Hypothalamopituitary Dysfunction Following Traumatic Brain Injury and Aneurysmal Subarachnoid Hemorrhage

Abstract

Context Neuroendocrine dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage may occur with a much higher prevalence than previously suspected. This sequela is a potentially serious but treatable complication of brain injury.Objective To review research on hypothalamopituitary dysfunction as an underdiagnosed consequence of traumatic brain injury and subarachnoid hemorrhage, the natural history of this complication, and the potential clinical and public health implications of posttraumatic hypopituitarism. Evidence AcquisitionThe MEDLINE database was searched for articles published between 2000 and 2007 using any combination of the terms traumatic brain injury or subarachnoid hemorrhage with pituitary, hypopituitarism, growth hormone deficiency, hypogonadism, hypocortisolism, hypothyroidism, or diabetes insipidus. The reference lists of articles identified by this search strategy were also searched. All articles reporting original data on endocrine outcomes after traumatic brain injury or aneurysmal subarachnoid hemorrhage in peer-reviewed journals with regard to prevalence, pathogenesis, risk factors, outcomes, and clinical course were selected. We pooled data and calculated prevalence rates and 95% confidence intervals (CIs). ResultsWe identified 19 studies including 1137 patients. The pooled prevalences of hypopituitarism in the chronic phase after traumatic brain injury and aneurysmal subarachnoid hemorrhage were 27.5% (95% confidence interval [CI], 22.8%-28.9%) and 47% (95% CI, 37.4%-56.8%), respectively. The pooled prevalence of hypopituitarism was greater in patients with severe compared with those with mild or moderate traumatic brain injury. Early neuroendocrine abnormalities were transient in some patients while, less commonly, hypopituitarism evolved over time in others. Patients with posttraumatic hypopituitarism showed an impaired quality of life and an adverse metabolic profile. ConclusionHypopituitarism is a common complication of both traumatic brain injury and aneurysmal subarachnoid hemorrhage and might contribute to morbidity and poor recovery after brain injury.

Should anterior pituitary function be tested during follow-up of all patients presenting at the emergency department because of traumatic brain injury?

“…In some previous studies, no association of pituitary dysfunction with TBI severity was reported (6,7,(10)(11)(12)(13), whereas others found pituitary dysfunction to be more prevalent in patients with more severe TBI (5,14). In their systematic review, Schneider et al pooled the reported prevalences in severe (35.3%, 95% CI 27.3-44.2%), Mod (10.9%, 95% CI 5.1-21.8%), and MTBI (16.8%, 95% CI 10.9-25.0%) (22), showing that the risk of pituitary dysfunction is higher in patients with STBI than in patients with a MTBI. In order to prevent the underestimation of the prevalence of pituitary dysfunction, our study enrolment procedure implied that the largest effort was made to include patients with Mod/STBI, resulting in an overrepresentation of Mod/STBI patients.…”

“…Additionally, hypogonadism may limit fertility, and hypocortisolism and hypothyroidism can be disabling and life-threatening (19,20). Consequently, it was proposed that pituitary function should be screened in all patients after Mod or STBI, even in the absence of symptoms of hypopituitarism (8,21,22).…”

Biomarcadores prognósticos no traumatismo crânio-encefálico grave

“…(76) Next, the luteinizant hormone (LH) and follicular stimulating hormone (FSH) deficiencies are significantly more common than deficiencies of the adrenocorticotropic hormone (ACTH) which are significantly more common than deficiencies of the thyroid stimulating hormone (TSH). (77) The pituitary gland responds to acute traumatic events and many changes in hormone levels become apparent in the first hours or days after trauma. (61,78) Recent studies have shown that various inflammatory mediators including cytokines and free radicals may affect endocrine function at the acute stage of TBI.…”

“…Serum levels of cortisol-binding globulin to cortisol may be decreased in catabolic conditions resulting in disproportionately low total cortisol levels when compared to free cortisol (biologically active). (77,81) Hyperprolactinemia is present in more than 50% of the patients at the acute post-TBI stage. Proof of a negative correlation between prolactine concentrations and TBI severity suggests a good prognostic role for prolactine responses at the acute stage after TBI.…”

“…Prevalence of diabetes insipidus after TBI at the acute stage may reach 26%. (77) Experimental studies have shown increases of leptin RNAm in the brain of rats, during the first hours after TBI. (82) Leptin is a hormone produced by adipocytes that regulates satiation and energy metabolism by activating receptors expressed in the hypothalamus.…”