Do I have polycystic ovary syndrome?

  People often ask: Am I suffering from polycystic ovary syndrome? Polycystic ovary syndrome is a syndrome of endocrine disorders characterized by persistent anovulation, hyperandrogenism and polycystic ovarian changes. It is the most common cause of menstrual disorders in adolescent and fertile women; it accounts for 1/3 of amenorrhea, 90% of menstrual scarcity and 90% of anovulatory infertility. The pathogenesis and diagnosis of the disorder are described in detail below (in).
  I. Pathogenesis
  The pathogenesis of PCOS is hitherto unknown and involves multiple factors.
  In the 1980s, polycystic ovaries were found to be the result of ovarian changes due to prolonged anovulation, called polycystic ovaries (PCO).
  Hyperandrogenemia and prolonged anovulation were known to characterize the disease in the 1990s, and some patients have insulin antagonism, which may eventually develop into endocrine and metabolic disorders with increased risk of coronary heart disease and type II diabetes mellitus. Current research suggests that it may be caused by the interaction of certain genetic and environmental factors.
  It is recognized that PCOS is a highly heterogeneous clinical syndrome with a multi-causal pathogenesis and polymorphic manifestations involving endocrine, metabolic and genetic factors. The incidence of hypertension is 8 times higher than normal women, diabetes 6 times higher, and endometrial and breast cancer 2 times higher due to abnormalities in the endocrine and metabolic systems.
  PCOS covers almost all of a woman’s life. Therefore, attention should be paid to the long-term treatment and prevention of PCOS patients.
  Clinical manifestations
  1. A complex group of syndromes
  The clinical manifestation of PCOS is a complex group of syndromes mainly manifested by irregular menstruation, infertility, hirsutism or acne, obesity, acanthosis nigricans, etc.
  2, PCOS distant comorbidities include.
  (1) malignant lesions: such as endometrial cancer, breast cancer.
  (2) diabetes mellitus: type II diabetes.
  (3) Cardiovascular disease: coronary heart disease, hypertension.
  3. Sporadic ovulation or anovulation, infertility
  (1) Clinical characteristics are as follows.
  (1) Sporadic menstruation, amenorrhea and, in a few cases, irregular bleeding.
  (2) Infertility due to non-ovulation and easy miscarriage after pregnancy.
  (2) Judgment criteria for sporadic ovulation or anovulation.
  Failure to establish regular menstruation two years after menarche; amenorrhea (menopause for more than 3 previous menstrual cycles or menstrual cycle R6 months).
  Regular menstruation cannot be taken as evidence of ovulation; basal body temperature (BBT), ultrasound monitoring of ovulation, and progesterone determination in the second half of menstruation can clarify whether ovulation is occurring; FSH and E2 levels should be normal, with the aim of excluding hypogonadism and premature ovarian failure with low gonadotropins.
  4.Kaohsiung
  The clinical manifestations of hyperandrogenism are an important feature of patients with PCOS.
  (1) Clinical manifestations of hyperandrogenic signs.
  Male features such as hirsutism, acne, seborrheic skin or hair loss.
  (2) Hyperandrogenic blood signs (testosterone levels)
  There are limitations, not all patients have high testosterone levels.
  (3) Characteristics of clinical manifestations of hyperandrogenism.
  Acne: recurrent, often located on the forehead, cheeks, nose, jaw, and in individuals on the forehead and back.
  Hirsutism: coarse and stiff hairs appear on the upper lip, jaw, around the areola, lower abdomen midline, etc., and dense pubic hair.
  5.Obesity
  50% of patients are centripetal obese, most of them have a family history of hypertension or diabetes mellitus.
  Acanthosis nigricans sign: 10% of obese patients in the labia, back of the neck, axilla, under the breast and groin and other parts of the skin appear gray-brown pigmentation, symmetrical, skin thickening, light touch soft as velvet. It is caused by high insulin/insulin antagonism.
  III. Examination and diagnostic criteria
  (A) Examination
  Whole body physical examination: obesity, hirsutism, male distribution, acne, acanthosis nigricans sign
  Gynecological examination: hirsutism next to the areola, increased pubic hair, male distribution, increased vulvar pigmentation; normal or slightly small uterus, slightly large cystic ovaries can be retrieved on both sides.
  Basal body temperature: monophasic.
  Ultrasound : polycystic ovaries.
  1. Yin ultrasound.
  (1) 2.5 diameter of one or both ovaries (not as diagnostic criteria, for auxiliary reference).
  (3) High prolactin in some patients.
  (4) Some patients have high insulin, insulin antagonism, and high blood glucose (not as diagnostic criteria and does not affect the treatment plan).
  Fasting insulin >15uIUH/ml or 2-hour insulin 10 times higher than fasting suggests insulin resistance.
  3.Diagnostic scraping
  To understand endometrial changes (hyperplasia, atypical hyperplasia or endometrial cancer); PCOS patients older than 35 years old should be routinely scraped if they have irregular vaginal bleeding for more than 15 days.
  4.Diagnostic items
  Table 1 Diagnostic items
  Clinical manifestations
  Endocrine examination
  Ovarian morphology
  Metabolism
  ◇Menstrual disorders (52%) ◇Obesity (50%) ◇Hirsutism and acne (52%) ◇High T (68%) ◇LH/FSH〉2.5 (50%) ◇High PRL (30%) ◇Large ovaries ◇Ovarian polycystic-like changes (52%) ◇Hyperinsulinemia (69%)
  (II) Diagnostic criteria
  Criteria established by the American and European Reproductive Societies Workshop in Rotterdam, the Netherlands, in 2003: 1) Sparse ovulation or anovulation (scanty menstruation, amenorrhea, or infertility). 2) Biochemical indicators/or clinical manifestations of hyperandrogenemia (hirsutism, acne). 3) Polycystic ovary sign under ultrasound.
  Diagnosis can be made by meeting two of the above three criteria and excluding other hyperandrogenic etiologies.
  (iii) Special instructions
  1. Hyperandrogenemia should exclude other diseases, such as adrenocortical hyperplasia, androgen-secreting tumors, Koch syndrome, etc.
  2, the presence of PCO alone cannot diagnose PCOS, PCOS does not necessarily have PCO.
  3, LH is not used as a diagnostic criterion for PCOS, but can be used as an auxiliary reference.
  4, insulin resistance is not used as a diagnostic criterion and does not affect the treatment plan. Screening for metabolic syndrome should be done for obese PCOS. For women with PCOS who are not obese, screening for metabolic syndrome can be done if there is a family history of diabetes.
  Additional content.
  Prefer metformin to lower blood insulin, improve ovulation and prevent distant complications.
  Dosage: 250-500mg tid, ovulation rate 10%-20% after 3 months of treatment, may improve the sensitivity of the organism to clomiphene.
  Other drugs: troglitazone, rosiglitazone (Vindia).
  At present, no drug can guarantee that there will be no more amenorrhea after stopping the drug. The purpose of menstrual regulation is to protect the endometrium and to counteract excessive endometrial hyperplasia, not to get menstruation.
  Total testosterone does not represent true body androgen activity and is not an absolute indicator of PCOS. It depends on whether the symptoms and signs improve and there is no need to dwell on whether the androgens have dropped to normal, the signs are more important than the androgen levels.