Traumatic brain injury as a relevant cause of growth hormone deficiency in adults: A KIMS-based study

Casanueva FF, Leal A, Koltowska-Haggstrom M, Jonsson P, Goth MI. Traumatic brain injury as a relevant cause of growth hormone deficiency in adults: a KIMS-based study. Objectives To characterize further the clinical manifestations and the efficacy of growth hormone (GH) replacement therapy in patients with adult-onset growth hormone deficiency (GHD) reported in the KIMS (Pfizer's international metabolic database) as caused by traumatic brain injury (TBI) and to compare them with nonirradiated patients whose GHD was due to a nonfunctioning pituitary adenoma (NFPA). Design Observational study. Setting Subjects selected from the KIMS database. Participants Fifty-one patients with GHD resulting from TBI and 688 patients with GHD resulting from NFPA. Both groups were selected from the KIMS and had adult-onset GHD with GH replacement therapy only after KIMS entry and before and after KIMS entry. Interventions Not applicable. Main outcome measures Age, body mass index, age at disease onset, age at disease diagnosis, age at KIMS entry, final height, GH peak at testing, GH replacement dose, routine biochemical analysis, clinical manifestations of disease, and quality of life measurements. Results Patients with TBI were significantly younger at study entry and were younger both at pituitary disease onset and at GHD diagnosis, but they showed a significant delay in treatment. When comparing patients not treated with GH before entering in the KIMS, patients with TBI were significantly shorter (167.2±1.7cm) than those with NFPA (171.6±0.4cm) in final height. TBI patients had lower GH reserves than NFPA patients, and although the latter group experienced more positive changes, both groups benefited from GH replacement therapy. Conclusions Patients with GHD due to TBI showed a significant reduction in height and a reduction in pituitary GH reserve and were diagnosed and treated with inappropriate delay.