CYCLIC MEDROXYPROGESTERONE TREATMENT INCREASES BONE-DENSITY - A CONTROLLED TRIAL IN ACTIVE WOMEN WITH MENSTRUAL-CYCLE DISTURBANCES

CYCLIC MEDROXYPROGESTERONE TREATMENT INCREASES BONE-DENSITY - A CONTROLLED TRIAL IN ACTIVE WOMEN WITH MENSTRUAL-CYCLE DISTURBANCES
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DOI:
10.1016/0002-9343(94)90092-2
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发表时间:
1994-06-01
影响因子:
5.9
通讯作者:
LENTLE, BC
LENTLE, BC
中科院分区:
医学2区
文献类型:
--
作者:
PRIOR, JC;VIGNA, YM;LENTLE, BC

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目的:骨丢失发生在经历闭经或排卵障碍的年轻女性。这项研究的目的是确定是否可以通过模拟更正常的激素模式,在有或没有补钙的体力活动女性中使用环状甲羟孕酮治疗来预防骨丢失。设计:这是一项为期1年的随机、双盲、安慰剂对照试验。根据月经周期紊乱进行分层的妇女被随机分为四组。研究的结果变量是通过双能技术测量的脊柱骨密度的变化。设定:一个大的都市地区。配对:61名健康的,正常体重的体力活动的绝经前妇女,年龄21到45岁,有闭经,月经过少,无排卵,或黄体周期较短的妇女完成了这项研究。干预:四组治疗:(A)(n=16)周期甲孕酮加碳酸钙;(B)(n=16)周期甲孕酮加钙安慰剂;(C)(n=15)甲羟孕酮加活性钙安慰剂;或(D)甲羟孕酮+安慰剂钙(n=14)。结果:初始骨密度(平均1.12g/cm(2))在不同组间无显著差异(P=0.85)。1年骨密度变化与甲孕酮治疗密切相关(P=0.0001),与补钙治疗弱相关(P=0.072)。甲羟孕酮治疗组(A、B)骨密度显著增加(+1.7%+/-0.5%,扫描电子显微镜+/-扫描电子显微镜,P=0.004),补钙组(C)骨密度无明显变化(-0.7%+/-0.6%);结论:在有闭经或排卵障碍的体力活动妇女中,环状甲孕酮增加了脊柱骨密度。潜在的临床意义:闭经、月经少、无排卵和黄体周期缩短在绝经前妇女中很常见,并与脊柱骨丢失有关,发生在骨密度正常稳定或增加的人生阶段。这项对照试验显示,在周期甲孕酮干预组中,女性的骨质显著增加,而安慰剂组的受试者骨质减少。补钙似乎有帮助,但没有达到统计学意义。这些发现对预防骨质疏松症的影响值得进一步研究。
OBJECTIVE: Bone loss occurs in young women, who experience amenorrhea or ovulatory disturbances. The purpose of this study was to determine whether bone loss could be prevented by simulating a more normal hormonal pattern, using treatment with cyclic medroxyprogesterone, with or without calcium supplementation, in physically active women with disturbed menstruation.DESIGN: This study was a 1-year randomized, double-blind, placebo-controlled trial. Women who were stratified by menstrual cycle disturbance were randomized into four groups. The outcome variable was the change in spinal bone density measured by dual energy techniques.SETTING: A large metropolitan area.PARTICIPANTS: Sixty-one healthy, normal-weight physically active premenopausal women aged 21 to 45 years who experienced amenorrhea, oligomenorrhea, anovulation, or short luteal phase cycles completed the study.INTERVENTION: Therapies were cyclic medroxyprogesterone (10 mg/day for 10 days per month) and calcium carbonate (1,000 mg/day of calcium) in four groups: (A) (n = 16) cyclic medroxyprogesterone plus calcium carbonate; (B) (n = 16) cyclic medroxyprogesterone with calcium placebo; (C) (n = 15) placebo medroxyprogesterone with active calcium; or (D) (n = 14) both medroxyprogesterone and calcium placebos.RESULTS: The initial bone density (mean = 1.12 g/cm(2)) did not differ by group (P = 0.85). The 1-year bone density change was strongly related to treatment with medroxyprogesterone (P = 0.0001) and weakly to calcium (P = 0.072) treatment. Bone density increased significantly (+1.7% +/- 0.5%, +/- SEM, P = 0.004) in the medroxyprogesterone-treated groups (A and B), did not change in the calcium-treated group (C) (-0.7% +/- 0.6%; P = 0.28), and decreased on both placebos (D) (-2.0% +/- 0.6%, P = 0.005).CONCLUSIONS: Cyclic medroxyprogesterone increased spinal bone density in physically active women experiencing amenorrhea or ovulatory disturbances.POTENTIAL CLINICAL SIGNIFICANCE: Amenorrhea, oligomenorrhea, anovulation, and short luteal phase cycles are common in premenopausal women and associated with spinal bone loss occurring at a stage of life when bone density would normally be stable or increasing. This controlled trial shows a significant gain in bone in women in the cyclic medroxyprogesterone intervention group, whereas those subjects in the placebo group lost bone. Calcium supplementation appeared to be helpful but did not reach statistical significance. The implications of these findings for the prevention of osteoporosis warrant further investigation.