Polycystic ovary syndrome (PCOS) is a common endocrine disorder closely related to metabolic syndrome, and the risk of type 2 diabetes and cardiovascular disease is increased. Dr. Fenglin Chen from Antai Hospital believes that the cause of PCOS is gonadal malstructure, that is, the remaining testicular tissue (ootestis) present in the ovaries during the differentiation period.
Therefore, the treatment can not stay on the change of the clinical symptoms of the disease, but through abdominal technology to reduce the ovarian testicular tissue (change the gonadal misstructure gene), and then according to the type supplemented by drug regulation. Simple surgical drilling can not achieve this purpose, therefore, the treatment effect, pregnancy rate is not ideal.
It is worth noting that the family aggregation phenomenon of polycystic ovary syndrome (PCOS) suggests that genetic factors play an important role in its pathogenesis, which has been confirmed by clinical and basic research at home and abroad.
Polycystic ovary syndrome (PCOS) has been shown to be a complex inheritance pattern rather than a single autosomal defect. Combined with the high heterogeneity of PCOS, the possibility of X2 linked dominant inheritance (X-linked) and polygenic forms and the influence of environmental factors cannot be ruled out. The pathophysiology of polycystic ovary syndrome (PCOS) is very complex, and a single pathological mechanism cannot fully explain the complex phenotype of PCOS. Currently, most scholars believe that PCOS is the result of the combined action of pathogenic genes and environmental factors.
Our doctors in Antai Hospital reviewed a large number of literature and combined with domestic and foreign studies, and believed that the hormonal environment in utero affected the endocrine state of adult individuals. When exposed to high concentration of androgens during pregnancy, ovulation and polycystic ovaries would occur in adults. It can be said that polycystic ovarian syndrome (PCOS) originated during fetal life, with the ovaries remaining testicular tissue (ovaltestis) during differentiation, or being exposed in utero before birth to high testosterone levels equivalent to those of male fetuses, who later exhibit many of the clinical and biochemical characteristics of PCOS. In particular, it is characterized by hypersecretion of luteinizing hormone (LH), abnormal insulin secretion or utilization, and hyperandrogenic anovulation in obese individuals (hyperinsulinemia).
Meanwhile, high concentration of sex hormone binding globulin in blood and high placental metabolism of androgens provide an effective buffer against maternal excess androgens entering fetal circulation. In other words, hyperandrogenemia can be passed from PCOS mother to daughter across the placenta.
Polycystic ovary syndrome (PCOS) is a complex polymorphic disorder, and most clinical and biochemical characteristics can be explained by the developmental disorder caused by ovarian androgen secretion. Excessive action of androgens in the hypothalamic-pituitary gland during fetal (gonadal dysstructure/hyperandrogenic environment) and/or during adolescence increases the distribution of visceral fat by controlling the LH hormone (thereby inducing insulin resistance and anovulation) and causes clinical manifestations of hyperandrogenemia in adulthood. Other cofactors include genetic and environmental factors that work together to alter phenotypes and produce polymorphic manifestations. In this way, in the treatment, the change of ovulation disorders is on the one hand (Antai uses ovaltestis diatosis, remove the fetal development period, ovarian differentiation testicular tissue), and then according to the polycystic ovary clinical more than ten types, respectively to give adjuvant treatment, not only can change the reproductive age of women difficult to conceive or not to conceive, but also can improve the metabolic disorders related to this disease.