Polycystic ovary syndrome

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

PCOS reflects interacting ovarian androgen production, altered gonadotrophin signalling and insulin resistance, with wide phenotypic variation. Some people present with infrequent bleeding, others with hirsutism, acne or difficulty conceiving, and some have few metabolic features. The ovarian follicles are not dangerous cysts requiring removal. Diagnosis is syndromic and requires active exclusion of pregnancy, thyroid dysfunction, hyperprolactinaemia, non-classic congenital adrenal hyperplasia and severe androgen disorders.

The consequences extend beyond fertility. Chronic anovulation can expose the endometrium to unopposed oestrogen, while dysglycaemia, sleep apnoea, fatty liver risk, anxiety, depression, eating disorders and body-image distress may coexist. Absolute cardiovascular-event evidence varies, so assess established risk factors rather than making deterministic predictions from the label.

The central decision is whether the presentation fits common PCOS or contains a clue to a tumour or another endocrine disorder, then which health goal matters now. A person can need contraception despite irregular ovulation, or fertility care despite intermittent bleeding; assumptions about pregnancy intentions, gender or sexual activity create preventable harm.

Key points

PCOS is a heterogeneous endocrine-metabolic syndrome, not an ultrasound description; polycystic ovarian morphology alone does not establish the diagnosis.
In adults, diagnose after excluding mimics when two of ovulatory dysfunction, clinical or biochemical hyperandrogenism, and polycystic ovarian morphology are present under the current guideline framework.
In adolescents, normal pubertal irregularity and multifollicular ovaries create overdiagnosis; require persistent cycle disturbance plus hyperandrogenism and use specialist age-from-menarche criteria rather than adult shortcuts.
Rapid progression, voice deepening, clitoromegaly, increased muscle bulk or severe biochemical androgen excess is not typical uncomplicated PCOS and needs urgent endocrine imaging pathways.
Long gaps without endometrial shedding increase hyperplasia risk; offer reliable cycle control or progestogen exposure even when contraception is not required.
Assess blood pressure, glucose status, lipids, sleep, weight trajectory, smoking and family cardiovascular risk without assuming that everyone with PCOS has obesity or insulin resistance.
Treatment follows the person's goal: menstrual and endometrial protection, unwanted hair or acne, metabolic health, contraception, fertility or psychological wellbeing.
Lifestyle support should be weight-neutral and stigma-aware where appropriate; clinically useful nutrition, movement and sleep interventions benefit health even without weight loss.
NHS public terminology moved toward polyendocrine metabolic ovarian syndrome in 2026 while established guidance and this route retain PCOS; check final current NICE wording and do not treat a consultation draft as enacted guidance.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Ovarian androgen dysregulation

Altered ovarian steroid production and gonadotrophin signalling increase androgen exposure and disrupt coordinated follicle maturation in susceptible patients.

Insulin resistance

Higher insulin concentrations can amplify ovarian androgen production and reduce sex-hormone-binding proteins, although metabolic severity varies widely.

Inherited and environmental susceptibility

Family pattern, body composition and wider metabolic context interact rather than one cyst or single hormone abnormality causing every phenotype.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Androgen activity increases
Ovarian androgen production and altered binding increase follicular and skin exposure, contributing to hirsutism and acne.
2
Follicle development becomes disordered
Multiple follicles begin development without reliably reaching ovulation, producing irregular or absent cycles and the characteristic ovarian appearance in some patients.
3
Progesterone exposure becomes intermittent
Infrequent ovulation reduces cyclical progesterone, leaving the endometrium exposed to continuing oestrogen without regular organised shedding.
4
Metabolic risks may cluster
Insulin resistance can coexist with dysglycaemia, sleep apnoea, fatty liver risk and adverse lipid or blood-pressure profiles.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Ovulatory dysfunction

Persistently long, irregular or absent cycles suggest infrequent ovulation, but pregnancy, lactation, hormonal contraception, perimenopause, energy deficit and chronic illness must be considered first.

Clinical hyperandrogenism

Terminal hair in androgen-sensitive sites, acne or scalp hair thinning may reflect androgen excess; severity, ethnicity, hair-removal practices and personal distress affect clinical recognition.

