Division of Reproductive Endocrinology, Department of Reproductive Medicine, University of California, San Diego, School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093-0633, United States.
Mol Cell Endocrinol. 2013 Jul 5;373(1-2):51-60. doi: 10.1016/j.mce.2012.07.011. Epub 2012 Jul 31.
Alterations of ovarian follicle morphology and function have been well documented in women with PCOS. These include increased numbers of growing preantral follicles, failure of follicle growth beyond the mid-antral stage, evidence of granulosa call degeneration, and theca cell hyperplasia. Functional abnormalities include paradoxical granulosa cell hyperresponsiveness to FSH which is clinically linked to ovarian hyperstimulation during ovulation induction. In addition, there is likely a primary theca cell defect that accounts for the majority of excess androgen production in this disorder. The precise mechanisms responsible for altered follicle function are not completely clear. However, several factors appear to influence normal advancement of follicle development as well as impair ovarian steroidogenesis. These include intra- as well as extraovarian influences that distort normal ovarian growth and disrupt steroid production by follicle cells.
多囊卵巢综合征患者的卵巢卵泡形态和功能发生改变已有充分的记载。这些改变包括生长前期卵泡数量增加、卵泡生长无法超过窦前中期、颗粒细胞退化变性、以及卵泡膜细胞增生。功能异常包括颗粒细胞对 FSH 的反常高反应性,这与排卵诱导时的卵巢过度刺激有关。此外,可能存在卵泡膜细胞的原发性缺陷,这是导致该疾病雄激素过多产生的主要原因。导致卵泡功能改变的确切机制尚不完全清楚。然而,有几种因素似乎影响了卵泡发育的正常进展,并损害了卵巢甾体生成。这些因素包括卵巢内外的影响,它们使正常的卵巢生长扭曲,并破坏了卵泡细胞的甾体生成。