Endocrine Abstracts

Purpose: Neuroendocrine dysfunction represents a frequent consequence of traumatic brain injury (TBI) but has not been studied longitudinally as yet. Here we attempt to identify predictors of late endocrine insufficiency following TBI.

Methods: 71 consecutive patients (age 18 – 87 yrs) with TBI assessed by an intial CT and the Glasgow Coma Score (GCS) were prospectively studied as to their pituitary function on day 0, 3 and 7 and dynamically 24–36 months post-injury. A multivariate analysis was performed.

Results: Trauma severity ranged from mild to severe (mean GCS 9.6±4.6). The CT revealed skull fracture (in 34 patients), skullbase fracture (16), open TBI (19), epidural hematoma (8), subdural hematoma (14), intracerebral hemorrhage (20) and traumatic subarachnoid hemorrhage (17). Initially most patients suffered from pituitary dysfunction (25 cortico-, 52 thyreo-, 57 gonado-, 39 somatotropic axes, 21 hyperprolactinaemia). During 36 months follow-up (available in 23 patients) 10 demonstrated clinical findings suggestive for pituitary dysfunction. While insufficiency of the thyreo- and gonadotropic axes and hyperprolactinaemia recovered, dynamic testing revealed an insufficient increase of the corticotropic axis (ACTH-test) in 11 patients. Growth hormone (GH) deficiency (GHRH-Arginine test) was found in 9 and low IGF1 in 13 patients. An early insufficiency of the somato- (r=0.391, P=0.032) and gonadotropic (r=0.425, P=0.019) axis predicted a persistent one. Age (r=0.455, P=0.015), body mass index (r=0.578, P=0.003), initial GCS (r=0.400, P=0.036) and mechanical ventilation (r=−0.563, P=0.004) were significantly correlated with a persistent GH deficiency.

Conclusions: Prevalence of hypopituitarism is detectable in up to 70% of patients initially and 50% late after TBI. As patients escaped diagnosis during follow-up and none was offered hormone replacement therapy we conclude that all patients at least with severe TBI should be followed with endocrine testing.