Beshyah S A, Kyd P, Thomas E, Fairney A, Johnston D G
Unit of Metabolic Medicine, St Mary's Hospital and Medical School, London, UK.
Clin Endocrinol (Oxf). 1995 Mar;42(3):249-54. doi: 10.1111/j.1365-2265.1995.tb01872.x.
Short-term GH replacement in hypopituitary adults increases bone turnover; data on the consequences of longer-term GH treatment are limited. We report on the effects of 12-18 months of GH replacement treatment with biosynthetic human GH on bone metabolism and bone mass in hypopituitary adults.
Patients were studied before and after GH treatment for 12 months (n = 11) and 18 months (n = 27) respectively in an open trial. GH dose was 0.04 +/- 0.01 IU/kg daily.
Plasma calcium, phosphate and intact PTH concentrations, 24-hour urinary calcium excretion, 3 markers of bone formation (total alkaline phosphatase, osteocalcin and procollagen 1 carboxy terminal peptide (P1CP)) and serum concentration of carboxyterminal cross-linked telopeptide of type 1 collagen (ICTP), as a marker of bone resorption, were measured at 6-month intervals. Lumbar spine and total body bone mineral mass was measured by dual-energy X-ray absorptiometry.
Small increases were observed in plasma calcium and phosphate concentrations at 12 months of GH therapy but the differences at 18 months were not statistically significant. Serum intact PTH concentration did not change. Plasma total alkaline phosphatase increased significantly on GH from 75 +/- 26 to 92 +/- 30 (P < 0.01) and 85 +/- 31 U/I (NS) at 12 and 18 months respectively. Serum osteocalcin increased from 6.5 +/- 3.7 to 15.7 +/- 6.2 (P < 0.0001) and 16.6 +/- 5.7 micrograms/I (P < 0.001) at 12 and 18 months respectively and P1CP increased significantly from 106.0 +/- 47.3 micrograms/I to 165.5 +/- 95.3 (P < 0.0001) and 177.2 +/- 72.2 micrograms/I (P < 0.01) at 12 and 18 months respectively. Plasma ICTP concentration increased also from 3.4 +/- 1.8 to 7.3 +/- 3.4 (P < 0.0001) and 7.0 +/- 2.7 micrograms/I (P < 0.003) at 12 and 18 months of GH therapy respectively. No significant change was observed in total body or lumbar spine bone mass, over the 18 months of GH treatment
Replacement therapy with GH in hypopituitary adults for 6-18 months produced a sustained increase in bone turnover (both formation and resorption). Bone mass was maintained but did not increase over the study period.
垂体功能减退的成年人进行短期生长激素替代治疗会增加骨转换；关于长期生长激素治疗后果的数据有限。我们报告了使用生物合成人生长激素进行12 - 18个月生长激素替代治疗对垂体功能减退成年人骨代谢和骨量的影响。
在一项开放性试验中，分别对患者在生长激素治疗前以及治疗12个月（n = 11）和18个月（n = 27）后进行研究。生长激素剂量为每日0.04±0.01 IU/kg。
每隔6个月测量血浆钙、磷和完整甲状旁腺激素浓度、24小时尿钙排泄量、3种骨形成标志物（总碱性磷酸酶、骨钙素和I型前胶原羧基末端肽（P1CP））以及作为骨吸收标志物的I型胶原羧基末端交联端肽（ICTP）的血清浓度。通过双能X线吸收法测量腰椎和全身骨矿物质质量。
生长激素治疗12个月时血浆钙和磷浓度有小幅升高，但18个月时差异无统计学意义。血清完整甲状旁腺激素浓度未改变。生长激素治疗时血浆总碱性磷酸酶在12个月时从75±26显著升高至92±30（P < 0.01），18个月时为85±31 U/L（无统计学差异）。血清骨钙素在12个月时从6.5±3.7升高至15.7±6.2（P < 0.0001），18个月时为16.6±5.7 μg/L（P < 0.001），P1CP在12个月时从106.0±47.3 μg/L显著升高至165.5±95.3（P < 0.0001），18个月时为177.2±72.2 μg/L（P < 0.01）。生长激素治疗12个月和18个月时血浆ICTP浓度也分别从3.4±1.8升高至7.3±3.4（P < 0.0001）和7.0±2.7 μg/L（P < 0.003）。在18个月的生长激素治疗期间，全身或腰椎骨量未观察到显著变化。
垂体功能减退的成年人进行6 - 18个月的生长激素替代治疗会使骨转换（形成和吸收）持续增加。在研究期间骨量得以维持但未增加。
