01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Androgens convert fine vellus hair into coarse terminal hair in genetically sensitive follicles. The same circulating androgen concentration can produce different visible hair according to age, ethnicity, follicular sensitivity and prior removal. A modified Ferriman–Gallwey score can structure examination but should not overrule the individual's distress or under-recognise hair removed before review.
Virilisation is more than hirsutism. Voice deepening, clitoral enlargement, breast atrophy, rapid scalp recession, marked muscularity or erythrocytosis suggests stronger or more abrupt androgen exposure. Ovarian tumours and hyperthecosis may raise testosterone, while adrenal tumours can produce adrenal androgens; patterns overlap, so imaging follows specialist biochemical confirmation rather than a simplistic single-marker rule.
The central decision is whether the presentation is a common chronic phenotype suitable for outpatient symptom management or severe androgen excess needing urgent tumour-focused investigation. Once the cause is addressed, treatment should combine hair removal, hormonal suppression when appropriate, metabolic and menstrual care, and psychological support without describing the concern as merely cosmetic.
Key points
- Hirsutism is terminal hair growth in androgen-dependent areas; hypertrichosis is diffuse non-androgen-pattern hair growth and has a different medicine and systemic differential.
- PCOS is the commonest cause of hirsutism, but rapid tempo, virilisation, postmenopausal onset or severe laboratory abnormality must not be squeezed into that diagnosis.
- Ask how quickly hair changed, what removal methods conceal, whether cycles altered, and whether voice, scalp hair, muscles, libido or genital anatomy changed.
- Measure testosterone with a reliable method and sex hormone-binding globulin, then use the 2025 Society for Endocrinology androgen-excess pathway for additional ovarian, adrenal and dynamic tests.
- Hormonal contraception changes ovarian production and sex hormone-binding globulin; record it and involve specialists before stopping essential contraception solely to obtain an ideal sample.
- Non-classic congenital adrenal hyperplasia, Cushing syndrome, severe insulin resistance, ovarian hyperthecosis, medicines and androgen exposure are important alternatives to PCOS.
- Hair removal is legitimate treatment at every stage; shaving does not increase follicle number or make biological androgen excess worse.
- Medical improvement takes at least several hair cycles, so define a six-month or longer review and pair androgen suppression with the person's chosen physical method.
- Systemic anti-androgens can affect development of a male fetus and require reliable pregnancy prevention, clear off-label consent and medicine-specific monitoring.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Polycystic ovary syndrome
Chronic ovarian androgen excess with irregular ovulation is a common cause of gradually progressive terminal hair growth.
Follicular sensitivity
Some people develop substantial hirsutism at circulating androgen concentrations that remain within the population range because hair follicles respond more strongly.
Severe ovarian or adrenal androgen excess
Ovarian tumours, hyperthecosis, adrenal tumours or congenital adrenal hyperplasia can produce higher or more rapidly rising androgen exposure.
Exogenous androgenic exposure
Prescribed hormones, supplements or indirect household contact can increase androgen effect and should be sought sensitively before invasive localisation.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Follicles receive androgen signal
Androgens convert fine vellus hair into coarse pigmented terminal hair in androgen-sensitive skin regions as the process continues.
- 2Hair growth becomes clinically visible
Repeated follicular cycling makes progression gradual, while ethnicity, age and previous hair removal alter how severity appears on examination.
- 3Higher exposure causes virilisation
Strong or rapidly rising androgen action affects voice, clitoris, scalp hair, muscle and breast tissue beyond the hair follicle alone.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Gradual terminal hair growth from adolescence with irregular cycles, acne and no virilisation commonly accompanies PCOS, but exclusion and metabolic assessment remain necessary.
Regular ovulatory cycles and normal androgen measurements can coexist with clinically important hair through follicular sensitivity; this is a diagnosis after appropriate assessment.
Change over months with deep voice, clitoromegaly, accelerated scalp loss or muscle change is a tumour or severe androgen-excess red flag rather than routine PCOS.
New or rapidly worsening hirsutism after menopause raises concern for ovarian hyperthecosis or an androgen-secreting ovarian or adrenal lesion and needs specialist review.
Androgen excess with an adrenal mass, bruising, proximal weakness, broad purple striae, hypertension or hypokalaemia may indicate adrenal tumour or Cushing syndrome.
Long-standing androgen features, early pubic hair, family or ethnic risk and raised 17-hydroxyprogesterone suggest non-classic 21-hydroxylase deficiency requiring endocrine confirmation.
Extensive acanthosis nigricans, dysglycaemia, lipodystrophy or striking hyperandrogenism suggests a severe insulin-resistance syndrome beyond common PCOS.
Anabolic steroids, testosterone gels transferred from a household member, supplements or compounded hormones can virilise; ask non-judgementally about prescribed, private and performance-enhancing products.
05InvestigationsWhat to request, why it matters and how to interpret it.
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
Total testosterone by validated assayFirst step - Why
- Confirm androgen excess and identify a result severe enough to accelerate specialist assessment.
- Interpretation and limitations
- Use the laboratory reference range and Society for Endocrinology pathway rather than a memorised universal cut-off. Repeat a discordant or severe result with high-quality mass-spectrometry methodology where available.
