The DOI matches its Crossref record; 107 of the 107 references it cites were found in a registry or an index; 2 of the 220 sources its claims cite were checked for support.
Chapter 1: pathophysiology of hypopituitarism in the setting of brain injury
Open accessAbstract
The complex pathophysiology of traumatic brain injury (TBI) involves not only the primary mechanical event but also secondary insults such as hypotension, hypoxia, raised intracranial pressure and changes in cerebral blood flow and metabolism. It is increasingly evident that these initial insults as well as transient events and treatments during the early injury phase can impact hypothalamic-pituitary function both acutely and chronically after injury. In turn, untreated pituitary hormonal dysfunction itself can further hinder recovery from brain injury. Secondary adrenal insufficiency, although typically reversible, occurs in up to 50% of intubated TBI victims and is associated with lower systemic blood pressure. Chronic anterior hypopituitarism, although reversible in some patients, persists in 25–40% of moderate and severe TBI survivors and likely contributes to long-term neurobehavioral and quality of life impairment. While the rates and risk factors of acute and chronic pituitary dysfunction have been documented for moderate and severe TBI victims in numerous recent studies, the pathophysiology remains ill-defined. Herein we discuss the hypotheses and available data concerning hypothalamic-pituitary vulnerability in the setting of head injury. Four possible pathophysiological mechanisms are considered: (1) the primary brain injury event, (2) secondary brain insults, (3) the stress of critical illness and (4) medication effects. Although each of these factors appears to be important in determining which hormonal axes are affected, the severity of dysfunction, their time course and possible reversibility, this process remains incompletely understood.
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48 Not checked yet · 24 Own interpretation · 1 Partly supported · accuracy not yet measured
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In the paper
“new corticotroph, thyrotroph and posterior pituitary deficiencies (permanent diabetes insipidus) are less common with rates averaging 8%, 5% and 2%, respectively”
§ Pathophysiology of hypopituitarism in the setting of brain injury > The growing awareness of TBI-induced hypopituitarsim
What the sources say
- Not checked yetcites [30] Agha A, Rogers B, Mylotte D et al (2004) Neuroendocrine dysfunction in the acute phase of traumatic brain injury. Clin Endocrinol (Oxf) 60:584–591. doi: 10.1111/j.1365-2265.2004.02023.x source
- Partly supportedcites [32] Agha A, Rogers B, Sherlock M et al (2004) Anterior pituitary dysfunction in survivors of traumatic brain injury. J Clin Endocrinol Metab 89:4929–4936. doi: 10.1210/jc.2004-0511 sourceExperimental — accuracy not yet measured
The corticotrophic-adrenal axis section reports ACTH deficiency in 13 of 102 TBI survivors (12.7%), assessed months after moderate or severe injury. This supports chronic corticotroph deficiency in this population, but the paper does not report an average rate of 8%. (LLM, conf=0.86)
- Not checked yetcites [33] Aimaretti G, Ambrosio MR, Di Somma C et al (2005) Hypopituitarism induced by traumatic brain injury in the transition phase. J Endocrinol Invest 28:984–989 source
- Not checked yetcites [38] Herrmann BL, Rehder J, Kahlke S et al (2006) Hypopituitarism following severe traumatic brain injury. Exp Clin Endocrinol Diabetes 114:316–321. doi: 10.1055/s-2006-924254 source
- Not checked yetcites [39] Kelly DF, Gonzalo IT, Cohan P, Berman N, Swerdloff R, Wang C (2000) Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report. J Neurosurg 93:743–752 source
- Not checked yetcites [40] Leal-Cerro A, Flores JM, Rincon M et al (2005) Prevalence of hypopituitarism and growth hormone deficiency in adults long-term after severe traumatic brain injury. Clin Endocrinol (Oxf) 62:525–532. doi: 10.1111/j.1365-2265.2005.02250.x source
- Not checked yetcites [41] Lieberman SA, Oberoi AL, Gilkison CR, Masel BE, Urban RJ (2001) Prevalence of neuroendocrine dysfunction in patients recovering from traumatic brain injury. J Clin Endocrinol Metab 86:2752–2756. doi: 10.1210/jc.86.6.2752 source
- Not checked yetcites [42] Tanriverdi F, Senyurek H, Unluhizarci K, Selcuklu A, Casanueva FF, Kelestimur F (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 91:2105–2111. doi: 10.1210/jc.2005-2476 source
- Not checked yetcites [43] Bavisetty S, Bavisetty S, McArthur DL et al (2008) Chronic hypopituitarism after traumatic brain injury: risk assessment and relationship to outcome. Neurosurgery 62 (in press) source
- Not checked yetcites [44] Aimaretti G, Ambrosio MR, Di Somma C, Gasperi M, Cannavo S, Scaroni C, Fusco A, Del Monte P, De Menis E, Faustini-Fustini M, Grimaldi F, Logoluso F, Razzore P, Rovere S, Benvenga S, Uberti EC, De Marinis L, Lombardi G, Mantero F, Martino E, Giordano G, Ghigo E (2005) Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study. J Clin Endocrinol Metab 90:6085–6092 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.
None of the sources cited for this claim have been checked yet.
