Robin G, Catteau-Jonard S, Dewailly D, Decanter C
hôpital Jeanne-de-Flandre, CHRU de Lille, France.
Gynecol Obstet Fertil. 2010 Jun;38(6):405-8. doi: 10.1016/j.gyobfe.2010.04.006. Epub 2010 Jun 4.
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.
多囊卵巢综合征（PCOS）是月经紊乱和高雄激素血症最常见的病因。其特征是卵巢卵泡过多。PCOS中卵泡发生障碍的机制似乎源于原发性卵巢高雄激素血症。这可由激素因素调节，如促黄体生成素（LH）或胰岛素。卵巢高雄激素血症是由真正的卵泡膜细胞功能障碍引起的，其起源仍知之甚少。似乎复杂的遗传因素可能与之有关，但尚未明确识别。PCOS也由颗粒细胞功能障碍引起。例如，卵巢内因素，如抗苗勒管激素，可能通过阻断卵泡募集的生理过程而参与排卵障碍。反过来，卵母细胞也可能是参与PCOS卵泡过多的因素之一。