Biochemical hyperandrogenism

Raised total or calculated free testosterone supports androgen excess when measured with a reliable assay, but hormonal contraception and altered sex hormone-binding globulin can distort interpretation.

Metabolic phenotype

Acanthosis nigricans, central adiposity, hypertension, dysglycaemia, obstructive sleep apnoea or metabolic liver disease indicates higher metabolic burden but is not required for diagnosis.

Endometrial riskRed flag

Very infrequent bleeding, prolonged amenorrhoea, persistent abnormal bleeding or a thickened endometrium increases concern for hyperplasia and requires a protection and investigation plan.

Androgen red flagRed flag

Rapid onset over months, postmenopausal presentation, deep voice, clitoromegaly, marked muscle change or a severe laboratory elevation suggests ovarian or adrenal pathology rather than routine PCOS.

Psychological burden

Depression, anxiety, disordered eating, weight stigma, sexual distress and unwanted-hair burden can be more disabling than laboratory abnormalities and should be assessed directly.

Adolescent uncertainty

Irregular cycles soon after menarche and multifollicular ovarian appearance can be physiological; premature labelling may cause lifelong anxiety, while persistent combined features merit review and support.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Pregnancy testFirst step
Why
Exclude the commonest physiological cause of absent or irregular bleeding before endocrine interpretation.
Interpretation and limitations
Test according to pregnancy possibility rather than stated fertility intention alone. Pain, bleeding, syncope or haemodynamic change needs the urgent early-pregnancy pathway even with PCOS.
02
Total testosterone and sex hormone-binding globulin
Why
Confirm and quantify biochemical androgen excess using a validated laboratory method.
Interpretation and limitations
Calculate or report free androgen status as locally validated. Repeat unexpected severe results with a high-quality assay and escalate rapidly rather than assuming PCOS; combined contraception changes SHBG and results.
03
Thyroid-stimulating hormone and prolactin
Why
Exclude thyroid dysfunction and hyperprolactinaemia as alternative causes of cycle disturbance.
Interpretation and limitations
Repeat prolactin under appropriate resting conditions and review medicines, pregnancy, renal function and macroprolactin according to the laboratory pathway before pituitary imaging.
04
Early-morning 17-hydroxyprogesterone
Why
Screen for non-classic congenital adrenal hyperplasia when androgen excess is being evaluated.
Interpretation and limitations
Timing, cycle phase and assay reference range matter; an abnormal result requires endocrine confirmation and dynamic testing rather than treatment from one value.
05
Pelvic ultrasound
Why
Assess ovarian morphology and endometrium when imaging contributes to diagnosis or investigates bleeding and pain.
Interpretation and limitations
Use current age and time-from-menarche criteria. Ultrasound is unnecessary when adult ovulatory dysfunction and hyperandrogenism already establish the syndrome, and morphology alone is not PCOS.
06
HbA1c or oral glucose tolerance assessment
Why
Detect dysglycaemia and establish metabolic risk using the current PCOS pathway.
Interpretation and limitations
Choose the test and interval from guideline risk factors, pregnancy planning and prior results. A normal fasting glucose alone may miss impaired glucose tolerance.
07
Blood pressure and lipid profile
Why
Identify treatable cardiovascular risk without making weight-based assumptions.
Interpretation and limitations
Interpret with age, smoking, family history, diabetes and pregnancy plans and manage through current primary-prevention guidance rather than a PCOS-specific unvalidated score.
08
Targeted cortisol or adrenal imaging pathway
Why
Investigate Cushing syndrome or an androgen-secreting lesion only when clinical or biochemical red flags exist.
Interpretation and limitations
Endocrine specialists select the appropriate cortisol test and ovarian or adrenal imaging sequence. Indiscriminate testing creates false positives, but rapid virilisation must not wait.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Pregnancy

Pregnancy remains an immediate explanation for absent bleeding and can occur despite irregular ovulation, so context must be confirmed.

Non-classic congenital adrenal hyperplasia

Abnormal adrenal steroid precursors and relevant family or childhood features suggest an inherited adrenal androgen disorder rather than PCOS.

