Key result
Childhood-onset growth hormone deficiency in young men is linked to lower volumetric bone density.
Why the study?
Does childhood-onset adult growth hormone deficiency after cessation of treatment impair volumetric bone density and microarchitecture in young male adults compared to healthy controls?
Case-Control (n=50)
No
Does childhood-onset adult growth hormone deficiency after cessation of treatment impair volumetric bone density and microarchitecture in young male adults compared to healthy controls?
p-value: p=<0.001
Young adult males with childhood-onset growth hormone deficiency who stop replacement therapy have significantly impaired bone density, microarchitecture, and estimated bone strength.
May warrant bone assessment in young males stopping GH therapy; leaves open whether resumption improves density or strength.
Context Adult growth hormone deficiency (AGHD) is characterized by low bone density and increased risk of fracture. Bone microarchitecture is insufficiently evaluated in patients with childhood-onset AGHD (CO AGHD). Objective To assess volumetric bone density (vBMD) and bone microarchitecture in CO AGHD in early adulthood after cessation of recombinant growth hormone (rhGH) treatment. Design and subjects Case-control study in a major academic medical center in Beijing, including 20 young male adults with CO AGHD and 30 age- and weight-matched non-athletic healthy men. High-resolution peripheral quantitative computerized tomography (HR-pQCT) of distal radius and tibia was performed. Outcomes The main outcomes were vBMD and morphometry parameters from HR-pQCT. Results Compared with healthy controls, CO AGHD group had significantly decreased insulin-like growth factor 1 (IGF-1) level and IGF-1 SDS (P < 0.001). β-CTX and alkaline phosphatase levels in CO AGHD group were significantly increased (P < 0.001). CO AGHD group had significantly decreased total vBMD, cortical vBMD, trabecular vBMD, cortical area, cortical thickness as well as trabecular thickness and trabecular bone volume fraction of both tibia and radius (P < 0.001). CO AGHD patients had an 8.4 kg decrease in grip strength and a significant decrease in creatinine levels (P = 0.001). At both tibia and radius, by finite element analysis, bone stiffness and failure load of the CO AGHD patients were significantly decreased (P < 0.001). After adjusting for age, BMI and serum levels of testosterone and free thyroxin, serum IGF-1 level was a positive predictor for total vBMD, cortical vBMD, cortical area, trabecular vBMD, bone stiffness and failure load of both tibia and distal radius in all subjects. Conclusions Young adult male patients with childhood-onset adult growth hormone deficiency who are no longer receiving growth hormone replacement have prominently impaired volumetric bone density and bone microarchitecture and lower estimated bone strength.
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Yang et al. (2018) conducted a case-control in Childhood-onset adult growth hormone deficiency (CO AGHD) (n=50). Childhood-onset adult growth hormone deficiency vs. Healthy controls was evaluated on Volumetric bone density (vBMD) and morphometry parameters from HR-pQCT (p=<0.001). Childhood-onset growth hormone deficiency in young adult males was associated with significantly decreased total, cortical, and trabecular volumetric bone density compared to healthy controls (P<0.001).
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