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O&G TopicsGynaecological health — menstrual disorders and androgen excess

O&G · Gynaecological health — menstrual disorders and androgen excess

Polycystic ovary syndrome: Rotterdam criteria, phenotypes & life-stage management (International Guideline 2023)

Also known as PCOS · Polycystic ovarian syndrome · Stein-Leventhal syndrome · Hyperandrogenic chronic anovulation · Rotterdam phenotypes

Exam-exhaustive FRANZCOG fellowship topic on polycystic ovary syndrome at fellowship depth: the Rotterdam 2003 criteria reproduced verbatim (2 of 3, after exclusion of mimics), the four phenotypes (A, B, C, D) and their cardiometabolic stratification, the pathophysiology triad (insulin resistance, theca-cell androgen excess, follicular arrest), the investigation panel with assay-quality caveats, the life-stage management ladder (lifestyle, COCP, metformin, letrozole-first fertility pathway, gonadotrophins, ovarian drilling, the IVF/OHSS pathway), the cardiometabolic and psychological burden, and lifelong follow-up. The 2023 Monash-led International Evidence-based Guideline (Teede et al, Fertil Steril 2023) is the global anchor; an MBBS-level PCOS leaf exists and is cross-linked. RANZCOG-primary, globally tagged to MRCOG, ABOG, FRCSC and MRCPI.

high16 referencesUpdated 27 July 202615 min readSource-verified · Oct 2026

Checked against its sources on 14 Oct 2026

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FRANZCOGMRCOGABOGFRCSCMRCPI

Red flags

  • Rapid-onset virilisation (clitoromegaly, voice deepening, frontal balding) or total testosterone over 5 nmol/L or DHEAS over 700 microg/dL — exclude an androgen-secreting tumour before labelling PCOS
  • Late-onset congenital adrenal hyperplasia mimics PCOS — send a morning seventeen-hydroxyprogesterone (over 6 nmol/L) before committing to the diagnosis
  • Prolonged amenorrhoea or cycles over 90 days — unopposed oestrogen; sample the endometrium to exclude hyperplasia or carcinoma (around 3x background risk, up to 9x with obesity)
  • Pregnancy conceived with ovulation induction or IVF — 2 to 3x baseline risk of ovarian hyperstimulation syndrome; anticipate and mitigate
  • An adolescent within 8 years of menarche — do not diagnose PCOS on ultrasound alone; irregular cycles and polycystic morphology are physiologic at this age
  • Depression, anxiety and eating disorders are 3 to 4x more common in PCOS — screen at every visit, not only when the woman volunteers
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Your progress

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Practise this topic8 MCQs with explanations

Target exams

FRANZCOGMRCOGABOGFRCSCMRCPI

Red flags

  • Rapid-onset virilisation (clitoromegaly, voice deepening, frontal balding) or total testosterone over 5 nmol/L or DHEAS over 700 microg/dL — exclude an androgen-secreting tumour before labelling PCOS
  • Late-onset congenital adrenal hyperplasia mimics PCOS — send a morning seventeen-hydroxyprogesterone (over 6 nmol/L) before committing to the diagnosis
  • Prolonged amenorrhoea or cycles over 90 days — unopposed oestrogen; sample the endometrium to exclude hyperplasia or carcinoma (around 3x background risk, up to 9x with obesity)
  • Pregnancy conceived with ovulation induction or IVF — 2 to 3x baseline risk of ovarian hyperstimulation syndrome; anticipate and mitigate
  • An adolescent within 8 years of menarche — do not diagnose PCOS on ultrasound alone; irregular cycles and polycystic morphology are physiologic at this age
  • Depression, anxiety and eating disorders are 3 to 4x more common in PCOS — screen at every visit, not only when the woman volunteers
One-line fellowship answer

Polycystic ovary syndrome (PCOS) is a lifelong, heterogeneous, reproductive-metabolic disorder defined by the Rotterdam 2003 criteria — any two of three: oligo/anovulation, hyperandrogenism (clinical or biochemical), and polycystic ovarian morphology — after exclusion of other causes (congenital adrenal hyperplasia, Cushing, androgen-secreting tumour, thyroid and prolactin disease). It produces four phenotypes (A, B, C, D), each with a different cardiometabolic and endometrial risk. Insulin resistance with compensatory hyperinsulinaemia is a central driver, fuelling ovarian androgen excess and follicular arrest. Manage it as a chronic disease by life stage: lifestyle first for all, the COCP for cycles/endometrium/acne/hirsutism, letrozole (superior to clomiphene) first-line for fertility, the gonadotrophin–drilling–IVF ladder next, and lifelong annual cardiometabolic and psychological surveillance. The 2023 International Evidence-based Guideline (Monash) is the global anchor.[1][2][5]

