Hypopituitarism has been reported in 28-65% of long-term survivors of traumatic brain injury (TBI). We attempted to define the natural history of post-traumatic hypopituitarism in order to devise guidelines for the optimal timing of patient assessment and hormone replacement.
Fifty consecutive patients with severe or moderate TBI were enrolled in a prospective study of pituitary function during the acute phase, at 6 months and, at 12 months following TBI. Growth hormone (GH) and adrenocorticotrophin hormone (ACTH) reserves were assessed using the glucagon stimulation test (GST). Baseline serum concentrations of other anterior pituitary hormones were measured. Results were compared against normative data obtained from matched healthy controls.
Nine patients (18 %) had GH deficiency (GHD) in the acute phase; at six month, five patients recovered function and 2 new deficiencies were detected; at twelve months, one patient recovered leaving 5 patients (10.4%) with GHD. Eight patients (16%) showed subnormal cortisol responses in the acute phase; at six months, four had recovered and five new deficiencies were detected; all nine patients (18.8%) had persistent abnormalities at twelve months. Forty patients (80%) had gonadotrophin deficiency in the acute phase, of whom, 85% recovered by six months and 88% by 12 months. Thyrotrophin deficiency was present in 1 patient in the acute phase, which recovered by six months; one new case was diagnosed at six months, which persisted by twelve months.
Following TBI, early neuroendocrine abnormalities are sometimes transient while late abnormalities present during the course of rehabilitation. A follow-up strategy with periodic evaluation is a necessary part of optimal care for TBI patients.
04 - 06 Apr 2005
British Endocrine Societies