[Etiology and pathogenesis]
Date is still unknown, some researchers believe the following aspects.
(1) of hypothalamus-pituitary dysfunction in PCOS patients LH, FSH normal or low value, it is more than 3 FSH. LH synthetic luteinizing hormone releasing hormone (LH-RH) reaction, it is that the hypothalamus-pituitary dysfunction of the initial incidence of the levy, resulting in abnormal ovarian steroid hormone synthesis. chronic anovulation. Not only increased the level of LH pulse amplitude increased, but the frequency has increased, this may be due to excessive hormone Zhou Xiong. Aromatase was excessive androgen continued interference into the hypothalamic-pituitary function.
(2) adrenal dysfunction in some patients with PCOS higher adrenal androgen secretion. This may be the adrenal P450c17 enzyme complex disorders make adjustments in the biosynthesis of steroid hormones way medroxyprogesterone acetate from 17 to estrone lack the enzyme blocked. Hypothalamus-pituitary-adrenal dysfunction can affect-ovarian axis and the relationship between the abnormal secretion.
(C) insulin resistance (insulin resistance) and high blood insulin Currently disease that hyperinsulinemia and insulin resistance are common manifestations of PCOS. Women with PCOS make higher insulin levels ovarian androgen synthesis. androgenic activity increased significantly affect glucose and insulin stable environment. Kaohsiung hyperprolactinemia associated with the obese PCOS patients whether or not, even the normal menstrual cycle. both significantly associated with the insulin resistance. Some scholars think that high concentrations of insulin and insulin-like growth factor I (IGF-I) receptor binding. PCOS patients with ovarian stromal tissue on the number of IGF-I receptors were higher than normal in a state of insulin resistance. Ovarian insulin on the role of IGF-I receptors might play a role. Luteinizing hormone and insulin synergy, the former granulosa cells so that it can stimulate the secretion of progesterone, luteinizing granulosa cells. granulosa cells induced by the LH receptor, change adrenal sensitivity to ACTH.
(4) ovarian local autocrine and paracrine mechanism of abnormal Most scholars infer PCOS patients Follicular memory in certain substances, such as epidermal growth factor (EGF). transforming growth factor a (TGFa), and inhibin (inhibin). FSH sensitivity to inhibition of granulosa cells, FSH raise their own threshold. choice and thereby hinder the further development of the dominant follicle. Ovarian autocrine or paracrine mechanism of abnormal disruption of dominant follicles was chosen because the incidence of PCOS.
(5) Some genetic factors that PCOS is genetic diseases may be linked dominant hereditary pattern. Most patients had a normal 46, XX karyotype. Performance of the long arm of chromosome X chromosome abnormalities were missing and the number of X chromosome abnormalities and the chimera.
(6) High prolactin about 20% -30% of PCOS patients with hyperprolactinemia. PRL was that the cells can stimulate the adrenal androgen secretion, as a prolactin receptor adrenocortical cells.

This article was posted on 2007-02-27