Hirsutism
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Direct answer
Hirsutism is excess terminal hair in a male-pattern distribution (face, chest, abdomen, back, thighs) in women, scored by the modified Ferriman-Gallwey system — nine body areas graded 0-4, with 8 or more conventionally defining hirsutism — and caused in over 80 per cent of Indian clinic practice by polycystic ovary syndrome, followed by idiopathic hirsutism, non-classic congenital adrenal hyperplasia, Cushing syndrome, androgen-secreting tumours, drugs (minoxidil, phenytoin, anabolic steroids) and hyperprolactinaemia. The workup pairs total testosterone, dehydroepiandrosterone sulphate (an adrenal marker), 17-hydroxyprogesterone (screening for 21-hydroxylase deficiency), prolactin, thyroid function and a pelvic ultrasound; testosterone above 150-200 ng/dL or rapid virilisation (clitoromegaly, voice deepening) triggers tumour search. Treatment combines cosmetic measures, combined oral contraceptives as first-line pharmacotherapy, and anti-androgens such as spironolactone 100 mg daily with contraception cover.
What you must remember
- Ferriman-Gallwey: nine androgen-sensitive areas (upper lip, chin, chest, upper and lower abdomen, upper and lower back including sacrum, upper arm, thigh) each scored 0-4; a modified total of 8 or more defines hirsutism — the number the exam wants.
- Cause hierarchy: polycystic ovary syndrome first (with oligo-anovulation, ultrasound morphology, androgen excess), idiopathic hirsutism second (normal androgens, likely increased 5-alpha-reductase skin sensitivity), then non-classic congenital adrenal hyperplasia, Cushing syndrome, hyperprolactinaemia, acromegaly, and tumours.
- Laboratory set: total testosterone (tumour threshold around 150-200 ng/dL), dehydroepiandrosterone sulphate (adrenal tumour marker above roughly 700 microgram/dL), early-morning 17-hydroxyprogesterone (basal over about 2-4 ng/mL proceeds to ACTH stimulation), prolactin, thyroid-stimulating hormone, and androstenedione where available.
- Red flags for tumour: rapid onset, progression over months, virilisation (clitoromegaly, deepening voice, male-pattern balding, muscle bulk), testosterone or dehydroepiandrosterone sulphate in tumour range, or postmenopausal onset.
- Pharmacotherapy ladder: combined oral contraceptive (e.g., ethinylestradiol with drospirenone or cyproterone acetate) as first line — suppresses ovarian androgen and raises sex hormone-binding globulin; add spironolactone 100 mg daily (up to 200 mg) if inadequate after 6 months; alternatives finasteride 5 mg, cyproterone acetate 50-100 mg; flutamide rarely, for hepatotoxicity.
- Mechanism note: all anti-androgens are teratogenic to a male fetus — mandatory contraception while on them, a standard exam caveat.
- Physical methods: laser photoepilation and electrolysis give durable reduction and combine well with drugs, since pharmacotherapy takes 6-12 months to show (hair cycle length) and stops working when stopped.
- Metformin treats insulin resistance, not hair: it improves cycle regularity in polycystic ovary syndrome but is a weak agent for hirsutism itself — a discriminating option in exams.
Working through the clinic pathway
A 24-year-old presents with increasing facial and abdominal hair over three years, irregular cycles every 45-60 days, body mass index 29. Modified Ferriman-Gallwey totals 11. Screening: testosterone 68 ng/dL, dehydroepiandrosterone sulphate 240 microgram/dL, 17-hydroxyprogesterone 1.4 ng/mL (early morning), prolactin and thyroid-stimulating hormone normal; ultrasound shows 12+ follicles per ovary with increased stroma. The picture is polycystic ovary syndrome hirsutism: combined oral contraceptive started (weight-neutral progestin preferred), spironolactone 100 mg daily added at review for insufficient response at six months, with explicit contraception counselling. Laser sessions run alongside; weight loss of 7 kg over the year lowers free androgen further — the only intervention that treats the substrate.
The contrast case: a 38-year-old with six months of rapidly thickening hair, frontal balding, deepening voice and clitoromegaly — virilisation. Testosterone is 260 ng/dL, imaging (transvaginal ultrasound, then adrenal computed tomography) hunts the tumour, and surgery, not anti-androgens, is the treatment. The third variant, hirsutism with galactorrhoea, sends you to prolactin and thyroid-stimulating hormone — hypothyroidism raising prolactin is a reversible cause seen in Indian clinics.
How the exam frames it
Three question types recur: the score ("which cut-off on modified Ferriman-Gallwey defines hirsutism" — 8), the hormone map ("which marker suggests an adrenal tumour" — dehydroepiandrosterone sulphate; "which screens congenital adrenal hyperplasia" — 17-hydroxyprogesterone), and the therapy pick (first line combined pill; add-on spironolactone; teratogenicity caveat). Virilisation versus hirsutism is the discriminating concept — hirsutism alone never means tumour, but virilisation demands exclusion — and the idiopathic label (normal androgens, excess hair) is the "most common cause after polycystic ovary syndrome" answer. Time-to-response (6-12 months because of the hair growth cycle) is a favourite "why didn't the drug work in 3 months" stem.
Frequently asked questions
What score on the modified Ferriman-Gallwey chart defines hirsutism?
A total of 8 or more across nine androgen-dependent body areas, each graded 0 to 4 by hair density and extent.
Which investigations form the first-line workup of hirsutism?
Total testosterone, dehydroepiandrosterone sulphate, early-morning 17-hydroxyprogesterone, prolactin and thyroid-stimulating hormone, with pelvic ultrasound where polycystic ovary syndrome is suspected.
Which features argue for an androgen-secreting tumour?
Rapid onset, progression over months, virilisation (clitoromegaly, deepened voice, temporal balding), testosterone above roughly 150-200 ng/dL or dehydroepiandrosterone sulphate above 700 microgram/dL.
What is the first-line drug for hirsutism?
A combined oral contraceptive, which suppresses ovarian androgen production and increases sex hormone-binding globulin; anti-androgens like spironolactone 100 mg daily are added if response is inadequate.
Why must contraception accompany anti-androgen therapy?
Spironolactone, finasteride, cyproterone and flutamide can feminise a male fetus, so effective contraception is mandatory during therapy.