Hirsutism and hypertrichosis

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

Hair quantity becomes a medical presentation when growth is new, changing, associated with systemic features or unwanted by the person. Hirsutism is a pattern diagnosis based on terminal pigmented hair in androgen-responsive areas, not a judgement about femininity or ethnicity. Hypertrichosis may be localised or generalised and involves sites not primarily driven by androgen. Distinguishing them directs the history: menstrual and virilisation questions for hirsutism, and congenital, medicine, nutritional, porphyria and systemic review for hypertrichosis.

PCOS is the most common pathological context for hirsutism, yet the serious-disease gate is tempo. A new deep voice, clitoral enlargement, rapid muscle change, temporal recession or severe androgen result over months raises an ovarian or adrenal source even if a first ultrasound is normal. Combined hormonal contraception changes androgen production and binding proteins, so timing and interpretation of blood tests should be agreed rather than stopping contraception unsafely merely to obtain a sample.

Treatment runs in parallel with diagnosis. Physical removal provides immediate control and should not be withheld until endocrine tests finish. Medicines alter new growth over several cycles, so existing terminal hair still needs removal and meaningful review takes six months or longer. Laser parameters must reflect hair colour and skin pigmentation; darker skin carries a higher burn and post-inflammatory pigment risk when an unsuitable device or operator is used.

Key points

Hirsutism means coarse terminal hair in androgen-dependent sites such as chin, upper lip, chest, lower abdomen and back; hypertrichosis is excess hair outside that sexual distribution.
Ask what has changed from the person's baseline and what removal methods conceal. Hair density varies normally by family and ancestry, so a visual score is not a universal disease threshold.
Slowly progressive hirsutism with irregular cycles, acne or metabolic features commonly reflects PCOS, but normal cycles and hormones can coexist with idiopathic follicular androgen sensitivity.
Rapid virilisation, marked androgen elevation, an abdominal or pelvic mass and postmenopausal onset are tumour or ovarian-hyperthecosis warnings and need expedited specialist assessment.
Hypertrichosis can be congenital or follow minoxidil, ciclosporin, phenytoin, glucocorticoids, malnutrition, porphyria or systemic disease; the distribution and timeline determine investigation.
Measure total testosterone with a validated assay and sex hormone-binding globulin when androgen excess is plausible, then extend adrenal or ovarian tests through a specialist pathway rather than ordering an indiscriminate panel.
Shaving does not increase follicle number or make androgen excess worse. Waxing, depilation, electrolysis and laser are legitimate treatments while the cause is investigated.
Eflornithine slows facial hair growth but does not remove existing hair; apply twice daily at least eight hours apart and discontinue if no benefit after four months.
Systemic anti-androgens are off-label for hirsutism in the UK and require reliable pregnancy prevention plus medicine-specific renal, potassium, hepatic and interaction safeguards.

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

Polycystic ovary syndrome

Chronic ovarian androgen excess and insulin-related signalling make PCOS the commonest pathological cause of slowly progressive hirsutism before menopause.

Idiopathic follicular sensitivity

Terminal facial or body hair can increase despite regular cycles and androgen results within range because follicular response varies genetically.

Severe ovarian or adrenal excess

Androgen-secreting tumours, ovarian hyperthecosis, non-classic adrenal hyperplasia and Cushing syndrome can cause rapid hirsutism or virilisation.

Hypertrichosis drivers

Congenital traits, minoxidil, ciclosporin, phenytoin, glucocorticoids, malnutrition, porphyria and systemic illness increase hair outside an androgen distribution.

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

1
Vellus hair becomes terminal
Androgen signalling enlarges susceptible follicles and produces longer, coarser, pigmented hair in sexually responsive facial and body sites.
2
Local conversion varies
Follicular enzymes convert testosterone to more potent dihydrotestosterone to differing degrees, explaining variable hair despite similar circulating concentrations.
3
Growth phase is prolonged
Hypertrichosis-inducing medicines and systemic states can extend anagen or alter cycling across nonsexual sites without biochemical androgen excess.
4
Suppression takes several cycles
Hormonal or topical treatment affects new production rather than removing existing shafts, so visible benefit develops slowly alongside physical removal.

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

Androgen-dependent terminal hair

Coarse pigmented hair over upper lip, chin, chest, lower abdomen, back or inner thighs fits hirsutism when increased from baseline.

Generalised nonsexual growth

Excess hair over forearms, forehead, trunk or other non-androgen distribution supports hypertrichosis and shifts attention toward medicines or systemic illness.

