PCOS (now PMOS)

Terminology change (May 2026): PCOS has been renamed polyendocrine metabolic ovarian syndrome (PMOS). Following a 14-year, 56-organisation global consensus process (22,000 survey responses across all world regions; consensus reached February 2026; published in The Lancet, May 2026), “polycystic ovary syndrome” has been retired as inaccurate and stigmatising — the ovarian ultrasound appearance reflects arrested follicular development, not true cysts, and the name obscured the condition’s metabolic, cardiovascular, dermatological and psychological features. The diagnostic criteria and management recommendations below are completely unchanged — only the name has changed. “PCOS” and “PMOS” will co-exist for a 3-year managed transition; this note uses PMOS (formerly PCOS) throughout and both terms are kept in the page title so the note is still found by either search term.

Polyendocrine metabolic ovarian syndrome (PMOS, formerly polycystic ovary syndrome or PCOS) is a common reproductive, metabolic and endocrine disorder, affecting 8–13% of women of reproductive age (higher in Aboriginal and Torres Strait Islander women — up to 21%). It is not the same as ultrasound-visible polycystic- appearing ovaries, which occur in up to a quarter of all women and up to ~70% of adolescents without PMOS — the follicular appearance reflects disrupted ovarian steroidogenesis and impaired follicular maturation, not pathological cysts.

Presentation

Domain	Features
Reproductive/ovarian	Menstrual disturbance (oligomenorrhoea/amenorrhoea), subfertility, elevated AMH
Polyendocrine	Hyperandrogenism (ovarian + adrenal), increased GnRH pulsatility/LH, insulin resistance with compensatory hyperinsulinaemia (present in ~85% of those affected)
Cutaneous (a manifestation of hyperandrogenism)	Hirsutism, acne (weaker association), androgenic alopecia
Metabolic	Obesity (central), insulin resistance, impaired glucose tolerance, type 2 diabetes, dyslipidaemia, NAFLD/MASLD, obstructive sleep apnoea
Cardiovascular	Hypertension; significantly elevated odds of composite cardiovascular disease, myocardial infarction and stroke compared with women without PMOS
Psychological	Anxiety, depression, poor body image, eating disorders, sexual difficulties

Diagnosis — Rotterdam criteria (unchanged)

Diagnose PMOS in an adult if 2 of the following 3 are met, after excluding differentials:

1. Menstrual disturbance (oligomenorrhoea/amenorrhoea) — irregular cycles shorter than 21 days or longer than 35 days
2. Clinical or biochemical hyperandrogenism
3. Polycystic-appearing ovaries on ultrasound

• If both (1) and (2) are present, ultrasound is not required for diagnosis.
• If only one of (1)/(2) is present, arrange a transvaginal ultrasound (first half of cycle) with a follicle count; transabdominal is an acceptable alternative if not yet sexually active. Without clinical or biochemical hyperandrogenism, a polycystic-appearing ovary on ultrasound alone has no diagnostic significance.
• Adolescents (<18yrs): refer for specialist assessment rather than diagnosing in primary care. Menstrual irregularity is only considered abnormal if it persists beyond 2 years post-menarche, and a polycystic-appearing ovary is normal for up to 8 years post-menarche — ultrasound is not recommended in this age group.

Biochemical hyperandrogenism: raised free androgen index (free testosterone/SHBG) or free testosterone. Stop the COCP for 3 months before testing (it suppresses androgens) and test on cycle days 1–14 where possible.

Differential diagnoses to exclude first

• Thyroid dysfunction, hyperprolactinaemia
• Late-onset congenital adrenal hyperplasia (17-OH-progesterone) — gene for the late-onset variant occurs in ~1:1000 of the population
• Cushing’s syndrome (purple striae, hypertension, supraclavicular fat pads)
• Androgen-secreting tumour (testosterone >5.2nmol/L, very high DHEAS, virilisation/clitoromegaly, deepening voice, increased musculature, balding)
• Premature ovarian insufficiency
• Hypogonadotrophic hypogonadism (decreased body fat, extensive exercise, low LH/FSH)
• Pregnancy

Initial investigations

Free testosterone, SHBG (→ FAI), LH/FSH, prolactin, TSH, DHEAS, 17-OH-progesterone, ±24h urine cortisol or dexamethasone suppression test if Cushingoid features. Add metabolic screening (below) and pelvic ultrasound only if indicated as above.

Management

Management is lifelong and tailored to the individual’s goals (menstrual control, hirsutism/acne, fertility, metabolic risk). Refer to a gynaecologist/ endocrinologist if diagnosis is uncertain (e.g. adolescents), hirsutism fails to respond to antiandrogen therapy after 6–12 months, or the patient is seeking fertility treatment.

