Traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarism: screening study at 3 months after the brain injury

Aimaretti, Gianluca; Ambrosio, Maria Rosaria; Somma, Carolina Di; Fusco, Alessandra; Cannavò, Salvatore; Gasperi, Maurizio; Scaroni, Carla; Marinis, Laura De; Benvenga, Salvatore; Uberti, Ettore C. degli; Lombardi, Gaetano; Mantero, Franco; Martino, Enio; Giordano, Giulio; Ghigo, Ezio

doi:10.1111/j.1365-2265.2004.02094.x

Cited by 309 publications

(330 citation statements)

References 28 publications

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“…Taken together, these observations suggest that cortical TBI inflicts long-lasting destructive changes in brain tissue that is remote from the site of the initial CCI. Specifically, our findings and others in humans with TBI (Kelly et al, 2000;Lieberman et al, 2001;Agha et al, 2004a;Aimaretti et al, 2004;Bondanelli et al, 2004) demonstrate that cortical TBI can have substantial effects on the expression of the GH system, supporting clinical studies and replicating the results in an animal model of CNS injury.…”

Section: Kasturi and Stein Discussionsupporting

confidence: 54%

“…Other signaling mechanisms could include trans-synaptic (Koliatsos et al, 2004) as well as anterograde and retrograde neuronal degeneration from the site of injury to the more distal sites (Sorensen et al, 1996;Bechmann and Nitsch, 1997), also eventually affecting some of the endocrine functions. While we know something about the effects of TBI on endocrine function based on human studies (Ceballos, 1966;Agha et al, 2004aAgha et al, , 2004bAgha et al, , 2005aAgha et al, , 2005bAimaretti et al, 2004Aimaretti et al, , 2005bBondanelli et al, 2004;Herrmann et al, 2006;Powner et al, 2006;Schneider et al, 2006;Tanriverdi et al, 2006), there is still some uncertainty about the mechanisms by which long-term alterations in the endocrine system (like suppression of serum GH in TBI subjects) evolve over time, and whether such changes could be prevented by therapeutic interventions.…”

Section: Introductionmentioning

confidence: 99%

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Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

Kasturi

Stein

2009

Journal of Neurotrauma

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In humans, traumatic brain injury (TBI) causes pathological changes in the hypothalamus (HT) and the pituitary. One consequence of TBI is hypopituitarism, with deficiency of single or multiple hormones of the anterior pituitary (AP), including growth hormone (GH). At present no animal model of TBI with ensuing hypopituitarism has been demonstrated. The main objective of this study was to investigate whether cortical contusion injury (CCI) could induce long-term reduction of serum GH in rats. We also tested the hypothesis that TBI to the medial frontal cortex (MFC) would induce inflammatory changes in the HT and AP. Methods: Nine young adult male rats were given sham surgery (n ¼ 4) or controlled impact contusions (n ¼ 5) of the MFC. Two months postinjury they were killed, trunk blood collected and their brains and AP harvested. GH was measured in serum and AP using ELISA and Western blot respectively. Interleukin-1b (IL-1b) and glial fibrillary acidic protein (GFAP) were measured in the cortex (Cx), HT, and AP by Western blot. Results: Lesion rats had significantly (p < 0.05) lower levels of GH in the AP and serum, unaltered serum IGF-1, and significantly (p < 0.05) higher levels of IL-1b in the Cx and HT and GFAP in the Cx, HT, and AP compared to that of shams. Conclusion: CCI leads to a long-term depletion of serum GH in male rats. This chronic change in GH post-TBI is probably the result of systemic and persistent inflammatory changes observed at the level of HT and AP, the mechanism of which is not yet known.

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Section: Kasturi and Stein Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

Kasturi

Stein

2009

Journal of Neurotrauma

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“…By contrast, other authors demonstrated a high prevalence of diabetes insipidus during the acute phase post-TBI in patients admitted to a neurosurgical center (22 -26%) (49,69) and in patients with head injury damaging the chiasm (37%) (70). However, diabetes insipidus is frequently transient and can spontaneously disappear within a few days or up to 1 month (66,70,71) after the acute event, as confirmed by its low prevalence (0 -6.9%) in patients evaluated after months or years following TBI (5,6,69).…”

Section: Consequences Of Tbimentioning

confidence: 99%

“…Musculoskeletal problems are also common, with an incidence of fractures of approximately 30% (8). Neuroendocrine dysfunction occurs in approximately 40% of patients with TBI (5,6,30). Medical complications occur not only in the immediate postinjury period with implications for early rehabilitation, but may persist for many months or become chronic.…”

Section: Consequences Of Tbimentioning

confidence: 99%

“…When the morning cortisol value is persistently in the lower limit of the normal range, a test of ACTH reserve should be performed, in order to demonstrate the presence of a subclinical corticotrope deficiency (96). In TBI patients, corticotropin hypothalamic -pituitary axis function has been studied by measuring basal ACTH and cortisol values (5,6) or by performing stimulation tests (ITT or ACTH) (7,30) with different results. Basal evaluation detected corticotropin deficiency in , 10% of the cases in three series (5,6,30).…”

Section: Kelly Et Al (30)mentioning

confidence: 99%

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Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

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185

152

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Traumatic brain injury (TBI) is one of the main causes of death and disability in young adults, with consequences ranging from physical disabilities to long-term cognitive, behavioural, psychological and social defects. Post-traumatic hypopituitarism (PTHP) was recognized more than 80 years ago, but it was thought to be a rare occurrence. Recently, clinical evidence has demonstrated that TBI may frequently cause hypothalamic -pituitary dysfunction, probably contributing to a delayed or hampered recovery from TBI. Changes in pituitary hormone secretion may be observed during the acute phase post-TBI, representing part of the acute adaptive response to the injury. Moreover, diminished pituitary hormone secretion, caused by damage to the pituitary and/or hypothalamus, may occur at any time after TBI. PTHP is observed in about 40% of patients with a history of TBI, presenting as an isolated deficiency in most cases, and more rarely as complete pituitary failure. The most common alterations appear to be gonadotropin and somatotropin deficiency, followed by corticotropin and thyrotropin deficiency. Hyper-or hypoprolactinemia may also be present. Diabetes insipidus may be frequent in the early, acute phase post-TBI, but it is rarely permanent. Severity of TBI seems to be an important risk factor for developing PTHP; however, PTHP can also manifest after mild TBI. Accurate evaluation and long-term follow-up of all TBI patients are necessary in order to detect the occurrence of PTHP, regardless of clinical evidence for pituitary dysfunction. In order to improve outcome and quality of life of TBI patients, an adequate replacement therapy is of paramount importance.European Journal of Endocrinology 152 679-691

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Adrenal Insufficiency

Salvatori¹

2005

JAMA

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Traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarism: screening study at 3 months after the brain injury

Abstract: TBI and SAH are conditions associated with high risk of acquired hypopituitarism. The pituitary defect is often multiple and severe GHD is the most frequent defect. Thus neuroendocrine evaluations are always mandatory in patients after brain injuries.

Cited by 309 publications

References 28 publications

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

Hypopituitarism after traumatic brain injury

Adrenal Insufficiency

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