Holmes S J, Shalet S M
Christie Hospital, Manchester, UK.
Horm Res. 1996;45 Suppl 1:69-71. doi: 10.1159/000184836.
Bone mineral density (BMD) is reduced in adults with growth hormone (GH) deficiency and the decrease in BMD appears more marked if the GH deficiency is childhood onset rather than adult onset. Recent epidemiological studies suggest an increased fracture rate in GH-deficient adults. The skeletal response to GH therapy depends on the variety of GH deficiency, the type of bone studied and the duration of therapy. In the childhood-onset, GH-deficient adult there is either no change or a reduction in cortical and integral bone mass over the first 6 months, whereas at 6 months there is an increase in vertebral trabecular BMD. Subsequently there is a steady rise in BMD at all sites over the next 12-18 months. In the adult-onset, GH-deficient adult, the long-term results are more contentious. It is too early to determine whether GH therapy modifies fracture risk.
生长激素(GH)缺乏的成年人骨矿物质密度(BMD)降低,并且如果GH缺乏始于儿童期而非成年期,BMD的降低似乎更为明显。最近的流行病学研究表明,GH缺乏的成年人骨折率增加。骨骼对GH治疗的反应取决于GH缺乏的类型、所研究的骨类型以及治疗持续时间。在儿童期起病的GH缺乏成年人中,最初6个月皮质骨和整体骨量要么没有变化,要么减少,而在6个月时椎骨小梁BMD增加。随后在接下来的12 - 18个月里,所有部位的BMD都稳步上升。在成年期起病的GH缺乏成年人中,长期结果更具争议性。现在确定GH治疗是否会改变骨折风险还为时过早。