What are the consequences and risks of depleted ovarian reserve?

What are the consequences and risks of depleted ovarian reserve?

Premature depletion of ovarian reserve is defined as cessation of ovarian function before the age of 40 years. Initially, there is an absence of menstruation for a period of at least 4 months, which is combined with an increase in the levels of follicle-stimulating hormone – FSH. Premature ovarian failure is associated with a permanent decrease in estrogen levels – hypoestrogenism, which leads to significant consequences for the health of many organs and systems. In the short term, hot flashes, night sweats, palpitations and headaches are observed. In the long term, however, the health risk is multifaceted. The increased frequency of infertility, osteoporosis, cardiovascular and neurological diseases is characteristic. In addition, numerous psychosocial problems are observed, including irritability, insomnia, concentration disorders, and memory difficulties. The decrease in estrogen leads to atrophy of the epithelium lining the vagina. This causes vaginal dryness, irritation and itching in the vaginal area. These changes have a negative impact on sexual desire and can cause pain during intercourse – dyspareunia. A leading cause of decreased life expectancy in patients with premature ovarian failure is the increased risk of developing cardiovascular disease. This is due to dysfunction of the endothelium � the inner layer covering the blood vessels, impaired function of the autonomic nervous system, changes in cholesterol levels, as well as insulin resistance and impaired insulin action. Low osteogen levels also have a negative impact on bone health. Hypoestrogenemia is a cause of decreased bone density. Changes in the levels of the follicle-stimulating hormone – FSH – also contribute to bone health disorders. Maintaining optimal bone density is directly related to the length of ovulatory cycles. Autoimmune oophoritis – autoimmune inflammation of the ovaries was described for the first time in patients with Addison’s disease and adrenal immunity. Much more often, the ovaries are subject to an autoimmune attack associated with autoimmune processes in the thyroid gland or other, often non-organ-specific, autoimmune reactions. It is estimated that 4�30% of cases of primary ovarian failure are due to autoimmune causes. Therefore, the risk of autoimmune diseases is increased in affected patients. According to available data, the incidence of autoimmune hypothyroidism, adrenal insufficiency, type 1 diabetes, hypoparathyroidism and pernicious anemia is increased in patients with primary ovarian failure. Autoimmune thyroiditis appears to be the most common autoimmune disease seen in association with primary ovarian failure. It was found that in nearly 24% of the patients, high serum concentrations of autoantibodies against thyroid peroxidase – antithyroid peroxidase antibodies – antiTPO were found.Clinical hypothyroidism – reduced thyroid gland function is observed in about 8-20% of patients with primary ovarian failure. Adrenal insufficiency is another disease that is often seen as a cause of ovarian failure. Increased levels of 21-hydroxylase were observed in 3.2% of patients. Observations have shown that approximately 2-3% of women have asymptomatic autoimmune adrenal insufficiency. According to other studies, patients with autoimmune involvement of the adrenal glands, detected by the presence of autoantibodies, have a 50% higher risk of developing adrenal insufficiency. The frequency of type 1 diabetes in patients with primary ovarian failure, according to the studies performed, is 2.5%. On the other hand, non-autoimmune forms of ovarian failure may be associated with an increased risk of developing autoimmune diseases. Early menopause, including due to surgical removal of the ovaries, as well as that which occurs naturally before the age of 45, has been found to be associated with an increased risk of developing systemic lupus erythematosus and rheumatoid arthritis. The pathophysiological mechanisms involved in these processes are complex. The immunomodulatory effects of estradiol, particularly on T helper cell function, have been suggested to be key in these processes. References: https://www.ncbi.nlm.nih.gov/books/NBK589674/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059950/

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