In the paper
“new corticotroph, thyrotroph and posterior pituitary deficiencies (permanent diabetes insipidus) are less common with rates averaging 8%, 5% and 2%, respectively”
§ Pathophysiology of hypopituitarism in the setting of brain injury > The growing awareness of TBI-induced hypopituitarsim
What the sources say
- Not checked yetcites [30] Agha A, Rogers B, Mylotte D et al (2004) Neuroendocrine dysfunction in the acute phase of traumatic brain injury. Clin Endocrinol (Oxf) 60:584–591. doi: 10.1111/j.1365-2265.2004.02023.x source
- Could not verifycites [32] Agha A, Rogers B, Sherlock M et al (2004) Anterior pituitary dysfunction in survivors of traumatic brain injury. J Clin Endocrinol Metab 89:4929–4936. doi: 10.1210/jc.2004-0511 sourceExperimental — accuracy not yet measured
The Discussion mentions that post-TBI diabetes insipidus may spontaneously recover, but gives no rate of permanent diabetes insipidus. The reported prevalence figures concern anterior pituitary deficiencies; searches for posterior pituitary deficiency and diabetes insipidus did not establish the claimed 2% rate. (LLM, conf=0.77)
- Not checked yetcites [33] Aimaretti G, Ambrosio MR, Di Somma C et al (2005) Hypopituitarism induced by traumatic brain injury in the transition phase. J Endocrinol Invest 28:984–989 source
- Not checked yetcites [38] Herrmann BL, Rehder J, Kahlke S et al (2006) Hypopituitarism following severe traumatic brain injury. Exp Clin Endocrinol Diabetes 114:316–321. doi: 10.1055/s-2006-924254 source
- Not checked yetcites [39] Kelly DF, Gonzalo IT, Cohan P, Berman N, Swerdloff R, Wang C (2000) Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report. J Neurosurg 93:743–752 source
- Not checked yetcites [40] Leal-Cerro A, Flores JM, Rincon M et al (2005) Prevalence of hypopituitarism and growth hormone deficiency in adults long-term after severe traumatic brain injury. Clin Endocrinol (Oxf) 62:525–532. doi: 10.1111/j.1365-2265.2005.02250.x source
- Not checked yetcites [41] Lieberman SA, Oberoi AL, Gilkison CR, Masel BE, Urban RJ (2001) Prevalence of neuroendocrine dysfunction in patients recovering from traumatic brain injury. J Clin Endocrinol Metab 86:2752–2756. doi: 10.1210/jc.86.6.2752 source
- Not checked yetcites [42] Tanriverdi F, Senyurek H, Unluhizarci K, Selcuklu A, Casanueva FF, Kelestimur F (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 91:2105–2111. doi: 10.1210/jc.2005-2476 source
- Not checked yetcites [43] Bavisetty S, Bavisetty S, McArthur DL et al (2008) Chronic hypopituitarism after traumatic brain injury: risk assessment and relationship to outcome. Neurosurgery 62 (in press) source
- Not checked yetcites [44] Aimaretti G, Ambrosio MR, Di Somma C, Gasperi M, Cannavo S, Scaroni C, Fusco A, Del Monte P, De Menis E, Faustini-Fustini M, Grimaldi F, Logoluso F, Razzore P, Rovere S, Benvenga S, Uberti EC, De Marinis L, Lombardi G, Mantero F, Martino E, Giordano G, Ghigo E (2005) Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study. J Clin Endocrinol Metab 90:6085–6092 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Secondary adrenal insufficiency, although typically reversible, occurs in up to 50% of intubated TBI victims”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Abstract
What the sources say
- Not checked yetcites [35] Cohan P, Wang C, McArthur DL et al (2005) Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study. Crit Care Med 33:2358–2366. doi: 10.1097/01.CCM.0000181735.51183.A7 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Secondary adrenal insufficiency, although typically reversible, occurs in up to 50% of intubated TBI victims and is associated with lower systemic blood pressure.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Abstract
What the sources say
- Not checked yetcites [35] Cohan P, Wang C, McArthur DL et al (2005) Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study. Crit Care Med 33:2358–2366. doi: 10.1097/01.CCM.0000181735.51183.A7 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“in our prior study of acute adrenal insufficiency which occurred in 50% of intu-bated TBI subjects within 10 days of injury”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [35] Cohan P, Wang C, McArthur DL et al (2005) Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study. Crit Care Med 33:2358–2366. doi: 10.1097/01.CCM.0000181735.51183.A7 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Interestingly, in our study, no association was seen between long-term hypopituitarism and acute hypotension, hypoxia, anemia or intracranial hypertension.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [43] Bavisetty S, Bavisetty S, McArthur DL et al (2008) Chronic hypopituitarism after traumatic brain injury: risk assessment and relationship to outcome. Neurosurgery 62 (in press) source
plainn = 70- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“our recently published study of 70 TBI patients with long-term follow-up suggests that the degree of brain injury as defined by acute CT (presence of diffuse brain swelling and evacuated intracerebral hematoma or multiple contusions, in particular) is the strongest predictor of subsequent hypopituitarism [43].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [43] Bavisetty S, Bavisetty S, McArthur DL et al (2008) Chronic hypopituitarism after traumatic brain injury: risk assessment and relationship to outcome. Neurosurgery 62 (in press) source
hedgedcorrelationaln = 70- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Although ischemia factors of hypotensions, hypoxia and severe anemia were found to be important, medication effects were significantly more contributory to the development of adrenal insufficiency. [35].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Stress of critical illness and medication effects
What the sources say
- Not checked yetcites [35] Cohan P, Wang C, McArthur DL et al (2005) Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study. Crit Care Med 33:2358–2366. doi: 10.1097/01.CCM.0000181735.51183.A7 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Those TBI patients with acute adrenal insufficiency who survived, all returned to normal adrenal functioning on chronic follow-up.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Stress of critical illness and medication effects
What the sources say
- Not checked yetcites [35] Cohan P, Wang C, McArthur DL et al (2005) Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study. Crit Care Med 33:2358–2366. doi: 10.1097/01.CCM.0000181735.51183.A7 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.
