Impact of the growth hormone replacement on bone status in growth hormone deficient adults

Introduction: Growth hormone deficiency (GHD) is associated with reduced bone mineral density (BMD). GH replacement has positive effect on BMD but the magnitude of this effect and its mechanism are debated. Objectives: The objectives of this study was first, to assess the effect of GH replacement on BMD, and second, to evaluate the effect of GH treatment on bone turnover and microarchitecture and to assess the factors influencing the effect of the therapy on BMD. Patients and Methods: Adult GHD (AO-GHD) and childhood onset GHD (CO-GHD) patients treated with GH using IGF-I normalization GH replacement regimen were prospectively followed during 2 years. Lumbar spine (L1-L4) and total femur BMD by Hologic discovery, in the subset of patients also bone turnover markers; osteocalcin and carboxy-terminal collagen crosslinks (CTx) were assessed at baseline and at months 3, 6,12 and 24, respectively. The trabecular bone score (TBS) derived from lumbar spine DXA by the iNsight (R) software was assessed in a subset of study population at baseline and months 12 and 24. Results: In total, 147 GHD patients (age 35.1 years, 84 males/63 females, 43 of childhood onset GHD/104 AO-GHD) were included. BMD of lumbar spine and femur increased significantly during the treatment (14% and 7% increase at 2 years, respectively; p < 0.0001). Bone markers increased during the first 12 months of treatment with subsequent decrease of CTx. At month 24, significant increase in TBS was observed (4%, p = 0.02). BMD increase was significantly higher in males (15% increase in males vs. 10% in females, p = 0.037) and childhood onset GHD (CO-GHD) patients (13% increase in CO-GHD, p = 0.004). Conclusion: GH supplementation leads to an increase of BMD with corresponding changes in bone turnover markers and changes in microarchitecture as assessed by trabecular bone score. Positive effect of GH on bone status is more pronounced in males and CO-GHD adults. (C) 2013 Elsevier Ltd. All rights reserved.