Hirsutism and Unwanted Hair: Turning Down the Androgen Signal

Hirsutism is not just "too much hair"

The word means one precise thing: male-pattern terminal hair in a woman. Hirsutism is excess coarse, dark terminal hair appearing in a female in an androgen-dependent distribution — the upper lip, chin, jawline, chest, upper abdomen, lower back and inner thighs. These are exactly the sites where hair growth in men depends on testosterone, which is the whole clue: hirsutism is an androgen story. It is the biological mirror image of androgenetic alopecia covered in the alopecia chapter — the same 5-alpha-reductase converting testosterone to the more potent dihydrotestosterone (DHT), the same receptor, but here the follicles respond by growing rather than shrinking. On the scalp androgens miniaturise; on the face and body they do the reverse, driving vellus down toward thick terminal hair.

The crucial distinction — and a favourite exam trap — is hirsutism versus hypertrichosis. Hypertrichosis is generalised excess hair anywhere on the body, in a non-sexual, non-androgen-dependent pattern. It is not driven by hormones at all; classically it is drug-induced — ciclosporin, minoxidil and phenytoin are the three names to know, and (as in the alopecia chapter) minoxidil's unwanted-hair effect is exactly the side of the same coin that makes it a scalp treatment. If a woman has fine hair increasing all over, including non-androgenic sites like the forearms and back, on one of those drugs, think hypertrichosis and review her medications — not an anti-androgen.

Where the androgens come from — mostly PCOS

The overwhelming majority of hirsutism is caused by polycystic ovary syndrome (PCOS), the subject of its own discussion in the Endocrine section. In PCOS, insulin resistance drives the ovaries (and adrenal glands) to over-produce androgens, and the same high insulin lowers sex-hormone-binding globulin (SHBG) in the liver. That second effect matters enormously: SHBG is the protein that mops up circulating testosterone, so when it falls, the fraction of free, active testosterone rises even if the total looks only mildly raised. Less common causes include congenital adrenal hyperplasia (CAH, usually the non-classical late-onset form, from 21-hydroxylase deficiency), Cushing's syndrome, and androgen-secreting tumours of the ovary or adrenal. Idiopathic hirsutism — normal androgens but unusually sensitive follicles — is a diagnosis of exclusion.

The work-up is really a search for the one cause you must not miss. Most hirsutism is slow and benign, so the tests are aimed less at confirming PCOS than at ruling out something dangerous. The alarm features are rapid onset over months, frank virilisation (deepening voice, clitoromegaly, male-pattern balding, increased muscle bulk), and a markedly elevated testosterone. That combination suggests an androgen-secreting tumour and warrants urgent imaging. A raised 17-hydroxyprogesterone points to non-classical CAH; the clinical picture of Cushing's is screened separately. The point of the biochemistry is not to treat a number but to decide whether you are looking at ordinary PCOS — reassure and treat the skin — or a rare surgical cause hiding behind the same hairs.

First-line: combined oral contraceptives

Lower the free androgen at its two main levers at once. The combined oral contraceptive (COC) is first-line for most women with hirsutism, and especially fitting when PCOS also means irregular periods and a need for contraception. It works on both levers at once. The oestrogen component raises SHBG in the liver, mopping up more free testosterone, while the progestogen suppresses the pituitary LH drive to the ovaries, so they make less androgen in the first place. Make less, and bind more of what is left — free active androgen falls from both directions. The effect on SHBG is a direct counter to what insulin resistance did in PCOS, which is why the COC ties so neatly back to the Endocrine chapter's account of the same hormone-binding physiology. Some formulations pair the oestrogen with an anti-androgenic progestogen such as cyproterone acetate or drospirenone, giving a third mechanism in one pill.

Anti-androgens: blocking the receptor

When a COC alone is not enough, or is contraindicated, the next step is a direct anti-androgen, and the workhorse is spironolactone. It is best known from the Cardiovascular and Endocrine sections as an aldosterone antagonist (a potassium-sparing diuretic), but at higher doses it is also a competitive androgen-receptor blocker and a weak inhibitor of androgen synthesis. It quite literally sits on the same receptor the DHT would occupy in the follicle. Two safety points define its use. First, because it is anti-aldosterone, it raises potassium — check renal function and potassium, and be cautious alongside ACE inhibitors, ARBs or potassium supplements, exactly as taught in the Cardiovascular chapter. Second, and non-negotiable: an anti-androgen given to a woman who conceives can feminise the external genitalia of a male fetus, so spironolactone (and every anti-androgen here) must be paired with reliable contraception — which is one more reason the COC and spironolactone are so often prescribed together.

Beyond spironolactone sit the other anti-androgens. Cyproterone acetate is a potent androgen-receptor blocker that also suppresses gonadotrophins; it is often used within a COC formulation rather than alone. Finasteride blocks 5-alpha-reductase — the exact same enzyme it inhibits for male-pattern hair loss and prostate disease in the alopecia chapter — cutting conversion of testosterone to DHT; it is effective but, like all these agents, teratogenic to a male fetus. Flutamide is a pure androgen-receptor antagonist that works well but is now little used because of the risk of serious, occasionally fatal hepatotoxicity, so liver monitoring is mandatory and most clinicians reach for it last. Across the whole class the theme is identical: either stop the androgen being made, or stop it reaching its receptor.

Metformin, topical eflornithine, and physical removal

Metformin earns its place through the root cause rather than the receptor. In PCOS the engine is insulin resistance, and metformin — the same biguanide covered in the Endocrine section for type 2 diabetes — lowers insulin, which in turn reduces the ovarian androgen drive. It is not a hair drug and its effect on hirsutism alone is modest, but it addresses the metabolic disturbance (weight, glucose, cycles) that sits underneath, so it is a valuable adjunct in women with PCOS. Topical eflornithine cream takes an entirely different, local route: it irreversibly inhibits ornithine decarboxylase, an enzyme the follicle needs for the cell division that fuels hair growth. Applied to the face, it slows the rate of hair growth — it does not remove existing hair, and growth resumes when it is stopped, so it is used as an adjunct, classically alongside laser, to buy a smoother result while the systemic drugs work upstream.

Drugs quiet the follicle; only physical methods remove the hair that is already there. Because no anti-androgen can pull out an existing terminal hair, definitive removal is mechanical. Shaving, waxing and threading are temporary; laser and intense-pulsed-light target the pigment in the follicle for longer-lasting reduction and are the closest thing to a permanent solution (electrolysis alone is truly permanent, follicle by follicle). The clinical art is to combine the two arms: a systemic anti-androgen to stop new terminal hairs forming and to keep the problem from returning, plus physical removal to clear the hair already present. Neither alone is enough — the drug prevents the next crop, the laser clears this one.