None of the sources cited for this claim have been checked yet.
In the paper
“Collectively, these studies indicate that by 6–12 months post-injury, 25–40% of moderate and severe TBI patients will develop chronic hypopituitarism”
§ Pathophysiology of hypopituitarism in the setting of brain injury > The growing awareness of TBI-induced hypopituitarsim
What the sources say
- Not checked yetcites [5] Kelly DF, McArthur DL, Levin H et al (2006) Neurobehavioral and quality of life changes associated with growth hormone insufficiency after complicated mild, moderate, or severe traumatic brain injury. J Neurotrauma 23:928–942. doi: 10.1089/neu.2006.23.928 source
- Not checked yetcites [30] Agha A, Rogers B, Mylotte D et al (2004) Neuroendocrine dysfunction in the acute phase of traumatic brain injury. Clin Endocrinol (Oxf) 60:584–591. doi: 10.1111/j.1365-2265.2004.02023.x source
- Not checked yetcites [31] Bondanelli M, Ambrosio MR, Cavazzini L et al (2007) Anterior pituitary function may predict functional and cognitive outcome in patients with traumatic brain injury undergoing rehabilitation. J Neurotrauma 24:1687–1697. doi: 10.1089/neu.2007.0343 source
- Not checked yetcites [32] Agha A, Rogers B, Sherlock M et al (2004) Anterior pituitary dysfunction in survivors of traumatic brain injury. J Clin Endocrinol Metab 89:4929–4936. doi: 10.1210/jc.2004-0511 source
- Not checked yetcites [33] Aimaretti G, Ambrosio MR, Di Somma C et al (2005) Hypopituitarism induced by traumatic brain injury in the transition phase. J Endocrinol Invest 28:984–989 source
- Not checked yetcites [34] Bondanelli M, Ambrosio MR, Zatelli MC, De Marinis L, degli Uberti EC (2005) Hypopituitarism after traumatic brain injury. Eur J Endocrinol 152:679–691. doi: 10.1530/eje.1.01895 source
- Not checked yetcites [35] Cohan P, Wang C, McArthur DL et al (2005) Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study. Crit Care Med 33:2358–2366. doi: 10.1097/01.CCM.0000181735.51183.A7 source
- Not checked yetcites [36] Schneider M, Schneider HJ, Yassouridis A, Saller B, von Rosen F, Stalla GK (2008) Predictors of anterior pituitary insufficiency after traumatic brain injury. Clin Endocrinol (Oxf) 68:206–212 source
- Not checked yetcites [37] Klose M, Juul A, Poulsgaard L, Kosteljanetz M, Brennum J, Feldt-Rasmussen U (2007) Prevalence and predictive factors of post-traumatic hypopituitarism. Clin Endocrinol (Oxf) 67:193–201. doi: 10.1111/j.1365-2265.2007.02860.x source
- Not checked yetcites [38] Herrmann BL, Rehder J, Kahlke S et al (2006) Hypopituitarism following severe traumatic brain injury. Exp Clin Endocrinol Diabetes 114:316–321. doi: 10.1055/s-2006-924254 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. 24
- Probably not a substantial claim. 3
In the paper
“All patients with major chronic hormonal deficits in our series had severe parenchymal brain injury including 87% with diffuse brain swelling.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [43] Bavisetty S, Bavisetty S, McArthur DL et al (2008) Chronic hypopituitarism after traumatic brain injury: risk assessment and relationship to outcome. Neurosurgery 62 (in press) source
plaincorrelationaln = 70- 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 our study of acute secondary adrenal insufficiency we found that severity of injury, as measured by the injury severity score, younger age, ischemic factors and medication effects all had an impact on acute cortisol and ACTH levels [35].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Stress of critical illness and medication effects
What the sources say
- Not checked yetcites [35] Cohan P, Wang C, McArthur DL et al (2005) Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study. Crit Care Med 33:2358–2366. doi: 10.1097/01.CCM.0000181735.51183.A7 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
“indicate a greater resilience of the adrenal, thyroid and posterior pituitary axes and a relative vulnerability of the somatotroph and gonadotroph axes”
§ Pathophysiology of hypopituitarism in the setting of brain injury > The growing awareness of TBI-induced hypopituitarsim
