Increase in bone density and lean body mass during testosterone administration in men with acquired hypogonadism.
Increase in bone density and lean body mass during testosterone administration in men with acquired hypogonadism.
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DOI：
10.1210/jcem.81.12.8954042
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发表时间：
1996-12
期刊：
影响因子：
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通讯作者：
L. Katznelson;J. Finkelstein;D. Schoenfeld;D. Rosenthal;E. Anderson;A. Klibanski
中科院分区：
文献类型：
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作者：
L. Katznelson;J. Finkelstein;D. Schoenfeld;D. Rosenthal;E. Anderson;A. Klibanski
获得性性腺功能减退症在成年男性中越来越被认识到。然而，长期睾酮替代对骨密度和身体组成的影响在很大程度上是未知的。我们调查了36名成年男性获得性性腺功能减退症（年龄，22 - 69岁;中位数，58岁），包括29名男性中枢性性腺功能减退症和7名男性原发性性腺功能减退症，和44名年龄匹配的性腺功能正常的对照。基线评估包括生物阻抗法身体成分分析、腰椎双能定量计算机断层扫描（QCT）测定特定部位脂肪面积、双能X线骨密度仪测量脊柱骨矿物质密度（BMD）、QCT测量脊柱骨小梁BMD和单光子吸收法测量桡骨BMD。性腺功能减退男性的体脂百分比显著高于性腺功能正常男性（平均值+/-SEM，26.4 +/-1.1% vs. 19.2 +/-0.8%; P <0.01）。通过QCT测定的性腺功能减退男性的平均骨小梁BMD为115 +/-6 mg K2HPO4/cc。脊柱BMD显著低于正常性腺对照组（分别为1.006 +/-0.024和1.109 +/-0.028 g/cm 2; P = 0.02）。两组桡骨BMD相似。在29名性腺功能减退男性中开始了100 mg/周剂量的庚酸替尼酯治疗，并在18个月内每隔6个月对受试者进行评价。在睾酮治疗期间，体脂百分比下降14 +/-4%（P <0.001）。在睾酮治疗期间，皮下脂肪减少13 +/-4%（P <0.01），瘦肌肉质量增加7 +/-2%（P = 0.01）。脊柱骨密度和骨小梁骨密度分别增加5 +/-1%（P <0.001）和14 +/-3%（P <0.001）。桡骨BMD无变化。血清骨特异性碱性磷酸酶和尿脱氧吡啶啉排泄，骨形成和骨吸收的标志物，分别在18个月内显着下降（P = 0.003和P = 0.04，分别）。我们的结论是，睾酮治疗获得性性腺功能减退症的成年男性减少皮下脂肪和增加肌肉质量。此外，睾酮治疗可减少骨重建并增加骨小梁密度。雄激素给药对身体成分和骨密度的有益作用可能为性腺功能减退男性的睾酮治疗提供额外的适应症。
Acquired hypogonadism is being increasingly recognized in adult men. However, the effects of long term testosterone replacement on bone density and body composition are largely unknown. We investigated 36 adult men with acquired hypogonadism (age, 22-69 yr; median, 58 yr), including 29 men with central hypogonadism and 7 men with primary hypogonadism, and 44 age-matched eugonadal controls. Baseline evaluation included body composition analysis by bioimpedance, determination of site-specific adipose area by dual energy quantitative computed tomography scan (QCT) of the lumbar spine, and measurements of spinal bone mineral density (BMD) using dual energy x-ray absortiometry, spinal trabecular BMD with QCT, and radial BMD with single photon absorptiometry. Percent body fat was significantly greater in the hypogonadal men compared to eugonadal men (mean +/- SEM, 26.4 +/- 1.1% vs. 19.2 +/- 0.8%; P < 0.01). The mean trabecular BMD determined by QCT for the hypogonadal men was 115 +/- 6 mg K2HPO4/cc. Spinal BMD was significantly lower than that in eugonadal controls (1.006 +/- 0.024 vs. 1.109 +/- 0.028 g/cm2; P = 0.02, respectively). Radial BMD was similar in both groups. Testosterone enanthate therapy was initiated in 29 hypogonadal men at a dose of 100 mg/week, and the subjects were evaluated at 6-month intervals for 18 months. During testosterone therapy, the percent body fat decreased 14 +/- 4% (P < 0.001). There was a 13 +/- 4% decrease in subcutaneous fat (P < 0.01) and a 7 +/- 2% increase in lean muscle mass (P = 0.01) during testosterone therapy. Spinal BMD and trabecular BMD increased by 5 +/- 1% (P < 0.001) and 14 +/- 3% (P < 0.001), respectively. Radial BMD did not change. Serum bone-specific alkaline phosphatase and urinary deoxypyridinoline excretion, markers of bone formation and resorption, respectively, decreased significantly over the 18 months (P = 0.003 and P = 0.04, respectively). We conclude that testosterone therapy given to adult men with acquired hypogonadism decreases sc fat and increases lean muscle mass. In addition, testosterone therapy reduces bone remodeling and increases trabecular bone density. The beneficial effects of androgen administration on body composition and bone density may provide additional indications for testosterone therapy in hypogonadal men.