- 02
Sex hormone-binding globulin and calculated free androgen measure - Why
- Interpret biologically available androgen when binding protein varies.
- Interpretation and limitations
- Low SHBG with insulin resistance can increase calculated free androgen despite modest total testosterone; combined contraception raises SHBG and changes interpretation. Use the laboratory's validated calculation.
- 03
DHEAS and androstenedione - Why
- Characterise adrenal and ovarian androgen patterns when initial assessment warrants expansion.
- Interpretation and limitations
- Marked adrenal androgen elevation supports adrenal investigation but is not perfectly source specific. Coordinate imaging with the full biochemical phenotype rather than localising from one analyte.
- 04
Early-morning 17-hydroxyprogesterone - Why
- Screen for non-classic congenital adrenal hyperplasia.
- Interpretation and limitations
- Sample timing, menstrual phase and assay matter. An abnormal or borderline value requires endocrinology-directed confirmatory stimulation testing; do not diagnose from one untimed result.
- 05
Pregnancy test, prolactin and thyroid function - Why
- Exclude pregnancy and common endocrine explanations for associated cycle disturbance.
- Interpretation and limitations
- Select testing from pregnancy possibility and menstrual symptoms. Repeat prolactin appropriately and review medicines before pituitary imaging; thyroid disease rarely explains isolated severe virilisation.
- 06
Targeted cortisol testing - Why
- Investigate Cushing syndrome when discriminatory clinical features accompany androgen excess.
- Interpretation and limitations
- An endocrinologist selects late-night salivary cortisol, overnight dexamethasone suppression or urine testing according to context. Random serum cortisol is not a screening test.
- 07
Pelvic ultrasound or cross-sectional ovarian imaging - Why
- Identify an ovarian mass or hyperthecosis after clinical and biochemical triage.
- Interpretation and limitations
- Small androgen-producing tumours can be difficult to see and a negative ultrasound does not end evaluation in severe virilisation. Specialist teams choose MRI or further localisation when needed.
- 08
Adrenal CT or MRI - Why
- Evaluate a suspected adrenal androgen source and stage a concerning mass.
- Interpretation and limitations
- Reserve imaging for a supported biochemical or clinical indication to avoid incidentalomas. A suspicious mass needs urgent endocrine, radiology and adrenal multidisciplinary review.
- 09
Metabolic profile and blood pressure - Why
- Detect dysglycaemia, dyslipidaemia and fatty-liver risk associated with PCOS or severe insulin resistance.
- Interpretation and limitations
- Assess HbA1c or glucose, lipids, liver risk and blood pressure according to phenotype; metabolic normality does not negate distress or a tumour red flag.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Hypertrichosis
Diffuse non-androgen-pattern hair growth, often medicine-related, affects areas outside the usual androgen-sensitive distribution and lacks virilisation.
Polycystic ovary syndrome
Slow progression with irregular cycles, acne and metabolic features supports PCOS after thyroid, prolactin and severe androgen disorders are excluded.
Androgen-secreting tumour
Rapid onset, voice deepening, clitoral enlargement or marked biochemical elevation raises concern for an ovarian or adrenal tumour.
Non-classic congenital adrenal hyperplasia
A longstanding adrenal androgen pattern, relevant family background and abnormal steroid precursors distinguish this from idiopathic or ovarian disease.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01TriageHirsutism without virilisationFirst stepSlowly progressive unwanted terminal hair with no rapid systemic or genital change.+
- 1Document onset, tempo, cycle and pregnancy history, medicines and supplements, removal practices, family pattern and psychosocial impact; examine androgen distribution, scalp, skin, blood pressure and Cushing features.
- 2Measure validated testosterone and SHBG and screen selected mimics with pregnancy testing, thyroid, prolactin and early-morning 17-hydroxyprogesterone according to the clinical pattern.
- 3If findings fit PCOS, complete its menstrual, metabolic and fertility assessment; if hormones are normal with regular cycles, consider idiopathic follicular sensitivity after review.
- 4Offer physical hair removal immediately and agree whether hormonal or topical treatment is desired, with a realistic response interval and safety review.
02Red flagVirilisation or severe biochemical excessRapid progression, virilisation, postmenopausal onset, mass or marked androgen result.+
- 1Repeat and confirm unexpected androgen results promptly using a reliable assay while taking a focused examination and exposure history; do not delay urgent referral for obvious virilisation.
- 2Measure the specialist androgen panel and targeted cortisol or tumour markers under the Society for Endocrinology pathway, avoiding indiscriminate low-yield tests.
- 3Use pelvic and adrenal imaging sequenced by the biochemical pattern and specialist team; recognise that a small ovarian tumour may be occult on first ultrasound.
- 4DefinitiveRefer suspected tumour to the appropriate endocrine, gynaecological oncology or adrenal multidisciplinary service for definitive localisation and treatment.
03TreatLong-term unwanted-hair managementSerious causes have been excluded or treated and the person wants symptom reduction.+
- 1Discuss shaving, waxing, depilation, electrolysis and laser or light treatment, considering skin tone, hair colour, access, burns and post-inflammatory pigment change.