Hyperprolactinaemia or thyroid disease

Raised prolactin or abnormal thyroid feedback can disrupt cycles and should be excluded before a syndromic PCOS diagnosis.

Androgen-secreting tumour

Rapid virilisation, voice change, clitoral enlargement or marked biochemical androgen excess requires urgent ovarian and adrenal evaluation.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01DiagnoseAdult PCOS assessmentFirst stepPersistent irregular cycles, hirsutism, acne or biochemical androgen excess in an adult.

1Clarify cycle pattern, pregnancy possibility, medications, hair progression, weight trajectory, sleep, mood, eating, fertility goals and red-flag virilisation; examine blood pressure, androgen signs and thyroid or Cushing features.
2Exclude pregnancy and common mimics with testosterone and SHBG, thyroid testing, prolactin and early-morning 17-hydroxyprogesterone, adding specialist tests only when indicated.
3Apply the current diagnostic criteria; use ultrasound only if it contributes and explain that ovarian morphology alone is neither dangerous nor diagnostic.
4EscalationDocument the phenotype, endometrial and metabolic risks, psychological needs and the individual's priorities, then agree a review and escalation plan.

02ProtectInfrequent bleeding and endometrial safetyLong or unpredictable gaps between spontaneous bleeds without current desire to conceive.

1Exclude pregnancy and investigate persistent, heavy or intermenstrual bleeding according to age and risk rather than attributing every pattern to PCOS.
2Offer a combined hormonal contraceptive, progestogen-only method, levonorgestrel intrauterine system or scheduled progestogen strategy after checking contraindications and preferences.
3Explain that bleeding induced by hormone treatment protects the endometrium but does not prove spontaneous ovulation and that irregular ovulation is not reliable contraception.
4EscalationEscalate persistent abnormal bleeding, anaemia, ultrasound concern or failure of protection to gynaecology for endometrial assessment under the local pathway.

03SymptomsHirsutism and metabolic goalsUnwanted hair, acne, higher metabolic risk or treatment distress after serious androgen causes are excluded.

1Offer respectful hair-removal options and a suitable combined hormonal contraceptive when desired, setting expectations that hair-cycle improvement takes months.
2Consider eflornithine for facial hair and specialist anti-androgen treatment only with reliable pregnancy prevention and adverse-effect monitoring.
3Provide individual nutrition, movement, sleep and smoking support; consider metformin for current metabolic or cycle indications after discussing off-label aspects and gastrointestinal or B12 effects.
4Review glucose, blood pressure, lipids, bleeding pattern, mood and treatment burden, stopping ineffective therapy rather than adding drugs indefinitely.

04FertilityAnovulatory conception pathwayPregnancy is desired and infrequent ovulation is likely after initial assessment of all contributing factors.

1Provide preconception folate, medicine and metabolic review and assess semen and tubal or uterine factors in parallel rather than treating PCOS in isolation.
2Refer according to current NICE NG257 and local access criteria for monitored ovulation induction; oral agents may be off-label and require informed specialist prescribing.
3Use ultrasound and hormone monitoring specified by the fertility service to minimise multiple pregnancy and ovarian hyperstimulation, with explicit cycle cancellation rules.
4EscalationEscalate non-response to specialist gonadotrophin, surgical or assisted-conception options and provide psychological support throughout.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

Provides contraception, predictable endometrial shedding and suppression of ovarian androgen effects on acne and hirsutism.

Combined hormonal contraception

Use a licensed low-risk preparation and schedule selected through the current UK contraceptive eligibility framework.

Assess migraine with aura, thrombosis, smoking, blood pressure and other UKMEC factors. It alters androgen testing and is unsuitable when conception is desired.

Induces withdrawal bleeding and opposes unopposed oestrogen when combined contraception or an intrauterine system is not chosen.

Intermittent oral progestogen

Give the locally recommended course often enough to provide endometrial protection when spontaneous bleeding is infrequent.

Exclude pregnancy first and investigate persistent abnormal bleeding. The regimen does not treat hirsutism, guarantee ovulation or provide contraception unless the selected product is licensed for it.

Improves insulin sensitivity and may support metabolic outcomes and cycle regularity in selected people with PCOS.

