Polycystic ovary syndrome: A model of follicular excess

被引:5
|
作者
Robin, G. [1 ]
Catteau-Jonard, S. [1 ]
Dewailly, D. [1 ]
Decanter, C. [1 ]
机构
[1] CHRU Lille, Hop Jeanne de Flandre, Serv Gynecol Endocrinienne & Med Reprod, F-59037 Lille, France
来源
GYNECOLOGIE OBSTETRIQUE & FERTILITE | 2010年 / 38卷 / 06期
关键词
Polycystic ovary syndrome; Hyperandrogenism; Follicular excess; Physiopathology; ACUTE REGULATORY PROTEIN; ANTI-MULLERIAN HORMONE; STIMULATING-HORMONE; LUTEINIZING-HORMONE; GRANULOSA-CELLS; THECA CELLS; CYTOCHROME-P450; 17-ALPHA-HYDROXYLASE; ANDROGEN EXCESS; WOMEN; FOLLICLES;
D O I
10.1016/j.gyobfe.2010.04.006
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Polycystic ovary syndrome (PCOS) is the most common etiology of menstrual disorders and hyperandrogenism. It is characterized by an excess of ovarian follicles. The mechanisms that underlie folliculogenesis disorder in PCOS appear to arise from primitive ovarian hyperandrogenism. This can be modulated by hormonal factors, such as LH or insulin. Ovarian hyperandrogenism results from a real theca cells dysfunction, whose origin is still poorly understood. It seems that complex genetic factors may be involved, but these have not yet been clearly identified. PCOS also results from granulosa cells dysfunction. For example, intra-ovarian factors, such as anti-mullerian hormone, are possibly involved in ovulation's disorders by blocking the physiological process of follicular recruitment. In turn, the oocyte could also be one of the actors possibly involved in the follicular excess in PCOS. (C) 2010 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:405 / 408
页数:4
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