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Androgen Deficiency and Osteopenia in Anorexia Nervosa

Androgen Deficiency and Osteopenia in Anorexia Nervosa
神经性厌食症的雄激素缺乏和骨质减少
批准号:
6317677
负责人:
Karen K Miller
金额:
$8.65万
依托单位国家:
美国
项目类别:
财政年份:
2001
资助国家:
美国
项目状态:
已结题
起止时间:
2001-05-01 至 2003-04-30

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中文摘要
翻译
说明(改编自应用程序) 神经性厌食症在年轻女性中越来越常见。骨量减少症 是一种严重、频繁且通常是永久性的并存的内科并发症 神经性厌食症,导致虚弱的脊椎粉碎性骨折。这个 骨丢失的病理生理学机制还不完全清楚,也没有有效的方法。 治疗是存在的。在这一人群中发生的骨量减少是独一无二的 不同于绝经后骨质疏松症。的代理标记数据 骨周转率除了增加外,还表现为骨形成减少 在雌激素缺乏状态下出现的吸收。我们的初步数据 证明患有神经性厌食症的女性有相对的 合成代谢激素睾酮,已知可刺激骨形成 体外培养。我们假设睾丸激素缺乏,主要是卵巢 起源,导致骨形成和骨密度下降 神经性厌食症。这一假设将通过调查是否 服用生理替代剂量的睾丸素可增加骨骼 这一人群的骨形成和骨密度。 在这项提案的第一阶段,我们计划调查流行率和 神经性厌食症患者雄激素缺乏的发病机制 特别是为了确定卵巢或肾上腺雄激素是否减少。在……里面 在第二阶段的研究中,我们将调查 睾酮缺乏与睾酮补充对骨标记物的影响 将患有神经性厌食症和睾酮缺乏症的女性随机接受 生理替代剂量的睾酮或安慰剂,为期12周 测量骨转换标志物的变化。在研究的第三阶段,我们 将研究注射睾丸素对骨密度和身体的影响 质量。
英文摘要
DESCRIPTION (adapted from the application) Anorexia nervosa is becoming increasingly common among young women. Osteopenia is a severe, frequent and often permanent comorbid medical complication of anorexia nervosa which results in debilitating vertebral crush fractures. The pathophysiology of the bone loss is incompletely understood, and no effective therapy exists. The osteopenia that occurs in this population is unique and differs from that of postmenopausal osteoporosis. Data of surrogate markers of bone turnover have shown decreased bone formation in addition to increased resorption seen in states of estrogen deficiency. Our preliminary data demonstrate that women with anorexia nervosa have a relative deficiency of the anabolic hormone testosterone which is known to stimulate bone formation in vitro. We hypothesize that testosterone deficiency, primarily of ovarian origin, contributes to the decreased bone formation and bone density seen in anorexia nervosa. This hypothesis will be tested by investigating whether administration of a physiologic replacement dose of testosterone increases bone formation and bone density in this population. In the first phase of this proposal we plan to investigate the prevalence and pathogenesis of androgen deficiency in women with anorexia nervosa and specifically to determine whether ovarian or adrenal androgens are reduced. In the second phase of the study we will investigate the metabolic effects of testosterone deficiency compared with testosterone repletion on bone markers by randomizing women with anorexia nervosa and testosterone deficiency to receive a physiologic replacement dose of testosterone or placebo for 12 weeks and measuring changes in bone turnover markers. In the third phase of the study, we will examine the effects of administering testosterone on bone density and body mass.
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