PCOS constellation

Gradual hirsutism with irregular ovulation, acne, central metabolic risk or infertility supports PCOS after appropriate exclusion of mimics.

VirilisationRed flag

Deep voice, clitoral enlargement, rapid temporal recession, increased muscle bulk or reduced breast tissue indicates androgen effect beyond ordinary hirsutism.

Medicine-shaped timeline

Diffuse growth after minoxidil, ciclosporin, phenytoin, systemic corticosteroid or an exogenous androgen exposure supports a pharmacological cause.

Porphyria pattern

Facial hypertrichosis with fragile blistering sun-exposed hands, milia or dark urine raises porphyria cutanea tarda and needs a specific pathway.

Red flags requiring action

Rapid progression over months, deepening voice, clitoromegaly, increased muscle bulk, temporal scalp recession, severe biochemical androgen excess or new postmenopausal hirsutism requires urgent endocrine and gynaecological or adrenal localisation.

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
Total testosterone by validated assayFirst step
Why
Confirm biochemical androgen excess and identify a result requiring faster specialist localisation.
Interpretation and limitations
Interpret against the laboratory range, cycle and hormonal medicines; repeat a discordant or severe result with high-quality methodology without delaying obvious virilisation referral.
02
Sex hormone-binding globulin and free-androgen measure
Why
Estimate biologically available androgen when binding protein is altered.
Interpretation and limitations
Insulin resistance can lower SHBG and contraception can raise it; use a validated calculation and do not interpret the index outside its analytical limits.
03
DHEAS, androstenedione and early-morning 17-hydroxyprogesterone
Why
Characterise adrenal contribution and screen selected patients for non-classic congenital adrenal hyperplasia.
Interpretation and limitations
Sampling time, assay and menstrual phase matter. A marked adrenal pattern or abnormal 17-hydroxyprogesterone needs endocrinology-led confirmation rather than self-directed imaging.
04
Pregnancy, thyroid and prolactin tests
Why
Assess common reproductive and endocrine explanations for associated cycle change.
Interpretation and limitations
Select from pregnancy possibility and symptoms; mild prolactin elevation should be repeated with medicine and sampling review before pituitary imaging.
05
Targeted cortisol testing
Why
Investigate Cushing syndrome when discriminatory features accompany hair change.
Interpretation and limitations
Endocrinology selects a validated late-night salivary, dexamethasone suppression or urine test; random serum cortisol is not a screening test.
06
Pelvic or adrenal imaging
Why
Localise a supported ovarian or adrenal source after clinical and biochemical triage.
Interpretation and limitations
Small ovarian tumours and hyperthecosis can be occult on initial ultrasound, while indiscriminate adrenal imaging creates incidentalomas; specialists sequence modality from the phenotype.
07
Hypertrichosis-directed tests
Why
Investigate a non-androgen pattern for medicine, nutrition, porphyria or systemic disease.
Interpretation and limitations
Review every prescribed and non-prescribed product first, then select blood count, thyroid, liver, nutritional or porphyrin studies only from associated clinical findings.

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

Normal familial hair pattern

Stable lifelong density matching family pattern without endocrine or systemic change may represent healthy variation rather than disease.

Hypertrichosis

Generalised or non-androgen-site growth, often linked to a medicine or systemic state, does not meet the biological definition of hirsutism.

Virilising androgen excess

Voice, genital, muscle and rapid scalp changes indicate stronger androgen effect and demand urgent localisation beyond routine PCOS care.

Hair-shaft visibility change

Shaving creates a blunt dark tip and weight loss changes contrast, which may make existing hair more noticeable without increased follicle number.

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

01Slow hirsutismDefine androgen context and personal goalsFirst stepTerminal hair has increased gradually without virilisation or a severe systemic feature.

1Document tempo, cycles, pregnancy goals, acne, scalp loss, medicines, supplements, family pattern and removal methods, then examine hair distribution, blood pressure and metabolic or Cushing features.
2Measure validated testosterone and SHBG and select pregnancy, thyroid, prolactin or 17-hydroxyprogesterone tests from the phenotype; complete a PCOS assessment when supported.
3PreferredOffer the person's preferred physical removal immediately and discuss eflornithine or hormonal treatment only after reproductive, vascular and medicine-safety assessment.

02VirilisationLocalise severe androgen excess urgentlyRapid progression, virilisation, postmenopausal onset, a mass or marked androgen result is present.

