Recent evidence suggests a high prevalence of neuroendocrine dysfunction in patients following traumatic brain injury (TBI), but dynamic anterior pituitary assessment were performed in relatively small number of patients and posterior pituitary function remains poorly investigated.
We studied 102 consecutive patients (84 males) who had survived severe or moderate TBI [initial Glasgow Coma Scale (GCS) score 3-13] at a mean (+/- standard deviation) of 19 +/- 10 months post event. Growth hormone (GH) and adreno-corticotrophin hormone (ACTH) reserves were assessed using the glucagon stimulation test (GST). Baseline thyroid function, prolactin, IGF-1, gonadotrophins, testosterone or estradiol were performed in all patients. 31 matched controls underwent GST for GH and cortisol responses; other parameters were compared to local reference ranges. All patients had the standard 8-hour water deprivation test.
In controls, a normal response was a stimulated GH peak of greater than 5 microgram per litre (μg/l) and cortisol greater than 450 nanomole per litre (nmol/l), following glucagon stimulation. 18 TBI patients had GH response less than 5 μg/l including13 with a peak less than 3μg/l. GH deficient patients had significantly higher body-mass index (p < 0.001) and lower IGF-1 concentrations (p = 0.02) than GH sufficient patients. Twenty-four patients had cortisol responses less than 450 nmol/l. GH and cortisol deficiencies were not related to age, computerised tomography appearance, GCS or Glasgow Outcome Scale scores (p > 0.05). Twelve patients had gonadotrophin and one had thyrotrophin deficiencies. Hyperprolactinemia was present in 12 patients. 41 patients had at a least one anterior pituitary hormone deficiency. Diabetes insipidus was diagnosed in 7 patients.
This is the largest study, to date, on post-traumatic hypopituitarism and confirms a high prevalence of pituitary hormone abnormalities. In addition to conventional pituitary hormone replacement, the potential of GH treatment to enhance recovery needs to be examined in a prospective study.
22 - 24 Mar 2004
British Endocrine Societies