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“most of the pituitary hormones have been shown to have important cerebral effects that impact not only brain development, but also allow normal brain function and are integral for effective brain repair and recovery.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > The growing awareness of TBI-induced hypopituitarsim
What the sources say
- Not checked yetcites [47] D’Ercole AJ, Ye P, Calikoglu AS, Gutierrez-Ospina G (1996) The role of the insulin-like growth factors in the central nervous system. Mol Neurobiol 13:227–255. doi: 10.1007/BF02740625 source
- Not checked yetcites [48] Hana V, Prazny M, Marek J, Skrha J, Justova V (2002) Reduced microvascular perfusion and reactivity in adult GH deficient patients is restored by GH replacement. Eur J Endocrinol 147:333–337. doi: 10.1530/eje.0.1470333 source
- Not checked yetcites [49] Napoli R, Guardasole V, Angelini V et al (2003) Acute effects of growth hormone on vascular function in human subjects. J Clin Endocrinol Metab 88:2817–2820. doi: 10.1210/jc.2003-030144 source
- Not checked yetcites [50] Saatman KE, Contreras PC, Smith DH et al (1997) Insulin-like growth factor-1 (IGF-1) improves both neurological motor and cognitive outcome following experimental brain injury. Exp Neurol 147:418–427. doi: 10.1006/exnr.1997.6629 source
- Not checked yetcites [51] Scheepens A, Sirimanne ES, Breier BH, Clark RG, Gluckman PD, Williams CE (2001) Growth hormone as a neuronal rescue factor during recovery from CNS injury. Neuroscience 104:677–687. doi: 10.1016/S0306-4522(01)00109-9 source
- Not checked yetcites [52] Scheepens A, Williams CE, Breier BH, Guan J, Gluckman PD (2000) A role for the somatotropic axis in neural development, injury and disease. J Pediatr Endocrinol Metab 13(Suppl 6):1483–1491 source
- Not checked yetcites [53] Silha JV, Krsek M, Hana V et al (2005) The effects of growth hormone status on circulating levels of vascular growth factors. Clin Endocrinol (Oxf) 63:79–86. doi: 10.1111/j.1365-2265.2005.02303.x source
- Not checked yetcites [54] Ye P, D’Ercole AJ (1999) Insulin-like growth factor I protects oligodendrocytes from tumor necrosis factor-alpha-induced injury. Endocrinology 140:3063–3072. doi: 10.1210/en.140.7.3063 source
- Not checked yetcites [55] Ye P, Li L, Richards RG, DiAugustine RP, D’Ercole AJ (2002) Myelination is altered in insulin-like growth factor-I null mutant mice. J Neurosci 22:6041–6051 source
- Not checked yetcites [56] Zhong J, Deng J, Phan J et al (2005) Insulin-like growth factor-I protects granule neurons from apoptosis and improves ataxia in weaver mice. J Neurosci Res 80:481–490. doi: 10.1002/jnr.20490 source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“IGF-1 appears to be an important factor in myelination, re-myelination, prevention of demyelination and protection of oligodendrocytes from tumor necrosis factor-α induced apoptosis [47–56].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > The growing awareness of TBI-induced hypopituitarsim
What the sources say
- Not checked yetcites [47] D’Ercole AJ, Ye P, Calikoglu AS, Gutierrez-Ospina G (1996) The role of the insulin-like growth factors in the central nervous system. Mol Neurobiol 13:227–255. doi: 10.1007/BF02740625 source
- Not checked yetcites [48] Hana V, Prazny M, Marek J, Skrha J, Justova V (2002) Reduced microvascular perfusion and reactivity in adult GH deficient patients is restored by GH replacement. Eur J Endocrinol 147:333–337. doi: 10.1530/eje.0.1470333 source
- Not checked yetcites [49] Napoli R, Guardasole V, Angelini V et al (2003) Acute effects of growth hormone on vascular function in human subjects. J Clin Endocrinol Metab 88:2817–2820. doi: 10.1210/jc.2003-030144 source
- Not checked yetcites [50] Saatman KE, Contreras PC, Smith DH et al (1997) Insulin-like growth factor-1 (IGF-1) improves both neurological motor and cognitive outcome following experimental brain injury. Exp Neurol 147:418–427. doi: 10.1006/exnr.1997.6629 source