1Arrange expedited endocrinology and gynaecological assessment, confirm unexpected assays promptly and take a precise exogenous androgen and supplement history.
2Extend ovarian and adrenal biochemistry under the Society for Endocrinology pathway and select pelvic or adrenal imaging from the pattern.
3Continue localisation despite a normal first ultrasound when clinical and biochemical evidence remains strong, because a small ovarian lesion or hyperthecosis may be occult.

03HypertrichosisFollow distribution back to causeExcess hair is generalised or outside androgen-dependent sites without virilisation.

1Distinguish lifelong from acquired growth and map onset against minoxidil, ciclosporin, phenytoin, steroids, supplements, weight loss, blistering photosensitivity and systemic symptoms.
2Discuss changing a suspected medicine with its prescriber rather than stopping essential treatment abruptly, and arrange targeted laboratory investigation when the associated phenotype supports it.
3Provide physical hair-management choices during recovery, explaining that drug-related growth can take months to recede after a safe change.

04Long-term reductionCombine immediate removal with slower suppressionSerious causes have been excluded or treated and unwanted hair remains distressing.

1Compare shaving, waxing, depilatories, electrolysis and laser by pain, cost, permanence, hair colour, skin pigmentation and pigment-change risk without claiming that shaving worsens growth.
2For facial hair, use licensed eflornithine alongside removal when suitable and review after four months; stop if ineffective.
3Seek specialist input before spironolactone or another systemic anti-androgen, secure reliable pregnancy prevention and review after multiple hair cycles with photographs only when consented.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Slows new facial hair growth and complements shaving, waxing or another physical removal method.

Eflornithine 11.5% facial cream

Apply a thin layer to clean dry affected facial skin twice daily at least eight hours apart; wait at least five minutes after hair removal and do not wash the treated area for four hours.

It is not a depilatory. Stop if there is no benefit after four months, avoid eyes and broken skin and review stinging, acne or dermatitis; use in pregnancy or breastfeeding only under current product advice.

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

Missed androgen-secreting disease

Normalising rapid change or stopping after one negative scan can delay treatment of an ovarian or adrenal tumour.

Metabolic and reproductive morbidity

PCOS-associated dysglycaemia, cardiovascular risk, irregular endometrial exposure and fertility concerns require care beyond visible hair reduction.

Treatment-related fetal harm

Systemic anti-androgens can disrupt development of a male fetus, making reliable contraception and pregnancy planning essential.

Skin and psychological injury

Burns, folliculitis, scarring, pigment change, shame and avoidance can follow removal treatment or insensitive clinical communication.

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

Review tempo, menstrual pattern, virilisation signs and androgen results promptly rather than waiting for a routine cosmetic-treatment appointment.
When PCOS is diagnosed, monitor blood pressure, glycaemia, lipids, cycles and endometrial protection through the appropriate reproductive and metabolic pathway.
Assess eflornithine response after four months and discontinue if ineffective; continuing physical removal remains necessary during successful treatment.
For systemic anti-androgen treatment, monitor pregnancy prevention and the medicine-specific renal, potassium, liver, blood pressure and interaction requirements.
Track distress, time spent removing hair, skin irritation and post-inflammatory pigment rather than relying only on a clinician hair score.

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

Pattern precedes laboratory

Androgen-dependent distribution determines whether hormone investigation is relevant; diffuse forearm growth does not become hirsutism because hair is coarse.

Tempo outranks amount

A small but rapidly changing amount with voice or genital change is more concerning than longstanding dense familial growth without virilisation.

Shaving changes the tip

A cut shaft feels blunt and looks darker as it emerges, but shaving does not create new follicles or alter circulating androgen.

Scans can miss small sources

Severe virilisation remains a biochemical and specialist problem after a negative first ultrasound because small ovarian tumours may be difficult to visualise.

Laser safety is pigment aware

Melanin-rich epidermis competes with hair pigment for laser energy, requiring an appropriate device, experienced operator and conservative test settings.

11Common pitfallsFrequent interpretation and management errors.

01
Using ethnicity or a visual hair score alone to define abnormal growth.
02
Calling generalised medicine-induced hypertrichosis PCOS because some facial hair is present.
03
Reassuring rapid postmenopausal virilisation after one normal pelvic ultrasound.
04
Stopping effective hormonal contraception without planning test timing and pregnancy risk.
05
Prescribing an anti-androgen without reliable pregnancy prevention and organ-specific monitoring.
06
Promising laser will be safe or permanent without accounting for skin pigmentation and hair colour.