Mahajan D K
Department of Obstetrics and Gynecology, Louisiana State University School of Medicine, New Orleans.
Endocrinol Metab Clin North Am. 1988 Dec;17(4):751-69.
Polycystic ovarian disease (PCOD) is a heterogenous condition with a broad clinical and pathologic spectrum that may reflect the effects of diverse etiologic factors. Depending on the diagnostic data available from patients, various steroidogenic enzyme blocks have been postulated, mostly implicating higher-than-normal production of circulating delta 4-androstenedione, testosterone, and, in some cases, dehydroisoandrosterone. These high levels of androgens, because of their peripheral conversion to estrogens, lead to inappropriate secretion of gonadotropins in PCOD. Whatever may be the etiologic factors, the common entity is a polycystic ovary. Such an ovary contains preantral follicles, few antral follicles, many atretic follicles, and follicular and degenerative cysts. The follicles lack a sufficient number of mature granulosa cells to produce enough estrogens. On the other hand, there is a hypertrophy of stromal and thecal tissue continuously producing androgens. The steroid analysis of the follicular fluid obtained from the cystic follicles of the polycystic ovary revealed high concentration of delta 4-androstenedione and absence of, or only minute amounts of, estrogens. Early studies of biosynthesis of steroids in the polycystic ovary demonstrated conversion of progesterone mainly to androgens. Arising from these observations was the suggestion that an aromatase enzyme block existed. That suggestion was corroborated in the findings of higher-than-normal circulating androgens in PCOD. Later, other partial enzymatic blocks of beta-hydroxydehydrogenase and 17-hydroxylase were also suggested. However, it is known that the therapies such as wedge resection, administration of FSH, or FSH/LH (Pergonal) and LHRH leads to ovulation and, in most cases, normal cyclicity in the polycystic ovary. The knowledge gained from these therapies clearly indicates that the enzymatic blocks or abnormal steroidogenesis in the polycystic ovary may be due to the absence of proper gonadotropin response, and the main defect may be at the hypothalamic-pituitary axis. In PCOD with hyperinsulinemia, insulin and IGF-I have been implicated in the production of androgens by the polycystic ovary. The mechanism of the action of insulin or IGF-I is not yet known, however.
多囊卵巢疾病（PCOD）是一种具有广泛临床和病理谱的异质性疾病，可能反映了多种病因的影响。根据患者可获得的诊断数据，已提出了各种类固醇生成酶阻断机制，大多涉及循环中的δ4-雄烯二酮、睾酮水平高于正常，在某些情况下，脱氢表雄酮水平也高于正常。由于这些高水平的雄激素在外周转化为雌激素，导致PCOD患者促性腺激素分泌异常。无论病因如何，共同特征是多囊卵巢。这样的卵巢包含窦前卵泡、少量窦卵泡、许多闭锁卵泡以及卵泡囊肿和退行性囊肿。这些卵泡缺乏足够数量的成熟颗粒细胞来产生足够的雌激素。另一方面，基质和卵泡膜组织肥大，持续产生雄激素。从多囊卵巢的囊性卵泡中获取的卵泡液的类固醇分析显示，δ4-雄烯二酮浓度高，雌激素缺乏或仅含微量雌激素。早期对多囊卵巢中类固醇生物合成的研究表明，孕酮主要转化为雄激素。基于这些观察结果，有人提出存在芳香化酶阻断。这一观点在PCOD患者循环雄激素高于正常的研究结果中得到了证实。后来，也有人提出了β-羟脱氢酶和17-羟化酶的其他部分酶阻断机制。然而，已知诸如楔形切除术、促卵泡激素（FSH）或FSH/LH（ Pergonal）以及促性腺激素释放激素（LHRH）的给药等治疗方法可导致多囊卵巢排卵，且在大多数情况下可恢复正常月经周期。从这些治疗方法中获得的知识清楚地表明，多囊卵巢中的酶阻断或异常类固醇生成可能是由于缺乏适当的促性腺激素反应，主要缺陷可能在于下丘脑 - 垂体轴。在伴有高胰岛素血症的PCOD中，胰岛素和胰岛素样生长因子 -I（IGF-I）与多囊卵巢产生雄激素有关。然而，胰岛素或IGF-I的作用机制尚不清楚。
