When women reach a certain age, their ovarian function will decline, so we must do a good job in preventing premature ovarian failure. First of all, we must pay attention to relevant dietary taboos, such as eating less fried eggs. In addition, women must carefully observe their menstruation, because when there is a problem with ovarian function, the first thing that happens is that the menstruation becomes abnormal. We must also adjust our emotions in daily life, etc. So what are the causes of premature ovarian failure? What causes premature ovarian failure? POF is a syndrome with multiple etiologies, which remain unknown in the majority of cases. At present, the causes of POF are mainly divided into the following aspects clinically. Each cause can reduce the reserve of the ovarian follicle pool or cause follicle dysfunction from one of the above aspects and lead to POF. 1. Genetic factors Through careful analysis of family history, the incidence of familial POF has been reported to be 4% to 31% in different populations, indicating that genetic factors play a major role in POF. X chromosome abnormalities have been recognized as the main cause of POF. With the progress of molecular biology, researchers have also found more and more candidate genes related to POF on autosomes. 2. Immune factors Since the 1950s, researchers have found that 9% to 40% of POF patients have concurrent autoimmune diseases of other endocrine glands or systems, such as autoimmune thyroiditis, systemic lupus erythematosus, myasthenia gravis, hypoparathyroidism, rheumatoid arthritis, idiopathic thrombocytopenic purpura, and diabetes. POF patients often have two or more autoimmune diseases. Among all the autoimmune diseases associated with POF, thyroid disease is the most common cause, and 12% to 33% of POF patients can be detected with thyroid disease. 18% of POF patients have hereditary thyroid disease in their families. The second most common is polyglandular autoimmune disease (PAGD, Addison's disease combined with endocrine dysfunction). In PGAD type I, the incidence of POF is 17% to 50%, and in PGAD type II, the incidence of POF is 3.6% to 7%. PGAD type II includes autoimmune Addison's disease, thyroid autoimmunity and insulin-dependent diabetes, as well as others such as vitiligo, baldness, chronic atrophic gastritis, pernicious anemia, etc. The natural course of these syndromes varies, and symptoms of POF may appear before or after the onset of the disease. For example, in Addison's disease, POF usually occurs earlier than adrenal symptoms. |
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