Hypopituitarism after traumatic brain injury

Abstract

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

Biomarcadores prognósticos no traumatismo crânio-encefálico grave

“…High levels of IL-6 in plasma and liquor are found after TBI. (3) IL-6 might stimulate vasopressin secretion and may be involved in the pathogenesis of the syndrome of inappropriate hormone secretion (ADHantidiuretic hormone) after TBI (61) .…”

“…(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. (78) Such changes represent part of the acute adaptive response to trauma and may also be influenced buy medication administered at this stage such as glucocorticoids, narcotics or dopaminergic agents.…”

“…(78) Such changes represent part of the acute adaptive response to trauma and may also be influenced buy medication administered at this stage such as glucocorticoids, narcotics or dopaminergic agents. (61) Hormone changes of the acute stage after TBI generally do not predict hypophysary dysfunction after one year. (78) Hypophysary function in TBI patient can improve with time, suggesting that isolated or even multiple failures diagnosed in the short time are transient.…”

“…(61) In some cases, abnormalities in the cortisol secretion dynamics ( fasting hypercortisolemia, abolition of normal day rhythm and inadequate suppression after dexamethasone) may persist for many months after TBI (78) . Tanriverdi et al (78) in a prospective study, in which dosages were measured during the first 24 hours after admission in the ICU and 12 months later, found that mean levels of cortisol were significantly higher at the acute stage in comparison to the levels of the ACTH triggering a central activation of the hypothalamus-hypophysis-adrenal axis.…”

“…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. (61,81) Posterior hypopituitarism can also be present after TBI with central diabetes insipidus. Prevalence of diabetes insipidus after TBI at the acute stage may reach 26%.…”