Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age all over the world; the prevalence of the polycystic ovary syndrome varies widely, depending on the ethnicity, body composition and definition used for diagnosis. The literature shows that the prevalence is 15% when the broader Rotterdam criteria are applied. Prevalence can reach almost 30% in women with overweight and obesity. Thus, polycystic ovary syndrome imposes a significant economic burden on national health systems.
Heterogeneous disorder affects several body systems and leads to reproductive and metabolic complications. It is also the most common cause of chronic anovulation and hyperandrogenism in young women.
Two of three criteria determines PCOS:
Menstrual irregularity (oligo-ovulation or anovulation),
Hyperandrogenism (clinical or biochemical),
Polycystic morphology of the ovaries.
Infertility, obesity, insulin resistance and dyslipidemia often accompany it.
Polycystic ovary syndrome is an extremely complex disorder that arises from a combination of heredity and environmental factors. Ethnic variations of PCOS are strongly determined by the genetic origin of humans. It is almost certainly a genetic condition, but the exact causes of hyperandrogenism, the cause of changes in ovarian function and the cause of anovulation that affects a subgroup of these women, remain unknown and are still under investigation. The genetic effect of the polycystic ovary syndrome has been suggested in many studies, including the identification of family clustering of the polycystic ovary syndrome and high heritability in twin studies.
Influence on Fertility
Polycystic ovary syndrome is the most common cause of anovulatory infertility and eugonadotropic hypogonadism in accordance with the WHO, and it is often diagnosed for the first time in a fertility clinic. Infertility is the main clinical consequence of ovulatory dysfunction in the syndrome of polycystic ovaries. Seventy five percent of these women suffer from infertility due to anovulation. This may explain the effects of obesity, metabolic, inflammatory and endocrine abnormalities on ovulatory function, oocyte quality and susceptibility to endometrium. Ovarian hyperandrogenism and hyperinsulinemia may contribute to premature luteinization of granulosa cells, and paracrine dysregulation of growth factors may disrupt the intrafocalic environment and worsen the cytoplasmic and/or nuclear maturation of oocytes. These features are not universal, and the quality of oocytes, fertilization and the speed of implantation in an individual woman with polycystic ovary syndrome can be normal.
Diagnosis of polycystic ovary syndrome is based mainly on clinical history and physical examination. The main clinical features of polycystic ovary syndrome are hyperandrogenism and menstrual dysfunction. It is generally recognized that polycystic ovary syndrome is not a specific endocrine disease, but a syndrome represented by a set of signs and symptoms, and that no one sign, symptom or test is diagnostic.
The establishment of criteria for the diagnosis of polycystic ovary syndrome proved to be complex and contradictory. Diagnostic criteria for polycystic ovary syndrome are based on consensus of experts, and not on evidence. In 2003, the Rotterdam Consensus expanded the diagnostic criteria to include at least two of the following characteristics:
Clinical or biochemical hyperandrogenism,
Oligo-anovulation (violation of the cycle),
Polycystic ovaries (PCO) (excess of antral follicle on ultrasound with ≥12 follicles from 2 to 9 mm per ovary and/or volume of ovaries ≥10 ml).
An Expert Panel from the 2012 NIH Evidence Based Methodology Workshop on polycystic ovary syndrome recommended that clinicians use earlier Rotterdam criteria for diagnosis.
Consensus opinion as a whole agreed that the ovary is central to the disorder and that other endocrinological disorders need to be excluded before the diagnosis is made (PCOS is the diagnosis of the exception). These disorders include non-classical adrenal hyperplasia, Cushing’s syndrome, androgen-producing tumors, and drug-induced excess of androgens. In addition, clinicians should exclude ovulatory dysfunction for other reasons, including thyroid dysfunction and hyperprolactinaemia, as well as pregnancy in women of reproductive age.
Evaluation of women with suspected polycystic ovary syndrome should include:
Serum thyroid-stimulating hormone (TSH),
Test for glucose tolerance for 2 hours,
Fasting lipid profile,
Endometrial sampling (in women whose history indicates a potential long-term effect of unresponsive estrogen stimulation),
Serum testosterone (in women with moderate or severe hirsutism),
Morning follicular phase of serum 17-hydroxyprogesterone (in women with precancerous perimenorrial origin of hirsutism, family history of congenital adrenal hyperplasia or high-risk),
A test to suppress dexamethasone at night (in women with signs or symptoms of hypercortisolism).
Improved and standardized androgenic analyzes, new methods for documenting chronic anovulation, beyond the menstrual history, and imaging technology can refine diagnostic criteria.
Management of Disease
Management of women with polycystic ovary syndrome should strive to correct or prevent both immediate and long-term clinical consequences, which may include all of the following:
An increased risk of developing endometrial hyperplasia and neoplasia,
Hyperandrogenism (hirsutism, acne, alopecia),
An increased risk of developing type 2 diabetes,
Increased risk of developing cardiovascular disease.
Women with polycystic ovary syndrome who do not want pregnancy need contraception. No contraceptive methods are contraindicated in the syndrome of polycystic ovaries. However, some of the signs associated with polycystic ovary syndrome (obesity, insulin resistance, etc.), can be a relative contraindication to the use of combined OCPs. OCPs suppress the secretion of LH and lead to a decrease in the production of oral androgen. The estrogen component increases the levels of SHBG, which in turn leads to a decrease in the number of free T circulation levels. The benefits of OCPs outweigh the risks in most patients with PCOS.
Those who seek to become pregnant are candidates for the induction of ovulation. An important point to be emphasized is that women with chronic anovulation require comprehensive clinical management that takes into account their immediate needs, but also takes into account their long-term health and includes appropriate risk reduction strategies.
Lifestyle and Dietary Interventions
In many cases, lifestyle changes will be an important part of clinical management, requiring careful training, counseling, support and follow-up. These changes included changes in diet, exercise and/or behavior that benefit overall health, including weight loss and weight gain. There is an opinion that weight and glycemic parameters improve. There are several randomized controlled trials of lifestyle actions, and they involve significant reproductive and metabolic benefits.
Management of Menstrual Abnormalities
Estrogen-progestin contraceptives are the most common treatment for menstrual anomalies associated with chronic anovulation because they cause regular cyclic menstruation and weaken the growth of the endometrium, thereby preventing dysfunctional uterine bleeding and eliminating the risk of developing endometrial hyperplasia and neoplasia. Cycle monitoring is usually achieved using OCPs in women with PCOS. In those who refuse or have a contraindication to the use of estrogen-progestin contraceptives, the same can be achieved with cyclic or continuous treatment with progestin alone. However, treatment with progestin deprives some of the other important actions of estrogen-progestin contraceptives, which help in the treatment of hyperandrogenism.
Knowledge and understanding of the health consequences and consequences of chronic anovulation and methods for their effective management is much more important than the purpose of a specific diagnosis of PCOS.
Management of Hyperandrogenism
Light focal hirsutism can be effectively controlled by cosmetic measures (shaving, plucking, waxing, depilatories), but most who make a complaint about hirsutism already use one or more of these techniques and will require treatment. Options for medical treatment include, first, estrogen-progestin contraceptives and anti-androgens (e.g., spironolactone). Anti-androgens are effective for the treatment of hirsutism, but they should be used in combination with the estrogen-progestin contraceptive or other highly reliable method (e.g., an intrauterine device) because of their potential adverse effects on sexual development in the fetus in men if the patient should have thought unexpectedly. Long-term (6 months) medical therapy for hirsutism is necessary for documenting the effectiveness. It is known that effective treatment of alopecia is not known.