moon, S. B., Lee, S. G. W., Park, G. J., Ryu, H. H., & Shin, S. D. (2022) · Journal of Neurotrauma · doi:10.1089/neu.2022.0053 · Cited by 17
Post-Traumatic Hypopituitarism: A Neglected Consequence of Traumatic Brain Injury
Kałas, M., Miksiewicz, M., Kowalke, A., & Siemiński, M. (2023) · Neuroendocrinology · doi:10.1159/000529327 · Cited by 17
Stem Cells in Neuroendocrinology
Pfaff, D., & Christen, Y. (2016) · Research and perspectives in endocrine interactions · doi:10.1007/978-3-319-41603-8 · Cited by 16
Traumatic brain injury and resultant pituitary dysfunction: insights from experimental animal models
Vennekens, A., & Vankelecom, H. E. J. (2019) · Pituitary · doi:10.1007/s11102-019-00961-z · Cited by 19
Elliott, S., Birkhäuser, V., Courtois, F. J., Gül, M., Ibrahim, E., Kiekens, C., New, P. W., Ohl, D. A., & Fode, M. M. (2025) · Sexual Medicine Reviews · doi:10.1093/sxmrev/qeaf030 · Cited by 14
Saliva Cortisol as a Biomarker of Injury in Youth Sport-Related Concussion
Tabor, J., La, P. L., Kline, G. A., Wang, M., Bonfield, S. P., Machan, M., Wynne‐Edwards, K. E., Emery, C. A., & Debert, C. T. (2022) · Journal of Neurotrauma · doi:10.1089/neu.2022.0190 · Cited by 15
“17 This may present as hypopituitarism post-TBI, which has been previously demonstrated in all severities of TBI, 20 where cortisol deficiency may require urgent intervention.”
Sports-Related Repetitive Traumatic Brain Injury: A Novel Cause of Pituitary Dysfunction
Sezgin Caglar, A., Tanriverdi, F., Karaca, Z., Unluhizarci, K., & Kelestimur, F. (2019) · Journal of Neurotrauma · doi:10.1089/neu.2018.5751 · Cited by 14
“4,22 Diagnosis of hypopituitarism, developing after TBI, is similar to hypopituitarism attributed to other hypothalamic or pituitary diseases.”
InfluentialSelf-citationThakur, M., Vasudeva, N., Sharma, S., & Datusalia, A. K. (2022) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527321666220830164432 · Cited by 14
Elliott, T. R., Hsiao, Y., Randolph, K. M., Urban, R. J., Sheffield‐Moore, M., Pyles, R. B., Masel, B. E., Wexler, T., & Wright, T. J. (2023) · PLoS ONE · doi:10.1371/journal.pone.0295593 · Cited by 13
“The symptom cluster is well-described in patients who experience deficiencies in pituitary hormones including growth hormone, the most frequent deficiency identified post-TBI [24].”
BackgroundSelf-citationPituitary dysfunction after traumatic brain injury: prevalence and screening strategies
Ntali, G., & Tsagarakis, S. (2020) · Expert Review of Endocrinology & Metabolism · doi:10.1080/17446651.2020.1810561 · Cited by 16
Bonert, V. S., & Melmed, S. K. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-804169-7.00004-0 · Cited by 14
EGF-GH Axis in Rat Steatotic and Non-steatotic Liver Transplantation From Brain-dead Donors
Álvarez‐Mercado, A. I., Negrete-Sánchez, E., Gulfo, J., León, C. G. A.-D., Casillas-Ramírez, A., Cornide‐Petronio, M. E., Bujaldon, E., Rotondo, F., Gracia‐Sancho, J., Jiménez‐Castro, M. B., et al. (2019) · Transplantation · doi:10.1097/tp.0000000000002636 · Cited by 13
“Clinical studies suggest that endocrine abnormalities in BD donors include a rapid decrease in hormones, such as growth hormone (GH), in the circulation.(7,8) GH is released from the anterior pituitary gland, circulates in plasma, and binds to its receptors in the liver.”
BackgroundRisk Factors for Anterior Hypopituitarism in Patients With Traumatic Brain Injury
You, W., Zhu, Y., Wen, L., Sun, Y., Pan, D.-S., & Yang, X. (2019) · Journal of Craniofacial Surgery · doi:10.1097/scs.0000000000005405 · Cited by 11
Duffy, D., Elliott-Sale, K. J., Gardner, H., Goldenstein, S. J., & Wideman, L. (2021) · Endocrines · doi:10.3390/endocrines2020010 · Cited by 12
“Following SRBI, the pituitary gland may not produce sufficient amounts of LH and FSH, ultimately altering the production of estrogen [64].”
BackgroundPituitary Stem Cells: Quest for Hidden Functions
Vankelecom, H. E. J. (2016) · Research and perspectives in endocrine interactions · doi:10.1007/978-3-319-41603-8_7 · Cited by 14
“In addition, traumatic brain injury, ranging from car accidents to sport-related impacts (e.g.,by boxing), represents an important cause of pituitary deficiency (Gasco et al. 2012; Tanriverdi et al. 2015).”
