Polycystic Ovary Syndrome



  • Polycystic ovarian syndrome (PCOS) is a syndrome of hyperandrogenism, altered ovarian morphology, and chronic anovulation with infertility.
  • Consensus guidelines recommend that although having two of the three features is enough to make a diagnosis of PCOS in adulthood, all three features of PCOS should be present before diagnosis in an adolescent. Additionally, the menstrual abnormality should have persisted for >2 years.
  • Obesity, hyperinsulinemia, and insulin resistance are common but not required for diagnosis.
  • Because features of PCOS overlap the androgen effects, ovarian morphology, and menstrual irregularity seen in normal puberty, diagnosis may be suspected but not confirmed in some adolescent girls. Thus, symptoms should be treated after appropriate hormonal investigation and do not require confirmation of PCOS diagnosis.


  • Present in 6–14% of postpubertal women
  • Risk factors may be noted in childhood, including low birth weight, premature adrenarche, and earlier menarche.
  • Insulin resistance, often with obesity, is a frequent accompanying feature.

Risk Factors


  • Multifactorial heritable syndrome
  • Polycystic ovaries appear to be inherited as an autosomal dominant trait.
  • PCOS may occur in mothers and sisters and in daughters of fathers with type 2 diabetes (T2D).
  • Fibrillin-3 (FBN-3), THADA, DENN/MADD domain containing 1A (DENND1A), follicle-stimulating hormone (FSH) receptor (FSHR), luteinizing hormone (LH) receptor (LHCGR), IL-6. TNF-α, GNRHR, FABP1, IL-1β, and IL-1Ra polymorphisms may contribute to the development of PCOS.


  • Developmental programming by androgens and/or glucocorticoids
  • Prenatal and childhood factors include being small for gestational age (SGA), rapid compensatory weight gain postnatally, and premature adrenarche.
  • Epigenetic factors observed in animal models include maternal hyperandrogenism and diabetes.
  • Ovarian follicular growth arrests at the antral stage before a dominant follicle occur, leading to chronic anovulation.
  • Insulin resistance or sensitivity varies by cell location.
    • Hepatic, adipose, and musculoskeletal insulin resistance
    • Adrenal, ovarian, and hypothalamic insulin sensitivity
  • Insulin resistance leads to hyperinsulinism. Hyperinsulinism leads to theca cell androgen production and decreased hepatic sex hormone–binding globulin (SHBG) production with increased free testosterone.
  • Obesity can worsen insulin resistance, PCOS symptoms, and risk of T2D.
  • 17-hydroxyprogesterone progesterone secretion is hyperresponsive to gonadotropins.
  • Decreased suppression of testosterone secretion by dexamethasone may be seen. This suggests ovarian hyperandrogenism.


  • Unknown
  • Several potential mechanisms may begin neuroendocrine abnormalities, excessive ovarian and adrenal hyperandrogenism, and metabolic dysfunction.
  • LH hypersecretion is common in women with PCOS and could be a primary neuroendocrine effect or due to hyperandrogenism.
  • Although the molecular mechanisms responsible for insulin resistance and hyperinsulinemia in PCOS are uncertain, improved insulin sensitivity by weight loss or metformin therapy improves PCOS symptoms.

Commonly Associated Conditions

  • Generalized obesity or overweight diagnosis
  • Insulin resistance
  • Impaired glucose tolerance
  • T2D
  • Dyslipidemia with low HDL and elevated triglycerides
  • Metabolic syndrome
  • Endometriosis
  • Hypertension (use age/sex tables)
  • Increased risk for cardiovascular disease
  • Nonalcoholic fatty liver disease
  • Sleep apnea
  • Depression, anxiety, impaired social functioning

There's more to see -- the rest of this topic is available only to subscribers.