The pathogenesis of infertility and early pregnancy loss in polycystic ovary syndrome
The pathogenesis of infertility and early pregnancy loss in polycystic ovary syndrome
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DOI：
10.1016/j.bpobgyn.2004.06.001
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发表时间：
2004-10-01
影响因子：
5.5
通讯作者：
Dyer, SJ
中科院分区：
文献类型：
--
作者：
van der Spuy, ZM;Dyer, SJ
多囊卵巢综合征（PCOS）常伴有生殖功能障碍。卵巢功能可能受到干扰，导致卵泡发育和甾体发育异常，尽管很难确定排卵的确切发病机制，但许多可能的机制已经被假设。不排卵的多囊卵巢综合征患者的卵泡发生的特点是优势性失败，卵巢有多个小卵泡，这些小卵泡被阻止，但能够产生类固醇。促性腺激素和胰岛素分泌异常和旁分泌功能紊乱已被确定。患有多囊卵巢综合征的妇女在自然排卵和诱导排卵后流产的发生率增加。高黄体生成素分泌、高雄激素血症和高胰岛素血症都被认为是多囊卵巢综合征的可能原因。这些因素可能是相互联系的，共同可能导致卵巢和子宫内膜功能紊乱。多种其他可能的异常被认为是导致生殖失败的因素。这些包括纤溶酶原激活物抑制剂活性降低、内皮功能障碍和肥胖。理想情况下，治疗应该针对潜在的疾病，但目前数据不足，在真正基于对病理生理学的理解提出治疗建议之前，需要进一步的调查。
Won-en with polycystic ovary syndrome (PCOS) frequently present with reproductive dysfunction. Ovarian function might be disturbed, with resultant abnormal folliculogenesis and sterodogenesis and, although it is difficult to define the exact pathogenesis of anovulation, many possible mechanisms have been postulated. Folliculogenesis in anovulatory women with PCOS is characterized by failure of dominance and the ovary has multiple small follicles, which are arrested but capable of steroidogenesis. Abnormalities in gonadotrophin and insulin secretion and disordered paracrine function have been identified. Women with PCOS have an increased prevalence of miscarriage, both after spontaneous and induced ovulation. Hypersecretion of LH, hyperandrogenaemia and hyperinsulinaemia have all been investigated as possible causes of PCOS. It is likely that these factors are interlinked and together might result in disordered ovarian and endometrial function. Multiple other possible abnormalities have been postulated as contributory factors in the reproductive failure. These include decreased plasminogen activator inhibitor activity, endothelial dysfunction and obesity. Ideally, therapy should target the underlying disorders but at present data are inadequate and further investigations are essential before therapeutic recommendations are truly based on an understanding of the pathophysiology.