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黄体功能不足与多囊卵巢综合征共有的病理生理学机制。对生育能力的影响。

Common pathophysiological mechanisms involved in luteal phase deficiency and polycystic ovary syndrome. Impact on fertility.

机构信息

Division of Endocrinology, First Department of Internal Medicine, Laiko General Hospital, Medical School, University of Athens, Aghiou Thoma 17 Street Goudi, Athens, Greece.

出版信息

Endocrine. 2013 Apr;43(2):314-7. doi: 10.1007/s12020-012-9778-9. Epub 2012 Aug 29.

DOI:10.1007/s12020-012-9778-9
PMID:22930247
Abstract

Luteal phase deficiency (LPD) is a consequence of the corpus luteum (CL) inability to produce and preserve adequate levels of progesterone. This is clinically manifested by short menstrual cycles and infertility. Abnormal follicular development, defects in neo-angiogenesis or inadequate steroidogenesis in the lutein cells of the CL have been implicated in CL dysfunction and LPD. LPD and polycystic ovary syndrome (PCOS) are independent disorders sharing common pathophysiological profiles. Factors such as hyperinsulinemia, AMH excess, and defects in angiogenesis of CL are at the origin of both LPD and PCOS. In PCOS ovulatory cycles, infertility could result from dysfunctional CL. The aim of this review was to investigate common mechanisms of infertility in CL dysfunction and PCOS.

摘要

黄体期缺陷(LPD)是黄体(CL)无法产生和维持足够水平的孕激素的结果。这在临床上表现为月经周期短和不孕。卵泡发育异常、新血管生成缺陷或黄体细胞中甾体生成不足与 CL 功能障碍和 LPD 有关。LPD 和多囊卵巢综合征(PCOS)是两种独立的疾病,具有共同的病理生理特征。高胰岛素血症、AMH 过多和 CL 血管生成缺陷等因素是 LPD 和 PCOS 的共同起源。在 PCOS 的排卵周期中,CL 功能障碍可能导致不孕。本综述的目的是探讨 CL 功能障碍和 PCOS 中不孕的共同机制。

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