多囊卵巢综合征病因有哪些？What is the etiology of polycystic ovary syndrome?

多囊卵巢综合征病因:The etiology of polycystic ovarian syndrome (PCOS):

1)家族遗传因素：依据多囊卵巢综合症发生所显示的家族高度聚集性，因此，遗传因素是其病因学上一个主要因素。多数多囊卵巢综合症与基因异常有关，少数多囊卵巢综合征有染色体异常，此发病因素很难进行避免，唯有早发现早治疗。

1. Genetic factors: Genetic factors are a major factor in the etiology of polycystic ovary syndrome (pcos), which is characterized by a high degree of familial aggregation. Most polycystic ovary syndrome (PCOS) is related to genetic abnormalities, and a few polycystic ovary syndrome (PCOS) is related to chromosomal abnormalities. This pathogenic factor is difficult to avoid, early detection and early treatment is necessary.

2)长期精神紧张、药物及疾病影响：由于精神紧张、药物及某些疾病影响到下丘脑一垂体一卵巢轴调节功能异常，导致卵巢间质、卵泡膜细胞产生过量雄激素;卵巢内高雄激素抑制卵泡成熟，从而出现一系列诸如闭经、多毛等多囊卵巢综合症的症状。

2. Long-term mental stress, drug and disease effects: As a result of mental stress, medicaments and certain disease influence hypothalamus ~ hypophysis ~ ovarian axis adjusts function abnormality, it causes the ovarian stroma, the follicle membrane cell to produce the excess androgen; High amount of androgens in the ovary inhibit the maturation of follicles, it will lead to a range of symptoms such as amenorrhea, hairiness and polycystic ovary syndrome (PCOS).

3)肥胖、高胰岛素血症患者：部分多囊卵巢综合症患者，尤其是肥胖患者可表现为高胰岛素血症和耐胰岛素，提示由胰岛素抵抗引起。引起胰岛素抵抗的原因有多种，多数情况是胰岛素受体后信息传导系统的障碍引起，也可有胰岛素受体缺陷引起。

3. Obesity, hyperinsulinemia: some patients with polycystic ovary syndrome (PCOS), Hyperinsulinemia and insulin resistance can occur in some patients with polycystic ovary syndrome (PCOS), especially obese patients, It’s due to insulin resistance. There are many causes of insulin resistance, most of which are caused by the disorder of the information transmission system after the insulin receptor, or the defect of the insulin receptor.

4)肾上腺功能异常：50%的多囊卵巢综合症患者存在肾上腺皮质功能异常现象，常由于肾上腺皮质功能亢进，导致分泌过量的雄激素，出现无排卵等症状。引起肾上腺皮质功能异常的疾病，主要有肾上腺肿瘤、肾上腺皮质增生等。

4. Adrenal dysfunction: 50% of patients with polycystic ovary syndrome (PCOS) have abnormal adrenocortical function, often due to adrenocortical hyperfunction, resulting in excessive secretion of androgens, not ovu