Polycystic Ovary Syndrome
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Direct answer
Rotterdam requires two of three features after other causes are excluded — oligo- or anovulation, clinical or biochemical hyperandrogenism, and polycystic ovarian morphology (updated thresholds: roughly 20 or more follicles per ovary and/or ovarian volume ≥10 mL) — making PCOS the commonest endocrinopathy of young women, with Indian studies suggesting a prevalence around one in ten urban women (estimates vary). Its engine is insulin resistance in most (though not all) patients — thin-PCOS is a well-recognised Indian phenotype — so management is metabolic at the core: weight loss where weight is present, cycle and endometrial protection with a combined oral contraceptive, metformin for metabolic dysfunction, and letrozole as first-line ovulation induction for infertility. Long-term obligations are diabetes screening and cardiovascular risk management, not just menstrual calendars.
What you must remember
- Rotterdam 2003 (two of three) versus AE-PCOS 2006 (hyperandrogenism mandatory) — quote the system; Rotterdam remains the widely used standard.
- Ultrasound definition (2018 consensus): ≥20 follicles per ovary and/or volume ≥10 mL; transabdominal scanning in virginal or adolescent patients cannot reliably apply adult criteria.
- Exclusion panel: TSH, prolactin, 17-OHP (non-classic CAH), testosterone/SHBG, DHEAS, FSH — and pregnancy where relevant.
- Insulin resistance: present in most (acanthosis nigricans as the bedside marker), drives hyperandrogenism and anovulation; screen glucose with OGTT (or fasting glucose plus HbA1c) at diagnosis and periodically thereafter.
- Cycle control: combined oral contraceptive (or cyclical progestogen) both regulates bleeding and protects the endometrium — aim for withdrawal bleeding at least every 3–4 months in untreated anovulation.
- Infertility: letrozole first line (superior ovulation and live-birth data versus clomiphene, without ovarian hyperstimulation); clomiphene second; metformin adjunct (particularly in obese PCOS); gonadotrophins and IVF later.
- Hirsutism therapy: OCP first, then spironolactone or cyproterone with strict contraception, eflornithine cream and cosmetic photoepilation.
- Weight loss of 5–10% restores spontaneous ovulation in a substantial share of overweight patients — the single most cost-effective intervention in the syndrome.
How the syndrome runs through a clinic
A 25-year-old presents with irregular cycles since menarche (3–5 per year), moderate hirsutism (Ferriman-Gallwey 12), BMI 27 with acanthosis over the neck, and ultrasound showing 24 follicles per ovary. Panel: TSH, prolactin and 17-OHP normal (excluding non-classic CAH), testosterone 78 ng/dL with low SHBG giving a raised free androgen index; OGTT two-hour glucose 152 mg/dL — impaired glucose tolerance, seen in a meaningful minority of young Indian PCOS patients. Diagnosis: PCOS by Rotterdam (all three criteria, mimics excluded). The plan unfolds in layers: 7% weight loss; a combined oral contraceptive for cycles, endometrial protection and hirsutism; metformin for the glucose intolerance (honestly framed — its strength is metabolic, not as a standalone fertility drug); and cosmetic measures.
Years later, wanting pregnancy: stop the pill, confirm anovulation, and start letrozole 2.5–5 mg on days 2–6 with follicular tracking and folic acid alongside.
The other phenotype visits the same clinic: a 23-year-old dancer, BMI 19, lean PCOS. Her care de-emphasises weight loss and centres cycle regulation plus metabolic surveillance — PCOS in Indian practice is frequently lean, and treating every patient as "obesity disease" misses her.
Where students slip
First, diagnosing PCOS on ultrasound alone: polycystic morphology occurs in a substantial share of normal ovulatory women, and Rotterdam demands symptoms or signs — "sono-PCOS" is not the syndrome. Second, skipping the exclusion panel and labelling every hirsute oligomenorrhoeic woman PCOS — non-classic CAH, hyperprolactinaemia and thyroid disease all wear the same coat. Third, forgetting the endometrium: years of unopposed oestrogen raise endometrial hyperplasia risk, so inducing withdrawal bleeds at least four times a year is protective medicine, not cosmetic. Fourth, offering metformin as the fertility drug of first choice — letrozole holds that place on current evidence — while metformin's role is metabolic and adjunctive. Fifth, treating the diagnosis once and discharging: diabetes risk persists lifelong, so periodic glucose, lipid and weight surveillance belongs to the long-term plan.
Frequently asked questions
What criteria diagnose PCOS?
Rotterdam: two of three — oligo/anovulation, clinical or biochemical hyperandrogenism, polycystic ovarian morphology — after excluding mimics (congenital adrenal hyperplasia, thyroid disease, hyperprolactinaemia, androgen tumours).
What is the updated ultrasound definition of polycystic ovaries?
Approximately 20 or more follicles per ovary and/or an ovarian volume of 10 mL or more, per the 2018 international consensus (raised from the earlier 12-follicle threshold, with modern high-resolution scanners in mind).
Which drug is first line for ovulation induction in PCOS?
Letrozole, the aromatase inhibitor, which improves ovulation and live-birth rates over clomiphene in randomised comparisons; clomiphene, gonadotrophins and IVF follow in sequence, with laparoscopic ovarian drilling a surgical niche option.
What metabolic screening does PCOS require?
Oral glucose tolerance testing (or fasting glucose with HbA1c) at diagnosis with periodic repetition, lipid profile, blood pressure and weight tracking — insulin resistance underlies the syndrome in most patients and type 2 diabetes risk is several-fold elevated.
Why must anovulatory PCOS patients have regular withdrawal bleeding?
Chronic unopposed oestrogen exposure thickens the endometrium and raises hyperplasia and carcinoma risk; cyclical progestogen or a combined contraceptive ensuring bleeding at least every 3–4 months provides protection.