Research Reports - Pituitary dysfunction after traumatic brain injury

Endocr Rev. 2015 Jun;36(3):305-42

Tanriverdi F, Schneider HJ, Aimaretti G, Masel BE, Casanueva FF, Kelestimur F

Traumatic brain injury (TBI) is a growing public health problem worldwide and is
a leading cause of death and disability. The causes of TBI include motor vehicle
accidents, which are the most common cause, falls, acts of violence,
sports-related head traumas, and war accidents including blast-related brain
injuries. Recently, pituitary dysfunction has also been described in boxers and
kickboxers. Neuroendocrine dysfunction due to TBI was described for the first
time in 1918. Only case reports and small case series were reported until 2000,
but since then pituitary function in TBI victims has been investigated in more
detail. The frequency of hypopituitarism after TBI varies widely among different
studies (15-50% of the patients with TBI in most studies). The estimates of
persistent hypopituitarism decrease to 12% if repeated testing is applied. GH is
the most common hormone lost after TBI, followed by ACTH, gonadotropins (FSH and
LH), and TSH. The underlying mechanisms responsible for pituitary dysfunction
after TBI are not entirely clear; however, recent studies have shown that genetic
predisposition and autoimmunity may have a role. Hypopituitarism after TBI may
have a negative impact on the pace or degree of functional recovery and
cognition. What is not clear is whether treatment of hypopituitarism has a
beneficial effect on specific function. In this review, the current data related
to anterior pituitary dysfunction after TBI in adult patients are updated, and
guidelines for the diagnosis, follow-up strategies, and therapeutic approaches
are reported.

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