Polycystic ovary syndrome is a syndrome with a multi-causal pathogenesis and a polymorphic clinical presentation. In recent years, the clinical features of this disorder have been further recognized as hyperandrogenism and persistent anovulation. The etiology is unclear, and polycystic ovary syndrome shows a familial clustering phenomenon, suggesting a genetic role. It is generally believed that hyperandrogenism and persistent anovulation are based on abnormalities in the endocrine activity of the ovaries, adrenal glands, pituitary gland, hypothalamus and peripheral fat, and that the pathogenesis may be due to the dysfunction of cytochromes, which are androgen-forming enzymes, present in both the ovaries and adrenal glands. Hyperprolactinemia occurs in about 25% of patients, probably due to feedback from abnormal estrogens to the pituitary gland, which in turn promotes androgen secretion by the ovaries and adrenal glands due to increased LH levels, further creating a vicious cycle of excessive androgens and persistent anovulation. It is now believed that the etiology of polycystic ovary syndrome may be related to hyperinsulinemia and insulin resistance. Insulin and insulin-like growth factor 1 receptors are present in the ovaries, and both insulin and insulin-like growth factor 1 affect the ovarian mesenchyme and follicles, causing the ovaries to secrete androgens and preventing normal follicle development. Polycystic ovary syndrome is a complex endocrine and metabolic abnormality common in women of reproductive age, and the cause is unclear.