- Not checked yetcites [51] Scheepens A, Sirimanne ES, Breier BH, Clark RG, Gluckman PD, Williams CE (2001) Growth hormone as a neuronal rescue factor during recovery from CNS injury. Neuroscience 104:677–687. doi: 10.1016/S0306-4522(01)00109-9 source
- Not checked yetcites [52] Scheepens A, Williams CE, Breier BH, Guan J, Gluckman PD (2000) A role for the somatotropic axis in neural development, injury and disease. J Pediatr Endocrinol Metab 13(Suppl 6):1483–1491 source
- Not checked yetcites [53] Silha JV, Krsek M, Hana V et al (2005) The effects of growth hormone status on circulating levels of vascular growth factors. Clin Endocrinol (Oxf) 63:79–86. doi: 10.1111/j.1365-2265.2005.02303.x source
- Not checked yetcites [54] Ye P, D’Ercole AJ (1999) Insulin-like growth factor I protects oligodendrocytes from tumor necrosis factor-alpha-induced injury. Endocrinology 140:3063–3072. doi: 10.1210/en.140.7.3063 source
- Not checked yetcites [55] Ye P, Li L, Richards RG, DiAugustine RP, D’Ercole AJ (2002) Myelination is altered in insulin-like growth factor-I null mutant mice. J Neurosci 22:6041–6051 source
- Not checked yetcites [56] Zhong J, Deng J, Phan J et al (2005) Insulin-like growth factor-I protects granule neurons from apoptosis and improves ataxia in weaver mice. J Neurosci Res 80:481–490. doi: 10.1002/jnr.20490 source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“GH has been shown to be directly involved in vascular reactivity, vascular tone and CNS repair processes after hypoxic injury”
§ Pathophysiology of hypopituitarism in the setting of brain injury > The growing awareness of TBI-induced hypopituitarsim
What the sources say
- Not checked yetcites [47] D’Ercole AJ, Ye P, Calikoglu AS, Gutierrez-Ospina G (1996) The role of the insulin-like growth factors in the central nervous system. Mol Neurobiol 13:227–255. doi: 10.1007/BF02740625 source
- Not checked yetcites [48] Hana V, Prazny M, Marek J, Skrha J, Justova V (2002) Reduced microvascular perfusion and reactivity in adult GH deficient patients is restored by GH replacement. Eur J Endocrinol 147:333–337. doi: 10.1530/eje.0.1470333 source
- Not checked yetcites [49] Napoli R, Guardasole V, Angelini V et al (2003) Acute effects of growth hormone on vascular function in human subjects. J Clin Endocrinol Metab 88:2817–2820. doi: 10.1210/jc.2003-030144 source
- Not checked yetcites [50] Saatman KE, Contreras PC, Smith DH et al (1997) Insulin-like growth factor-1 (IGF-1) improves both neurological motor and cognitive outcome following experimental brain injury. Exp Neurol 147:418–427. doi: 10.1006/exnr.1997.6629 source
- Not checked yetcites [51] Scheepens A, Sirimanne ES, Breier BH, Clark RG, Gluckman PD, Williams CE (2001) Growth hormone as a neuronal rescue factor during recovery from CNS injury. Neuroscience 104:677–687. doi: 10.1016/S0306-4522(01)00109-9 source
- Not checked yetcites [52] Scheepens A, Williams CE, Breier BH, Guan J, Gluckman PD (2000) A role for the somatotropic axis in neural development, injury and disease. J Pediatr Endocrinol Metab 13(Suppl 6):1483–1491 source
- Not checked yetcites [53] Silha JV, Krsek M, Hana V et al (2005) The effects of growth hormone status on circulating levels of vascular growth factors. Clin Endocrinol (Oxf) 63:79–86. doi: 10.1111/j.1365-2265.2005.02303.x source
- Not checked yetcites [54] Ye P, D’Ercole AJ (1999) Insulin-like growth factor I protects oligodendrocytes from tumor necrosis factor-alpha-induced injury. Endocrinology 140:3063–3072. doi: 10.1210/en.140.7.3063 source
- Not checked yetcites [55] Ye P, Li L, Richards RG, DiAugustine RP, D’Ercole AJ (2002) Myelination is altered in insulin-like growth factor-I null mutant mice. J Neurosci 22:6041–6051 source
- Not checked yetcites [56] Zhong J, Deng J, Phan J et al (2005) Insulin-like growth factor-I protects granule neurons from apoptosis and improves ataxia in weaver mice. J Neurosci Res 80:481–490. doi: 10.1002/jnr.20490 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.
None of the sources cited for this claim have been checked yet.