- 2Offer eflornithine for suitable facial hair and a combined hormonal contraceptive when desired and medically eligible, explaining that existing hair still needs removal.
- 3If distress persists after an adequate trial, seek specialist advice on spironolactone or another anti-androgen with reliable contraception and appropriate renal, potassium or liver monitoring.
- 4Photograph or score only with consent, review after several hair cycles and stop ineffective medicines while continuing valued physical methods.
04ExposureMedicine or exogenous androgen causeTemporal relationship to anabolic agents, testosterone transfer or a prescribed medicine associated with hair change.+
- 1Clarify the exact product, source, dose pattern, application site and household exposure without judgement, including private and online products not on the NHS record.
- 2Stop avoidable exposure safely or prevent secondary gel transfer through washing, covering and product-specific precautions, involving the original prescriber when treatment remains necessary.
- 3Assess gonadal axis, liver, lipids, full blood count and fertility consequences according to the exposure and refer endocrine or substance-use services when withdrawal or recovery is complex.
- 4Track biochemical and clinical resolution over months; persistent virilisation still requires endogenous tumour evaluation.
Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
Eflornithine cream
Apply a thin layer to affected facial skin twice daily following the licensed interval and application instructions.Skin irritation and acne can occur; avoid broken skin and eyes. It is not a depilatory, takes weeks to work and loses benefit after discontinuation.
Combined hormonal contraceptive
Choose a licensed formulation and regimen under UK contraceptive eligibility guidance after individual risk assessment.Review thrombosis, migraine with aura, smoking, hypertension and interactions. It changes androgen laboratory results and cannot be used when pregnancy is actively sought.
Spironolactone
Use the specialist-agreed off-label regimen with baseline and follow-up potassium and renal function.Ensure reliable contraception because fetal anti-androgen effects are possible. Avoid significant hyperkalaemia risk and review hypotension, renal impairment and interacting medicines.
Finasteride specialist anti-androgen
Prescribe only the specialist-selected off-label schedule with robust pregnancy-prevention arrangements.Exposure in pregnancy can harm development of a male fetus; tablets should not be handled crushed during pregnancy. Review sexual, mood and hepatic considerations and stop if ineffective.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Delayed tumour diagnosis
Treating rapidly progressive virilisation as routine PCOS can postpone identification of an aggressive ovarian or adrenal source.
Endometrial risk
When hirsutism accompanies chronic anovulation, prolonged unopposed oestrogen can increase endometrial hyperplasia and irregular bleeding risk.
Psychological burden
Unwanted hair, repeated removal and virilising change can affect body image, relationships and mental health and should not be dismissed as cosmetic.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Review hair progression, new virilisation, menstrual pattern and systemic symptoms; any acceleration overrides the planned routine interval.
- Assess treatment benefit after at least six months where safe, because hair cycles make early changes unreliable; include patient-reported distress rather than clinician appearance alone.
- For spironolactone, monitor potassium, renal function, blood pressure, pregnancy prevention and interacting medicines at the locally specified interval.
- For combined contraception, review blood pressure, thrombosis risk, migraine, smoking and adherence according to UK contraceptive standards.
- When androgen excess reflects PCOS or insulin resistance, monitor glucose risk, lipids, blood pressure, sleep and endometrial protection separately from cosmetic response.
- After tumour or exposure treatment, trend the relevant androgen panel with the specialist service and recognise that voice or clitoral changes may not fully reverse.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Hair removal does not confound dignity
People may remove nearly all visible hair before examination. Ask what would be present without treatment and never require regrowth solely to validate distress.
Tempo beats hair count
A modest distribution changing rapidly with voice or genital signs can be more dangerous than extensive stable familial hair present for years.
Assays matter greatly
Female-range testosterone challenges some immunoassays. A severe discordant result deserves confirmation with a high-quality method, not dismissal or automatic imaging alone.
Source markers overlap
DHEAS favours adrenal production and testosterone may favour ovarian production, but neither localises perfectly; specialist synthesis prevents false certainty.
Shaving does not multiply follicles
A blunt cut makes regrowth feel coarse but does not turn vellus follicles into androgen-sensitive terminal follicles or worsen the endocrine disorder.
Anti-androgens need contraception
Irregular cycles do not equal infertility. Systemic blockade can affect a male fetus, so pregnancy prevention is an essential part of prescribing.
Cosmetic is not trivial
Unwanted hair can affect employment, relationships, identity and mental health. Treating it alongside metabolic or tumour assessment is legitimate clinical care.
11Common pitfallsFrequent interpretation and management errors.
- 01
Calling all unwanted hair hirsutism without distinguishing hypertrichosis.
- 02
Diagnosing PCOS before asking about rapid progression and virilisation.
- 03
Using one unreliable testosterone assay to localise a tumour.
- 04
Ordering adrenal imaging for every mild hair complaint and creating incidentalomas.
- 05
Stopping contraception unsafely merely to obtain ideal androgen tests.
- 06
Starting spironolactone or finasteride without pregnancy prevention.
- 07
Promising visible improvement within a few weeks.
- 08
Dismissing severe psychosocial impact because no malignancy is found.