BackgroundTufan, E., Taheri, S., Karaca, Z., Mehmetbeyoğlu, E., Şükranlı, Z. Y., Bayramov, K. K., Ulutabanca, H., Tanrıverdi, F., Ünlühızarcı, K., Rassoulzadegan, M., et al. (2023) · Neuroendocrinology · doi:10.1159/000535748 · Cited by 9
“The possible mechanisms underlying the recovery or worsening of pituitary function remain to be discovered and cannot be explained simply by direct injury to the pituitary gland and/or vascular injury [5].”
InfluentialSelf-citationEbrahimi, F., Andereggen, L., & Christ, E. (2024) · Reviews in Endocrine and Metabolic Disorders · doi:10.1007/s11154-024-09888-8 · Cited by 8
“11% of these patients [64, 65].”
Fernández-Rodríguez, E., Taibo, R. V., & Bernabéu, I. (2023) · Endocrinología Diabetes y Nutrición (English ed ) · doi:10.1016/j.endien.2023.11.002 · Cited by 10
Umeano, O. A., Wang, H., Dawson, H. N., et al. (2017) · World Journal of Critical Care Medicine · doi:10.5492/wjccm.v6.i2.107 · Cited by 8
Toklu, H. Z., Sakarya, Y., & Tümer, N. (2017) · Methods in molecular biology · doi:10.1007/978-1-4939-6952-4_16 · Cited by 8
Traumatic brain injury and prolactin
Hacıoğlu, A., & Tanrıverdi, F. (2024) · Reviews in Endocrine and Metabolic Disorders · doi:10.1007/s11154-024-09904-x · Cited by 8
“Direct injuries may be caused by so called ‘primary insults’ such as skull base fractures, shearing injuries, or compression by a hematoma or brain edema [5, 26–28].”
InfluentialSelf-citationMiller, R. M., Dunn, J. A., O’Beirne, G. A., Whitney, S. L., & Snell, D. L. (2024) · Brain Injury · doi:10.1080/02699052.2024.2337905 · Cited by 7
“Symptoms that we have attributed to vestibular issues such as dizziness could also be attributed to ANS (106,108) or pituitary (43,44) dysfunction according to researchers.”
BackgroundEndocrine dysregulation in aneurysmal subarachnoid haemorrhage
Roe, T., Welbourne, J., & Nikitas, N. (2022) · British Journal of Neurosurgery · doi:10.1080/02688697.2022.2039378 · Cited by 7
“An observational study using traumatic SAH patient by Tanriverdi et al.(13) showed that increasing age was associated”
BackgroundMethodInfluentialTaheri, S., Karaca, Z., Mehmetbeyoglu, E., Hamurcu, Z., Yılmaz, Z., Dal, F., Cınar, V., Ulutabanca, H., Tanriverdi, F., Unluhizarci, K., et al. (2022) · doi:10.21203/rs.3.rs-1159219/v1 · Cited by 26
Self-citationWest, A. N., Diaz-Thomas, A., & Shafi, N. I. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.551923 · Cited by 7
“Generally, the chronic phase after TBI is thought to begin weeks after the injury and can last well beyond 3 months (50).”
BackgroundThe autoimmune basis of hypopituitarism in traumatic brain injury: fiction or reality?
Harsh, V., Jha, S., Kumar, H., & Kumar, A. (2019) · British Journal of Neurosurgery · doi:10.1080/02688697.2018.1485875 · Cited by 7
Endocrine dysfunction post-traumatic brain injury: challenges and therapeutic approaches
Soltani, Z. E., Nazari, M., Babaei, M., Shakeri, H., Jalali, S., Hajali, V., & Keshavarzi, Z. (2025) · Acta Neurologica Belgica · doi:10.1007/s13760-025-02755-6 · Cited by 8
“Research indicates that TBI can lead to both immediate and delayed onset of endocrine dysfunctions [13], including hypopituitarism, which can occur in up to 40% of TBI survivors [14 ].”
Evaluation of growth hormone deficiency in women with unexplained infertility
Ortac, M. S., Hacıoğlu, A., Uludağ, S. Z., Karaca, Z., Ünlühızarcı, K., Keleştimur, F., & Tanrıverdi, F. (2024) · Growth Hormone & IGF Research · doi:10.1016/j.ghir.2024.101571 · Cited by 6
Self-citationHuang, Y., Zhang, H., Yang, E., Yue, K., Gao, X., Dai, S., Wei, J., Yang, Y., Luo, P., Li, X., et al. (2022) · Journal of Molecular Neuroscience · doi:10.1007/s12031-021-01949-w · Cited by 5
“Recent research shows that growth hormone (GH) and IGF deficiency after TBI may inhibit the recovery of the axon and neurons, and thus, GH/IGF-I system would be benefit for the therapy of TBI (Feeney et al. 2017; Tanriverdi et al. 2015; Yuen et al. 2020).”
Sport-Related Concussion Preceding Adrenal Insufficiency and Hypopituitarism
Northam, W. T., Alexander, A. S., & Carneiro, K. A. (2020) · Current Sports Medicine Reports · doi:10.1249/jsr.0000000000000672 · Cited by 7
Famà, F., Vita, R., Sindoni, A., Vinci, S. L., Giorgianni, G. M., Grasso, L., Gioffré‐Florio, M., & Benvenga, S. (2018) · Journal of Clinical & Translational Endocrinology · doi:10.1016/j.jcte.2018.12.008 · Cited by 6
“For diagnosis of GH deficiency we relied only on IGF1, since basal circulating GH measurement is not helpful to diagnose GH deficiency [7].”
Method
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
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