In the paper
“it is now clear that there are both GH and insulinlike growth factor (IGF-1) receptors widely present in the brain.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > The growing awareness of TBI-induced hypopituitarsim
What the sources say
- Not checked yetcites [47] D’Ercole AJ, Ye P, Calikoglu AS, Gutierrez-Ospina G (1996) The role of the insulin-like growth factors in the central nervous system. Mol Neurobiol 13:227–255. doi: 10.1007/BF02740625 source
- Not checked yetcites [48] Hana V, Prazny M, Marek J, Skrha J, Justova V (2002) Reduced microvascular perfusion and reactivity in adult GH deficient patients is restored by GH replacement. Eur J Endocrinol 147:333–337. doi: 10.1530/eje.0.1470333 source
- Not checked yetcites [49] Napoli R, Guardasole V, Angelini V et al (2003) Acute effects of growth hormone on vascular function in human subjects. J Clin Endocrinol Metab 88:2817–2820. doi: 10.1210/jc.2003-030144 source
- Not checked yetcites [50] Saatman KE, Contreras PC, Smith DH et al (1997) Insulin-like growth factor-1 (IGF-1) improves both neurological motor and cognitive outcome following experimental brain injury. Exp Neurol 147:418–427. doi: 10.1006/exnr.1997.6629 source
- Not checked yetcites [51] Scheepens A, Sirimanne ES, Breier BH, Clark RG, Gluckman PD, Williams CE (2001) Growth hormone as a neuronal rescue factor during recovery from CNS injury. Neuroscience 104:677–687. doi: 10.1016/S0306-4522(01)00109-9 source
- Not checked yetcites [52] Scheepens A, Williams CE, Breier BH, Guan J, Gluckman PD (2000) A role for the somatotropic axis in neural development, injury and disease. J Pediatr Endocrinol Metab 13(Suppl 6):1483–1491 source
- Not checked yetcites [53] Silha JV, Krsek M, Hana V et al (2005) The effects of growth hormone status on circulating levels of vascular growth factors. Clin Endocrinol (Oxf) 63:79–86. doi: 10.1111/j.1365-2265.2005.02303.x source
- Not checked yetcites [54] Ye P, D’Ercole AJ (1999) Insulin-like growth factor I protects oligodendrocytes from tumor necrosis factor-alpha-induced injury. Endocrinology 140:3063–3072. doi: 10.1210/en.140.7.3063 source
- Not checked yetcites [55] Ye P, Li L, Richards RG, DiAugustine RP, D’Ercole AJ (2002) Myelination is altered in insulin-like growth factor-I null mutant mice. J Neurosci 22:6041–6051 source
- Not checked yetcites [56] Zhong J, Deng J, Phan J et al (2005) Insulin-like growth factor-I protects granule neurons from apoptosis and improves ataxia in weaver mice. J Neurosci Res 80:481–490. doi: 10.1002/jnr.20490 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.
In the paper
“The pituitary gland, typically weighing less than one gram and measuring approximately 8 mm by 10 mm, is located within the sella turcica in the skull base. It is separated from the suprasellar cistern by the diaphragma sella and is tethered to the hypopthalamus by the infundibulum which inserts on its superior surface [57].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Pituitary gland vascular anatomy and blood supply
What the sources say
- Not checked yetcites [57] Rhoton AL Jr (2002) The sellar region. Neurosurgery 51:S335–S374. doi: 10.1097/00006123-200208000-00007 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. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The short hypophyseal portal vessels arise from branches of the intracavernous internal carotid artery, the inferior hypophyseal arteries, which enter the sella from below the diaphragma sella and supply the anterior gland with less than 30% of its vascular supply, predominantly in the medial portion of the gland including the pars intermedia [58–60].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Pituitary gland vascular anatomy and blood supply
What the sources say
- Not checked yetcites [58] Adams JH, Daniel PM, Prichard MM (1966) The long-term effect of transection of the pituitary stalk on the volume of the pituitary gland on the adult goat. Acta Endocrinol (Copenh) 51:377–390 source
- Not checked yetcites [59] Daniel PM (1963) The pituitary gland and its blood supply. Sci Basis Med Annu Rev 84:83–98
- Not checked yetcites [60] Gorczyca W, Hardy J (1987) Arterial supply of the human anterior pituitary gland. Neurosurgery 20:369–378. doi: 10.1097/00006123-198703000-00003 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.
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 is likely that these factors individually and in varying combinations determine which hormonal axes are affected, the severity of abnormality and whether such deficits are reversible or permanent.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Overview
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 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
“Given the pituitary glands confinement within the bony sella and overlying diaphragma sella, and its tethering to the hypothalamus by the infundibulum, it has been hypothesized that the anterior and posterior gland may be susceptible to mechanical trauma at the moment of impact.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
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.
None of the sources cited for this claim have been checked yet.
In the paper
“Fractures through the skull base and sella turcica as well as rotational and shearing injuries of the brain stem and hypothalamic-pituitary axis may directly injure the gland, infundibulum and/or hypothalamus.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [10] Chesnut RM, Marshall LF, Klauber MR et al (1993) The role of secondary brain injury in determining outcome from severe head injury. J Trauma 34:216–222. doi: 10.1097/00005373-199302000-00006 source
- Not checked yetcites [39] Kelly DF, Gonzalo IT, Cohan P, Berman N, Swerdloff R, Wang C (2000) Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report. J Neurosurg 93:743–752 source
- Not checked yetcites [59] Daniel PM (1963) The pituitary gland and its blood supply. Sci Basis Med Annu Rev 84:83–98
- Not checked yetcites [61] Ceballos R (1966) Pituitary changes in head trauma (analysis of 102 consecutive cases of head injury). Ala J Med Sci 3:185–198
- Not checked yetcites [62] Daniel PM, Prichard MM, Treip CS (1959) Traumatic infarction of the anterior lobe of the pituitary gland. Lancet 2:927–931. doi: 10.1016/S0140-6736(59)91583-1 source
- Not checked yetcites [63] Kornblum RN, Fisher RS (1969) Pituitary lesions in craniocerebral injuries. Arch Pathol 88:242–248
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
“In these cases, the infarction pattern was in the blood supply pattern of the long hypophyseal portal veins while tissue in the vascular territory of the short portal veins survived.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [61] Ceballos R (1966) Pituitary changes in head trauma (analysis of 102 consecutive cases of head injury). Ala J Med Sci 3:185–198
- Not checked yetcites [63] Kornblum RN, Fisher RS (1969) Pituitary lesions in craniocerebral injuries. Arch Pathol 88:242–248
plaincorrelationaln = 200- 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 acute phase, the pituitary glands of TBI patients are significantly enlarged as compared with normal healthy control subjects and many also demonstrate other abnormalities such as hemorrhage, infarction, signal abnormalities and/or partial stalk transsection [67].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [67] Maiya B, Newcombe V, Nortje J et al (2008) Magnetic resonance imaging changes in the pituitary gland following acute traumatic brain injury. Intensive Care Med 34:468–475. doi: 10.1007/s00134-007-0902-x 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.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This cellular distribution is consistent with the area of irrigation of the long hypophyseal portal vessels. An infarction of this lateral and peripheral region of the gland will mostly affect somatotrophs and gonadotrophs.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
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.
