Endocrine sequelae of traumatic brain injury in childhood.

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Abstract

Anterior pituitary hormone dysfunction may be an important feature of long-term morbidity in survivors of traumatic brain injury (TBI). The hypothalamic-pituitary structures are vulnerable to damage following head injury. Therefore, pituitary dysfunction, which may be detected months or years after injury, is now well recognised as a long-term consequence of TBI in adults. In contrast, little is known about this potential complication in children and adolescents. This article reviews the available paediatric data, which show that hypopituitarism may occur after both mild and severe TBI, although there is little published data on its incidence or prevalence within this age group. A recent analysis of the KIGS (Pfizer International Growth Study database) highlights very few registered cases of TBI-related growth hormone deficiency, suggesting that this may be either an uncommon or an overlooked phenomenon. Prospective studies will be needed to determine the incidence, natural history and response to hormone replacement of post-TBI-induced hypopituitarism in children.

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Novel insights into the neuroendocrinology of critical illness.

G Van den Berghe (2000)

An unexplained hallmark of prolonged critical illness is the fact that food does not prevent or reverse protein wasting, while fat is paradoxically accrued. This 'wasting syndrome' often persists after the underlying disease has been resolved and thus perpetuates intensive care dependency. Although the crucial role of an intact hypothalamus-pituitary axis for homeostasis during stress is well recognized, the differences between the neuroendocrine changes observed in acute and prolonged critical illness were only recently described. Novel insights in this area are reviewed here. The initial endocrine stress response consists primarily of a peripheral inactivation of anabolic pathways while pituitary activity is essentially amplified or maintained. These responses presumably provide the metabolic substrates and host defense required for survival and to delay anabolism, and thus should be considered as adaptive and beneficial. Persistence of this acute stress response throughout the course of critical illness was hitherto assumed. This assumption has now been invalidated, since a uniformly reduced pulsatile secretion of ACTH, TSH, LH, prolactin (PRL) and GH has been observed in protracted critical illness, causing diminished stimulation of several target organs. Impaired pulsatile secretion of anterior pituitary hormones in the chronic phase of critical illness seems to have a hypothalamic rather than a pituitary origin, as administration of relevant releasing factors evoked immediate and pronounced pituitary hormone release. A reduced availability of TRH, one of the endogenous ligands of the GH-releasing peptide (GHRP) receptor (such as the recently discovered ghrelin) and, in very long-stay critically ill men, also of GHRH, appear to be involved. This hypothesis was further explored by investigating the effects of continuous i.v. infusion of GHRH, GHRP, TRH and their combinations for several days. Pulsatile secretion of GH, TSH and PRL was re-amplified by relevant combinations of releasing factors which also substantially increased circulating levels of IGF-I, GH-dependent binding proteins, thyroxine and tri-iodothyronine (T3) while avoiding a rise in reverse T3. Active feedback-inhibition loops prevented overstimulation of target organs and metabolic improvement was noted with the combined infusion of GHRP and TRH. Whether this novel endocrine strategy will also enhance clinical recovery from critical illness remains to be explored.

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Prevalence of Neuroendocrine Dysfunction in Patients Recovering from Traumatic Brain Injury

S. Lieberman (2001)

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Anterior pituitary dysfunction following traumatic brain injury (TBI).

Amar Agha, Elaine C. Thompson (2006)

Traumatic brain injury (TBI) is the commonest cause of death and disability in young adults living in industrialized countries. Several recent studies have convincingly shown that anterior hypopituitarism is a common complication of head trauma with a prevalence of at least 25% among long-term survivors. This is a much higher frequency than previously thought and suggests that most cases of post-traumatic hypopituitarism (PTHP) remain undiagnosed and untreated. These findings raise important questions about the potential contribution of PTHP to the high physical and neuropsychiatric morbidity seen in this group of patients. In this review, we examine the published reports on the neuroendocrine abnormalities in TBI patients and highlight new data that give novel insights into the natural history of this disorder. We discuss the potential contribution of PTHP to recovery and rehabilitation after injury and the need for the identification and the appropriate and timely management of hormone deficiencies to optimize patient recovery from head trauma, improve quality of life and avoid the long-term adverse consequences of untreated hypopituitarism.