Poster 6: Traumatic brain injury as a relevant cause of growth hormone deficiency in adults. Experience from KIMS (pharmacia international metabolic database)

Abstract

Objective: To compare baseline clinical characteristics and 1-year growth hormone (GH) replacement results in patients with adult onset growth hormone deficiency (GHD) caused by traumatic brain injury (TBI) versus nonfunctioning pituitary adenoma (NFPA). Design: Pharmacoepidemiologic survey of hypopituitary adults with GHD. Setting: Records were selected from the KIMS database, which contains information on >8500 patients with GHD, for 168 of whom TBI was identified as a cause. Participants: Both groups (NFPA group, n=207; TBI group, n=29) were age- (at pituitary disorder onset and entry into the KIMS database) and sex-matched (60% men, 40% women), previously not irradiated, and had not received GH. Interventions: Not applicable. Main Outcome Measures: Values given as mean ± SE. Results: The age at GHD diagnosis was 38.8±2.0 years for the TBI group and 41.5±0.5 years for the NFPA group. In both groups, the most frequent additional hypopituitary deficiency was luteinzing hormone/follicle-stimulating hormone, followed by adrenocorticotropic hormone and thyroid-stimulating hormone. The mean GH peak at diagnosis was 1.25±0.42ng/mL in the TBI group, which was significantly lower than that of the NFPA group (2.38±0.7ng/mL). There were no significant statistical differences in medical history, glucose level, lipids, waist circumference, or body composition measurements. Interestingly, patients with TBI were significantly shorter (168.2±1.5cm) than the NFPA patients (172.5±0.6cm). After 1 year of GH treatment, differences were shown in waist, lean mass, heart rate, glucose levels, quality of life as measured by the Quality of Life Assessment in Growth Hormone Deficient Adults and insulin-like growth factor I. Conclusions: Although hypopituitarism secondary to TBI was described more than 50 years ago, it is only now evident that a considerable number of patients experience severe GHD after TBI. It is suspected that a large number of patients after TBI have undiagnosed GHD. The present results confirm that clinical characteristics and GH treatment effects in GHD caused by TBI are indistinguishable from those in GHD caused by NFPA.