In the paper
“The somatotrophs are located primarily in the lateral wings of the anterior pituitary and the gonadotrophs are scattered throughout the pars distalis and are the major cell group in the pars tuberalis [69].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [69] Asa S, Kovacs K, Melmed S (1995) The hypothalamic-pituitary axis. In: Melmed S (ed) The pituitary. Blackwell Science Inc., Cambridge, pp 3–44
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
“The corticotrophs, found predominantly in the central mucoid wedge and pars intermedia, and the thyrotrophs, tending to cluster in the anteromedial portion of the gland, are thus in the less susceptible short hypophyseal portal territory.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [69] Asa S, Kovacs K, Melmed S (1995) The hypothalamic-pituitary axis. In: Melmed S (ed) The pituitary. Blackwell Science Inc., Cambridge, pp 3–44
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
“In the chronic phase, patients often demonstrate pituitary volume loss or empty sella, followed by abnormal pituitary gland signal heterogeneity, perfusion deficits and/or lack of posterior pituitary signal [68].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [68] Schneider HJ, Samann PG, Schneider M et al (2007) Pituitary imaging abnormalities in patients with and without hypopituitarism after traumatic brain injury. J Endocrinol Invest 30:RC9–RC12 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.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This reversibility of acute adrenal insufficiency and the fact that chronic adrenal insufficiency is so uncommon suggests that other factors (as discussed below) may be relevant in the acute setting.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
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
“a severe injury is not necessarily a prerequisite for development of chronic pituitary failure. Several studies have demonstrated chronic endocrinopathy after milder TBI [28, 29, 39, 45].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Primary and secondary brain injury
What the sources say
- Not checked yetcites [28] Benvenga S, Campenni A, Ruggeri RM, Trimarchi F (2000) Clinical review 113: hypopituitarism secondary to head trauma. J Clin Endocrinol Metab 85:1353–1361. doi: 10.1210/jc.85.4.1353 source
- Not checked yetcites [29] Edwards OM, Clark JD (1986) Post-traumatic hypopituitarism. Six cases and a review of the literature. Medicine (Baltimore) 65:281–290. doi: 10.1097/00005792-198609000-00001 source
- Not checked yetcites [39] Kelly DF, Gonzalo IT, Cohan P, Berman N, Swerdloff R, Wang C (2000) Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report. J Neurosurg 93:743–752 source
- Not checked yetcites [45] Bondanelli M, De Marinis L, Ambrosio MR, Monesi M, Valle D, Zatelli MC, Fusco A, Bianchi A, Farneti M, degli Uberti EC (2004) Occurrence of pituitary dysfunction following traumatic brain injury. J Neurotrauma 21:685–696. doi: 10.1089/0897715041269713 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.
None of the sources cited for this claim have been checked yet.
