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Conditions · Pelvis

Polycystic ovary syndrome !

Polycystic ovary syndrome (PCOS) is a common hormonal disorder with irregular ovulation, excess male hormones and many small ovarian follicles.

Updated 2026-10-29

Structures involved

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Why it happens

What it is

A common endocrine and metabolic disorder of reproductive age, defined by combinations of ovulatory dysfunction, androgen excess and polycystic ovarian morphology. Some recent sources use the new name Polyendocrine Metabolic Ovarian Syndrome, which stresses its metabolic side.

Who gets it

One of the most common endocrine disorders in women of reproductive age; prevalence depends on the criteria used. It often starts in adolescence and is under-diagnosed. In Latin America, high rates of obesity and insulin resistance add to its metabolic burden.

Causes

  • Polygenic, runs in families
  • Insulin resistance with compensatory hyperinsulinaemia
  • Faster GnRH pulses that favour LH over FSH
  • Developmental factors in utero (proposed)
  • Obesity worsens its expression

Risk factors

  • Family history of PCOS or type 2 diabetes
  • Obesity, especially central
  • Insulin resistance
  • Premature adrenarche in childhood

Pathophysiology

Rapid GnRH pulses raise LH relative to FSH. LH drives androgen production by theca cells, and relative FSH lack stops follicles maturing, leaving many small arrested follicles. Hyperinsulinaemia boosts ovarian androgens and lowers SHBG, raising free androgens. Without ovulation, the endometrium is exposed to unopposed oestrogen.

Classification

  • Rotterdam criteria: at least 2 of 3: ovulatory dysfunction, clinical or biochemical hyperandrogenism, polycystic ovarian morphology (ultrasound or, in adults, raised AMH)
  • Other causes must be excluded first (thyroid disease, hyperprolactinaemia, non-classic congenital adrenal hyperplasia, androgen-secreting tumours)
  • Phenotypes A–D by which criteria are present; A (all three) carries the greatest metabolic risk
  • Adolescents: both ovulatory dysfunction and hyperandrogenism are needed; ultrasound and AMH are not used in the first years after menarche

Symptoms and signs

  • Irregular or absent periods
  • Hirsutism, acne or androgenic hair loss
  • Subfertility from anovulation
  • Weight gain and central obesity
  • Acanthosis nigricans (sign of insulin resistance)
  • More frequent depression and anxiety

Diagnosis

Clinical
History of cycles and androgen signs, hirsutism scoring (modified Ferriman–Gallwey), weight, waist, blood pressure and acanthosis nigricans.
Tests
Pregnancy test; total and free testosterone; TSH, prolactin and 17-hydroxyprogesterone to exclude mimics; AMH may replace ultrasound in adults; oral glucose tolerance test or HbA1c and lipid profile.
Imaging
Transvaginal ultrasound counts follicles and measures ovarian volume (adults only); thresholds depend on equipment and criteria vary.

Differential diagnosis

  • Thyroid disease
  • Hyperprolactinaemia
  • Non-classic congenital adrenal hyperplasia
  • Androgen-secreting ovarian or adrenal tumour
  • Cushing syndrome
  • Functional hypothalamic amenorrhoea

Goal of treatment

Treat what matters most to the patient (cycles, androgen signs, fertility), protect the endometrium and lower long-term metabolic and cardiovascular risk.

Treatment

Lifestyle
Healthy eating and physical activity for everyone; modest weight loss in those with excess weight can restore ovulation and improve metabolic risk.
Medical
Combined hormonal contraceptives regulate cycles, protect the endometrium and reduce hyperandrogenism; cyclic progestins are an alternative for endometrial protection.
Medical
Insulin sensitisers (biguanides) for metabolic features; anti-androgens for hirsutism, only with reliable contraception; cosmetic hair removal.
Medical
Ovulation induction for infertility: aromatase inhibitors first line, then gonadotropins or IVF in specialist care.
Follow-up
Regular screening for glucose intolerance, dyslipidaemia, hypertension, mood disorders and sleep apnoea.

Drugs for this condition

Complications

  • Type 2 diabetes and gestational diabetes
  • Dyslipidaemia, metabolic syndrome and higher cardiovascular risk factors
  • Endometrial hyperplasia and cancer
  • Infertility and pregnancy complications such as preeclampsia
  • Obstructive sleep apnoea and fatty liver disease
  • Depression, anxiety and body-image distress

Prognosis

A lifelong condition whose features change with age: cycle and androgen problems often ease towards menopause, while metabolic risk persists. With treatment and follow-up most control their symptoms, and many conceive.

Test yourself

Think of the answer, then tap the question to see it.

What are the Rotterdam criteria for PCOS?

Two of three: ovulatory dysfunction, hyperandrogenism and polycystic ovarian morphology, after excluding other causes.

Why does chronic anovulation in PCOS raise the risk of endometrial cancer?

Unopposed oestrogen without cyclic progesterone leads to endometrial hyperplasia.

Which skin sign suggests insulin resistance in PCOS?

Acanthosis nigricans: dark, velvety skin in folds such as the neck and armpits.

Which drug class is first line for ovulation induction in PCOS?

Aromatase inhibitors.

What new name for PCOS appears in some recent sources?

Polyendocrine Metabolic Ovarian Syndrome, which highlights its endocrine and metabolic nature.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Polyendocrine Metabolic Ovarian Syndrome (StatPearls (NCBI Bookshelf), 2025).

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Representative model, for educational purposes only.

Ovaries highlighted on the Durgical 3D model