A woman in your fertility clinic has had irregular cycles since menarche, clinical hyperandrogenism, obesity, and polycystic ovaries on ultrasound. She is exhausted, anxious, and desperate to conceive. Your job is to confirm the diagnosis with the right test, exclude the mimics before labelling her, then walk the evidence-based ladder — lifestyle, letrozole, and an OHSS-aware IVF pathway if needed — while never losing sight of her cardiometabolic and psychological future. The Rotterdam framework and the 2023 International Guideline exist precisely to stop doctors calling the symptom a diagnosis and reaching for clomiphene first.[1][2]

Overview and definition

PCOS is the commonest endocrine disorder of reproductive-age women — prevalence around one in ten using Rotterdam criteria, rising with ethnicity — and the leading cause of anovulatory infertility.[5] It is a syndrome, not a single disease: a cluster of ovulatory dysfunction, androgen excess, and a characteristic ovarian morphology, set against a backdrop of insulin resistance and chronic low-grade inflammation that does not disappear at menopause.[5][14]

The defining act of every consultation is the structured application of the Rotterdam criteria after exclusion of mimics. The syndrome has no cure; the phenotype shifts across the life course. The clinician's job is to treat the symptom in front of the woman today and to set up the surveillance that protects her tomorrow.[2][11]

PCOS — the burden in numbers that frame every visit

~1 in 10Prevalence (Rotterdam)reproductive-age women; higher in South Asian and Middle Eastern populations
commonInsulin resistance95% of obese, 60–70% of lean phenotypes — present independent of obesity
commonAnovulatory infertilityleading cause worldwide
elevatedLifetime type 2 diabetesKakoly 2018 meta-regression; rises with ethnicity and BMI
~3xEndometrial cancerunopposed oestrogen; up to 9x with obesity
elevatedDepression and anxietyscreen at every visit, not only when volunteered
[2] [5] [7] [8]
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References16ShowHide
  1. [1]Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril, 2004.PMID 14711538
  2. [2]Teede HJ, Tay CT, Laven JJE, Dokras A, Moran LJ, Piltonen TT, et al. Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Fertil Steril, 2023.PMID 37589624
  3. [3]Legro RS, Brzyski RG, Diamond MP, et al. Letrozole versus clomiphene for infertility in the polycystic ovary syndrome. N Engl J Med, 2014.PMID 25006718
  4. [4]Teede HJ, Misso ML, Costello MF, Dokras A, Laven J, Moran L, et al. Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Fertil Steril, 2018.PMID 30033227
  5. [5]Stener-Victorin E, Teede H, Norman RJ, et al. Polycystic ovary syndrome. Nat Rev Dis Primers, 2024.PMID 38637590
  6. [6]Lizneva D, Kirubakaran R, Mykhalchenko K, Suturina L, Chernukha G, Diamond MP, Azziz R. Phenotypes and body mass in women with polycystic ovary syndrome identified in referral versus unselected populations: systematic review and meta-analysis. Fertil Steril, 2016.PMID 27530062
  7. [7]Barry JA, Azizia MM, Hardiman PJ. Risk of endometrial, ovarian and breast cancer in women with polycystic ovary syndrome: a systematic review and meta-analysis. Hum Reprod Update, 2014.PMID 24688118
  8. [8]Kakoly NS, Khomami MB, Joham AE, et al. Ethnicity, obesity and the prevalence of impaired glucose tolerance and type 2 diabetes in PCOS: a systematic review and meta-regression. Hum Reprod Update, 2018.PMID 29590375
  9. [9]Franik S, Le QK, Kremer JA, Kiesel L, Farquhar C. Aromatase inhibitors (letrozole) for ovulation induction in infertile women with polycystic ovary syndrome. Cochrane Database Syst Rev, 2022.PMID 36165742
  10. [10]Costello M, Shrestha B, Eden J, Sjoblom P, Johnson N. Insulin-sensitising drugs versus the combined oral contraceptive pill for hirsutism, acne and risk of diabetes, cardiovascular disease, and endometrial cancer in polycystic ovary syndrome. Cochrane Database Syst Rev, 2007.PMID 17253562
  11. [11]Legro RS, Arslanian SA, Ehrmann DA, et al. Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab, 2013.PMID 24151290
  12. [12]Fauser BC, Tarlatzis BC, Rebar RW, et al. Consensus on women's health aspects of polycystic ovary syndrome (PCOS): the Amsterdam ESHRE/ASRM-Sponsored 3rd PCOS Consensus Workshop Group. Fertil Steril, 2012.PMID 22153789
  13. [13]Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W, et al. Positions statement: criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an Androgen Excess Society guideline. J Clin Endocrinol Metab, 2006.PMID 16940456
  14. [14]McCartney CR, Marshall JC. Clinical practice. Polycystic ovary syndrome. N Engl J Med, 2016.PMID 27406348
  15. [15]Cooney LG, Dokras A. Cardiometabolic Risk in Polycystic Ovary Syndrome: Current Guidelines. Endocrinol Metab Clin North Am, 2021.PMID 33518188
  16. [16]Bahri Khomami M, Shorakae S, Hashemi S, et al. Systematic review and meta-analysis of pregnancy outcomes in women with polycystic ovary syndrome. Nature communications, 2024.PMID 38965226

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