In the paper
“the effect of the metabolic suppressive agents high-dose pentobarbital and propofol were more lasting but still reversible and dose-dependent [74–83].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Stress of critical illness and medication effects
What the sources say
- Not checked yetcites [74] Absalom A, Pledger D, Kong A (1999) Adrenocortical function in critically ill patients 24 h after a single dose of etomidate. Anaesthesia 54:861–867. doi: 10.1046/j.1365-2044.1999.01003.x source
- Not checked yetcites [75] Aitkenhead AR, Pepperman ML, Willatts SM et al (1989) Comparison of propofol and midazolam for sedation in critically ill patients. Lancet 2:704–709. doi: 10.1016/S0140-6736(89)90770-8 source
- Not checked yetcites [76] Brooks SM, Werk EE, Ackerman SJ, Sullivan I, Thrasher K (1972) Adverse effects of phenobarbital on corticosteroid metabolism in patients with bronchial asthma. N Engl J Med 286:1125–1128 source
- Not checked yetcites [77] Crozier TA, Beck D, Schlaeger M, Wuttke W, Kettler D (1987) Endocrinological changes following etomidate, midazolam, or methohexital for minor surgery. Anesthesiology 66:628–635. doi: 10.1097/00000542-198705000-00006 source
- Not checked yetcites [78] Fellows IW, Bastow MD, Byrne AJ, Allison SP (1983) Adrenocortical suppression in multiply injured patients: a complication of etomidate treatment. Br Med J (Clin Res ed) 287:1835–1837 source
- Not checked yetcites [79] Hoen S, Asehnoune K, Brailly-Tabard S et al (2002) Cortisol response to corticotrophin stimulation in trauma patients: influence of hemorrhagic shock. Anesthesiology 97:807–813. doi: 10.1097/00000542-200210000-00010 source
- Not checked yetcites [80] Malerba G, Romano-Girard F, Cravoisy A et al (2005) Risk factors of relative adrenocortical deficiency in intensive care patients needing mechanical ventilation. Intensive Care Med 31:388–392. doi: 10.1007/s00134-004-2550-8 source
- Not checked yetcites [81] Newman LH, McDonald JC, Wallace PG, Ledingham IM (1987) Propofol infusion for sedation in intensive care. Anaesthesia 42:929–937. doi: 10.1111/j.1365-2044.1987.tb05362.x source
- Not checked yetcites [82] Schenarts CL, Burton JH, Riker RR (2001) Adrenocortical dysfunction following etomidate induction in emergency department patients. Acad Emerg Med 8:1–7. doi: 10.1111/j.1553-2712.2001.tb00537.x source
- Not checked yetcites [83] Wagner RL, White PF, Kan PB, Rosenthal MH, Feldman D (1984) Inhibition of adrenal steroidogenesis by the anesthetic etomidate. N Engl J Med 310:1415–1421 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
“Therefore, this acute hypopituitarism appeared to be a transient and reversible effect largely related to metabolic suppressive agents or etomidate and did not lead to overt chronic adrenal deficiency.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Pathophysiology of hypopitutarism after TBI > Stress of critical illness and medication effects
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 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
“Based on prior autopsy studies of fatal head injuries and imaging studies of TBI survivors, it appears the site of injury leading to pituitary hormonal dysfunction is variable and may include the hypothalamus, infundibulum and pituitary gland itself.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Conclusions
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 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 the mechanism of post-TBI pituitary dysfunction remains incompletely understood, evidence suggests this is a multi-factorial process related to: (1) the primary brain injury event itself; (2) secondary insults such as hypotension, hypoxia and raised intracranial pressure; (3) the transient stress of critical illness; and (4) transient medication effects.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Conclusions
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: 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
“This hormonal dysfunction can impact the early and late recovery process, ultimately effecting longterm neurobehavioral function and quality of life.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Conclusions
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: 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
“It is likely that these factors individually and in varying combinations determine which hormonal axes are affected, the severity of abnormality and whether such deficits are reversible or permanent.”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Conclusions
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.
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 cited source says what the claim attributes to it.
In the citing 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”
From Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach (2015) · cites this paper as [133]
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
§ Pathophysiology of hypopituitarism in the setting of brain injury > Overview of TBI pathophysiolgy and current therapy
“mild TBI, defined as a post-resuscitation Glasgow Coma Scale score of 13–15 [3].”
§ Pathophysiology of hypopituitarism in the setting of brain injury > Overview of TBI pathophysiolgy and current therapy
“moderate (GCS 9–13) and severe (GCS 3–8) TBI”
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
§ Pathophysiology of hypopituitarism in the setting of brain injury > References
“Incidence of traumatic brain injury in the United States, 2006”
§ Pathophysiology of hypopituitarism in the setting of brain injury > References
“J Head Trauma Rehabil 2003 21 544 548”
Citations
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Rehabilitation of Persons With Traumatic Brain Injury
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Review: Traumatic brain injury and hyperglycemia, a potentially modifiable risk factor
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Tan, C. L., Alavi, S. A., Baldeweg, S. E., Belli, A., Carson, A., Feeney, C., Goldstone, A. P., Greenwood, R., Menon, D. K., Simpson, H. L., et al. (2017) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp-2016-315500 · Cited by 111
Metadata
- Authors
- Dusick, J. R., Wang, C., Cohan, P., Swerdloff, R., & Kelly, D. F.
- Affiliations
- University of California, Los Angeles (US)
- The Lundquist Institute (US)
- Saint John's Health Center (US)
- Corresponding author
- Kelly, Daniel F.
- Venue
- Pituitary
- Published
- 2008-05-15
- Volume
- 15
- Issue
- 1
- Pages
- 2-9
- ISSN
- 1386-341X (ISSN-L)
- 1573-7403
- PMC
- PMC4170072
- OpenAlex
- W2210815217
- Semantic Scholar
- 2e74496d8082e16b7594d7ea441d3a531a19c74d
- Cited by
- 121
- References
- 107
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 9 · 2023: 6 · 2022: 6 · 2021: 6 · 2020: 5 · 2019: 19 · 2018: 9 · 2017: 8 · 2016: 9 · 2015: 11 · 2014: 5 · 2013: 5 · 2012: 3
- FWCI
- 0.59
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Pituitary (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR000124)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Keywords
- traumatic brain injury, hypopituitarism, hypothalamic-pituitary dysfunction, secondary brain injury, adrenal insufficiency, medication effects, intracranial pressure, hypoxia, hypotension, cerebral blood flow
- MeSH terms
- Brain Injuries, Humans, Hypopituitarism
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-05, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-05 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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