Metformin

Start low with food and titrate gradually to the tolerated formulary dose for the agreed indication.

Discuss gastrointestinal effects and off-label use where relevant; check renal function, pause during severe dehydration or hypoxia and monitor vitamin B12 risk during long-term treatment.

Slows new facial terminal-hair growth while physical removal continues during the delayed treatment response.

Eflornithine facial cream

Apply a thin layer to affected facial areas using the licensed twice-daily instructions.

Avoid broken skin and contact with eyes; irritation can occur. It does not remove existing hair, and benefit is lost after stopping.

Reduces androgen action and may improve troublesome hirsutism when cosmetic and first-line hormonal measures are insufficient.

Spironolactone specialist anti-androgen

Use only the specialist-selected regimen after baseline renal and potassium assessment with reliable contraception.

Potential fetal anti-androgen effect means pregnancy prevention is essential. Monitor potassium and renal function, avoid relevant interactions and stop if benefit does not justify burden.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Endometrial hyperplasia

Chronic anovulation and prolonged unopposed oestrogen increase endometrial proliferation, causing irregular bleeding and raising the risk of hyperplasia and endometrial cancer.

Subfertility

Infrequent or unpredictable ovulation reduces conception opportunities; structured ovulation assessment and cause-specific fertility treatment can address the principal mechanism.

Dysglycaemia and metabolic disease

Insulin resistance increases risk of prediabetes, type 2 diabetes and associated cardiovascular and fatty-liver risk factors.

Psychological burden

Hirsutism, acne, weight stigma, fertility concerns and cycle unpredictability can contribute to anxiety, depression, disordered eating and body-image distress.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record cycle length and any unscheduled, heavy or postcoital bleeding, confirming that endometrial protection is actually being delivered rather than merely prescribed.
Review blood pressure, glucose risk, lipids, smoking, sleep apnoea symptoms and family history at a risk-based interval; do not use BMI as the sole gatekeeper for screening.
Assess hirsutism or acne response only after an adequate hair-cycle interval and ask about distress, skin effects, contraception and medicine adherence.
Revisit pregnancy intentions at every relevant review because irregular ovulation neither guarantees infertility nor protects against unplanned pregnancy.
Screen for depression, anxiety, disordered eating and weight stigma and offer appropriate psychological or eating-disorder services rather than framing distress as non-adherence.
In adolescents, reassess diagnostic certainty over time, avoiding both a permanent premature label and loss to follow-up when persistent hyperandrogenism or cycle dysfunction remains.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Follicles are not dangerous cysts

The ultrasound appearance reflects arrested follicles and does not imply ovarian tumours, inevitable pain or a need for surgical removal.

Two features can suffice

In an adult with well-established ovulatory dysfunction and hyperandrogenism after exclusions, ultrasound may add cost and incidental findings without changing the diagnosis.

Irregular does not mean infertile

Ovulation can occur unpredictably. Offer contraception when pregnancy is not desired and assess all fertility factors when it is.

Hair treatment takes time

Terminal hairs already present must complete their cycle; medicines slow new androgen-driven growth and work best alongside the person's chosen removal method.

Endometrium needs a plan

A person unconcerned by infrequent bleeding may still need progestogen exposure or a hormonal method to reduce prolonged unopposed oestrogen.

Lean phenotype still exists

Absence of higher weight does not rule out PCOS or remove glucose and psychological assessment; care should follow phenotype and risk, not stereotype.

Names are changing

The 2026 NHS use of PMOS reflects concern that PCOS under-describes systemic features. Stable care depends on current final guidance, not on assuming a new name changes diagnostic criteria overnight.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing PCOS from an ultrasound report alone.
02
Using adult ultrasound criteria during normal adolescent pubertal transition.
03
Missing pregnancy in a person told that irregular periods mean infertility.
04
Attributing rapid virilisation or a severe testosterone result to common PCOS.
05
Ignoring prolonged amenorrhoea because bleeding is not bothersome.
06
Offering weight loss as the only treatment and overlooking mood, sleep and endometrial risk.
07
Starting an anti-androgen without reliable pregnancy prevention.
08
Quoting a 2026 NICE consultation draft as though it were final guidance.