How bad are bilateral polycystic ovaries

Polycystic Ovary Syndrome (PCOS)

is one of the most common hormonal diseases in young women and affects about 5–10% of all women, androgenization symptoms (masculinization with increased hair growth (hirsutism), seborrhea (increased sebum production of the skin), acne, increased blood levels male sex hormone) anovulatory cycles and other cycle disorders and infertility possible. Polycystic Ovary Syndrome is the cause of up to 30% of secondary amenorrhoea and can also be the cause of primary amenorrhoea. 60-80% of women with secondary amenorrhea have hyperandrogenemia.

 PCOS is one of the most common reasons why women of childbearing age do not get pregnant. Usually the Diagnosis made during examinations because of unfulfilled desire to have children. Most women with PCOS have some level of insulin resistance, which is responsible for cardiovascular risks. Often the so-called Syndrome X is also present (insulin resistance, obesity, hypertension, and lipid metabolism disorders). There are several diagnostic criteria. US National Institutes of Health criteria for polycystic ovary syndrome, menstrual irregularities or anovulation, clinical and / or biochemical hyperandrogenemia, absence of hyperprolactinaemia or thyroid disease as a cause, no congenital adrenal hyperplasia, no Cushing's syndrome. Differential diagnoses there: Criteria for polycystic ovaries: Polycystic ovaries on ultrasound, no menstrual disorders or cosmetic symptoms, no biochemical hyperandrogenemia. Idiopathic hirsutism: excessive hair growth, no biochemical hyperandrogenemia. Criteria of the European Society of Human Reproduction and Embryology and the American Society for Reproductive Medicine: Polycystic Ovary Syndrome is diagnosed when 2 of the following criteria are met: polycystic ovaries on ultrasound, menstrual disorders or anovulatory cycles, biochemical hyperandrogenemia.

The cause is largely unknown. Oligoamenorrhea, infertility, centripetal obesity, hirsutism and an increased plasma testosterone level as well as bilaterally enlarged ovaries with several cysts occur symptomatically. Theca cells in the polycystic ovaries produce more androgens here. Evidence of another endocrine disorder must be absent for diagnosis.

The disorder usually becomes noticeable when an appropriate diagnosis is carried out if the desire to have children is not fulfilled. In anovulatory women with polycystic ovaries, the (abnormal) growth of the follicles stops at a diameter of 5-8 mm, well before the size at which a mature follicle can release its egg (ovulation). This disruption of follicle maturation is triggered by the hormonal disorder. Follicular maturation usually takes 6 months or more, only the last two weeks of follicular maturation depend on hormonal changes in the woman's menstrual cycle. In the earlier stages of development, the growth of the follicles is more dependent on local growth factors and the local hormones in the ovary. Few egg cells in healthy women reach the pre-ovulatory stage of maturity. Valproate treatment (but also other drugs) can favor this syndrome in women.

The spontaneous incidence of PCOD is estimated at up to 19% (predominantly 5-10% are given) in healthy women in western industrialized countries, so that it is difficult to decide in individual cases whether valproate is the cause. For valproate treatment, incidences of over 50% are reported. The cause is assumed to be in the hypothalamus with disorders of the LH secretion. Secondary disorders in the insulin metabolism are said to be responsible for the resulting obesity. However, many authors assume that the impaired insulin function is the decisive cause of the disorder. In any case, insulin resistance in adipose tissue and in skeletal muscle seems to be a very common phenomenon in this disorder. The associated hyperinsulinemia may cause increased androgen secretion in the ovaries and abnormal follicular growth that eventually leads to dysfunctional ovarian and menstrual activity. The oral antidiabetic drug metformin is effective in the treatment of PCOS even according to a new meta-analysis. PCOS increases the risk of developing diabetes and cardiovascular diseases.

Other investigators assume that the condition has its origins in childhood. One study found fundamental differences between the ovaries of healthy women and women with polycystic ovaries. With PCOS there is obviously a greatly increased density of even small follicles. PCOS could therefore also be due to an attachment with already increased follicles in the fetal ovary (the later adult woman, or from a reduced loss of egg cells during the late pregnancy of the mother, childhood or puberty A gene in the region of the insulin receptor may be largely responsible. The most common definition of polycystic ovary syndrome is the combination of hyperandrogenism and chronic anovulatory cycles in women with no prior knowledge of any specific adrenal or pituitary disease.

Hyperandrogenism leads clinically to hirsutism (male hair growth), acne, and androgen-dependent alopecia (hair loss) and biochemically to increased serum concentrations of androgens, especially testosterone and androstenedione. Disturbances in the insulin metabolism seem to be a priority, insulin influences the androgen secretion and its metabolism. Obesity is common but not common. Ultrasound studies showed that 30% of women with amenorrhea and 75% of women with oligomenorrhea had evidence of a polycystic ovary. More than 60% of these women had increased male hair growth (hirsutimus), and 90% had increased serum levels of LH (luteinizing hormone) or androgens (or both). 73% of women with anovulatory infertility have the syndrome. 87% of women with hirsutism and regular menses are also affected. Typically these changes lead to hypersecretion of LH (luteinizing hormone) and androgens with normal or low serum concentrations of FSH (follicle stimulating hormone).

Infertility is a common consequence. The pregnancies that come about don't have to be compromised. Early descriptions of the syndrome relied on the visible changes in the ovary (ovary), which were seen as a prerequisite for diagnosis. Other publications see the biochemical changes in the foreground.

There is evidence that PCOS patients also often suffer from severe depression and eating disorders. Some authors suspect that a dysfunction of the hypothalamic-pituitary-adrenal system (HPA system), which can be observed in PCOS, causes depressive disorders as a neurobiological risk factor. Likewise, between eating disorders such as bulimia nervosa or binge eating disorder and PCOS there may be hormonal and metabolic mechanisms that combine. It is possible that changes in behavior and psychological disorders favor the development of PCOS - or that PCOS can lead to psychological disorders via psychological or neuroendocrine mechanisms. PCOS leads to an endothelial dysfunction in the vessels and to resistance to the vasodilatory effects of insulin. This endothelial dysfunction leads to increased androgen levels and insulin resistance (risk of diabetes) Women with PCOS have an increased risk of vascular problems. Hyperinsulinemic insulin resistance and a metabolic syndrome that lead to an increased cardiovascular risk are common.


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