Saag K G, Emkey R, Schnitzer T J, Brown J P, Hawkins F, Goemaere S, Thamsborg G, Liberman U A, Delmas P D, Malice M P, Czachur M, Daifotis A G
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242-1081, USA.
N Engl J Med. 1998 Jul 30;339(5):292-9. doi: 10.1056/NEJM199807303390502.
Osteoporosis is a common complication of long-term glucocorticoid therapy for which there is no well-proved preventive or restorative treatment.
We carried out two 48-week, randomized, placebo-controlled studies of two doses of alendronate in 477 men and women, 17 to 83 years of age, who were receiving glucocorticoid therapy. The primary end point was the difference in the mean percent change in lumbar-spine bone density from base line to week 48 between the groups. Secondary outcomes included changes in bone density of the hip, biochemical markers of bone turnover, and the incidence of new vertebral fractures.
The mean (+/-SE) bone density of the lumbar spine increased by 2.1+/-0.3 percent and 2.9+/-0.3 percent, respectively, in the groups that received 5 and 10 mg of alendronate per day (P<0.001) and decreased by 0.4+/-0.3 percent in the placebo group. The femoral-neck bone density increased by 1.2+/-0.4 percent and 1.0+/-0.4 percent in the respective alendronate groups (P<0.01) and decreased by 1.2+/-0.4 percent in the placebo group (P<0.01). The bone density of the trochanter and total body also increased significantly in the patients treated with alendronate. There were proportionally fewer new vertebral fractures in the alendronate groups (overall incidence, 2.3 percent) than in the placebo group (3.7 percent) (relative risk, 0.6; 95 percent confidence interval, 0.1 to 4.4). Markers of bone turnover decreased significantly in the alendronate groups (P<0.001). There were no differences in serious adverse effects among the three groups, but there was a small increase in nonserious upper gastrointestinal effects in the group receiving 10 mg of alendronate.
Alendronate increases bone density in patients receiving glucocorticoid therapy.
骨质疏松症是长期糖皮质激素治疗的常见并发症，对此尚无经充分证实的预防或恢复性治疗方法。
我们对477名年龄在17至83岁、正在接受糖皮质激素治疗的男性和女性进行了两项为期48周的随机、安慰剂对照研究，给予两种剂量的阿仑膦酸盐。主要终点是各治疗组从基线至第48周腰椎骨密度平均变化百分比的差异。次要结果包括髋部骨密度变化、骨转换生化标志物以及新椎体骨折的发生率。
每日服用5毫克和10毫克阿仑膦酸盐的组中，腰椎平均（±标准误）骨密度分别增加了2.1±0.3%和2.9±0.3%（P<0.001），而安慰剂组降低了0.4±0.3%。在各自的阿仑膦酸盐组中，股骨颈骨密度分别增加了1.2±0.4%和1.0±0.4%（P<0.01），安慰剂组降低了1.2±0.4%（P<0.01）。接受阿仑膦酸盐治疗的患者转子和全身的骨密度也显著增加。阿仑膦酸盐组新椎体骨折的比例（总发生率为2.3%）低于安慰剂组（3.7%）（相对风险为0.6；95%置信区间为0.1至4.4）。阿仑膦酸盐组骨转换标志物显著降低（P<0.001）。三组之间严重不良反应无差异，但接受10毫克阿仑膦酸盐的组非严重上消化道不良反应略有增加。
阿仑膦酸盐可增加接受糖皮质激素治疗患者的骨密度。