Ensure the patient understands the diagnosis accurately — the metabolic, psychological and reproductive aspects, and that management is lifelong. PMOS can raise concerns about body image, weight, and infertility risk, sometimes with inappropriate eating/exercise responses; ask about anxiety, depression and social isolation, and manage hirsutism sensitively.

Lifestyle (first-line for almost everything)

• A 5% weight loss in overweight/obese women improves ovulatory function, fertility, insulin resistance, hyperandrogenism and psychological wellbeing, and can reduce diabetes risk by 50–60%. Aim to prevent further weight gain even in women with a normal BMI.
• Diet and exercise (150 min moderate or 75 min vigorous activity/week).
• Offer regular monitoring (weight, waist circumference, BMI) at least 6–12 monthly, frequency agreed with the patient.

Menstrual disturbance / endometrial protection

Anovulatory cycles cause unopposed oestrogen exposure → endometrial thickening, irregular/heavy bleeding, and a 2–6-fold increased risk of endometrial cancer (risk rises further if cycles are >90 days apart).

• First-line: combined oral contraceptive (COC) — most effective menstrual regulator, also helps hirsutism/acne/alopecia via androgen suppression. Use the lowest effective oestrogen dose (e.g. 20–30mcg ethinyloestradiol or equivalent); extended/continuous use minimises withdrawal bleeding. No clear evidence favours a specific progestogen, though anti-androgenic progestogens are second-line as per general population guidance.
• If COC contraindicated: 52mg levonorgestrel IUD (endometrial protection + contraception, replace 5-yearly), or another second-line endometrial-protection option.
• Oral cyclical progestogen: short-term option only if COC/LNG-IUD unsuitable — less effective, doesn’t address hyperandrogenism, poorly tolerated, and risks hypoestrogenism with long-term use.
• Metformin is NOT recommended for menstrual regulation (poor bleeding control, inadequate endometrial protection) — its role is limited to subfertility.
• Investigate heavy/irregular bleeding that persists despite 6 months of therapy (or earlier if other cancer-risk features) to exclude endometrial cancer; consider semi-urgent gynaecology referral if indicated.

Hyperandrogenism (hirsutism, acne, alopecia)

• COC first-line (as above).
• Cosmetic measures (laser, electrolysis, eflornithine cream — not PBS-subsidised, ~$90/30g tube, takes 6–8 weeks) alongside COC for at least 6 months.
• Spironolactone as an add-on after 6–12 months of COC + cosmetic therapy if hirsutism goals aren’t met, or usable alone with reliable contraception (teratogenic): hirsutism 100mg → 200mg daily; acne 25–50mg → up to 50–100mg daily. Check potassium at 1 month (no need to repeat unless renal impairment develops or a potassium-sparing agent like an ACE inhibitor is started); reassess at 6 months or refer to dermatology.

Metabolic / cardiovascular screening

• Screen all women with PMOS for glucose dysregulation at diagnosis and every 1–3 years: fasting glucose, HbA1c, or OGTT. OGTT preferred if high-risk (BMI >25kg/m² [>23 for Asian ethnicity], impaired fasting glucose/IGT, family history of diabetes, prior gestational diabetes, hypertension, high-risk ethnicity) or contemplating pregnancy.
• Pregnant women with PMOS: OGTT before 20 weeks, repeated at 24–28 weeks.
• Assess cardiovascular risk factors in every woman with PMOS (dyslipidaemia, weight, BP) — an explicit recommendation regardless of diabetes status, reflecting the significantly elevated composite CVD/MI/stroke risk in this population.
• Assess psychological wellbeing at every review; refer for mental health support as needed.

Metformin

Consider for:

• High risk of type 2 diabetes (even with normal glucose tests)
• Subfertility with irregular cycles despite lifestyle change
• BMI >25 with insufficient weight loss after a 6-month lifestyle trial (doesn’t cause weight loss itself, but may prevent further gain); most benefit seen at BMI <30

Dosing: immediate-release 250mg BD with food initially, increasing by 500mg/week to a maximum of 2.5g/day in adults (2g/day in adolescents) in divided doses, or extended-release preparations to minimise gastrointestinal side-effects.

Subfertility

PMOS is the most common cause of anovulatory infertility.

• First-line: lifestyle changes (diet/exercise/weight loss, aiming for BMI <25 over ~6 months if age <36); folic acid + iodine; smoking cessation. Even 5% weight loss can restore regular cycles and ovulation.
• Refer for ovulation induction (e.g. letrozole/clomiphene) if lifestyle measures fail — metformin can be used as a bridge while awaiting specialist review, and adds benefit when combined with ovulation-induction agents, but is less effective alone. If BMI >30, refer for clomiphene instead of or alongside metformin.
• Bariatric surgery may be considered for BMI >40 (or >35 with obesity-related comorbidity), but pregnancy should be deferred ≥12 months post-surgery and benefit on fertility itself is unclear.