Hirsutism and androgen excess approach

• Hirsutism is terminal (coarse, pigmented) hair growing in a male (androgen-dependent) pattern in a woman. It is not the same as hypertrichosis, which is generalized excess hair.
• It affects 5% to 10% of women worldwide and is usually benign but distressing. It is a sign of androgen action in the skin, not a disease in itself.
• Polycystic ovary syndrome (PCOS) explains 75% to 80% of cases; idiopathic hirsutism explains 5% to 20%; NCCAH, androgen-secreting tumours, Cushing syndrome and drug effects together make up less than 5%. ^[1]
• Score with the Ferriman-Gallwey score, but cut-offs vary by ethnicity, and patient-important hirsutism can exist with a normal score.
• Test when the score is abnormal or the history suggests a disorder: baseline total testosterone, then early-morning confirmatory testosterone, a 17-hydroxyprogesterone (17-OHP) screen, and DHEAS when an adrenal cause is suspected.
• Treat first with a combined oral contraceptive for most women not seeking pregnancy, add an antiandrogen after 6 months if needed, and use direct hair removal as an adjunct. Surgery is reserved for androgen-secreting tumours. ^[1]

By the end of this page you should be able to:

1. Define hirsutism and distinguish it from hypertrichosis, and explain why hair-follicle biology shapes the 6-month timeline of treatment.
2. Score hirsutism with the Ferriman-Gallwey system and apply ethnicity-based cut-offs.
3. List the common and rare causes by stage of life and name the red flags that point to a tumour or Cushing syndrome.
4. Choose and interpret the correct androgen tests (total and free testosterone, 17-OHP and DHEAS) and know when to image.
5. Outline the management algorithm, including oral contraceptives, antiandrogens and their doses, direct hair removal, and when to refer or operate.
6. Adapt the approach to adolescents, pregnancy, the postmenopausal woman and low-resource settings.

Hirsutism is male-pattern terminal hair growth in a woman. A follicle can produce vellus (fine, pale) or terminal (coarse, pigmented) hair depending on circulating androgens and the follicle's own 5-alpha-reductase activity, which converts testosterone to dihydrotestosterone (DHT), the active androgen in skin. Terminal hairs can exceed 5 mm when untreated and vary in shape, texture and pigmentation. Only terminal hairs count when scoring hirsutism.

Androgens in women come from two places. About 33% of circulating testosterone is produced by ovarian theca cells; most of the rest is synthesised peripherally from androstenedione made by the ovaries and adrenals. The adrenal zona reticularis alone produces dehydroepiandrosterone sulphate (DHEAS), the best biomarker of adrenal hyperandrogenism because it has a long half-life. Androgens act directly through the androgen receptor and indirectly through conversion to oestrogen. ^[3]

Hirsutism is therefore a sign, the skin's response to androgen, rather than a disease. Hirsutism affects 5% to 10% of women worldwide, and the distress it causes (social, psychological and financial, through cosmetics and hair removal) is real even when the score is modest. "Patient-important hirsutism" is now used for unwanted hair growth of any degree that causes enough distress for a woman to seek treatment, and is a legitimate reason to treat even with a normal Ferriman-Gallwey score. ^[1]

The single most useful rule of thumb in management is biological. The hair cycle takes many months, so pharmacologic treatment needs 6 months before judging success, before changing the dose, switching drugs or adding one. Starting pharmacologic treatment and direct hair removal together is acceptable when a quicker cosmetic result is wanted.

• Hirsutism affects 5% to 10% of women worldwide. ^[1]
• PCOS is the most common endocrine disorder of reproductive-age women, affecting 10% to 13% of women globally, and is present in 75% to 80% of women with hirsutism. ^{[1][2] [3]}
• Idiopathic hirsutism (normal tests, normal ovaries, no menstrual disorder) accounts for 5% to 20% of cases. ^[1]
• Rare causes (NCCAH, androgen-secreting tumours, Cushing syndrome and drug effects) together make up less than 5% of cases. ^[1]
• In women presenting with hyperandrogenism, 57% to 82% meet criteria for PCOS; among women with PCOS, 65% to 75% have hyperandrogenism, with hirsutism the most common sign. ^[3]

Approach first by asking three questions: how old is she, how quickly did it start, and is she virilised? Premenopausal women most often have PCOS or NCCAH; postmenopausal women with new hirsutism need exclusion of an ovarian or adrenal tumour or ovarian hyperthecosis.

PCOS is the single most common cause and is diagnosed on the 2003 Rotterdam criteria, retained in the 2023 international guideline: at least two of (1) clinical or biochemical hyperandrogenism, (2) ovulatory dysfunction and (3) polycystic ovarian morphology on ultrasound (or AMH in adults). ^[2] In a woman with irregular cycles and hyperandrogenism, imaging is not needed for diagnosis. ^[2] Androgens should be checked at least 3 months after stopping hormonal contraception, because the pill raises SHBG and lowers gonadotrophin-driven androgen production, masking the result. ^[2][3] New-onset, severe or worsening hyperandrogenism calls for exclusion of a tumour and ovarian hyperthecosis rather than assuming PCOS. ^[2]

NCCAH is the most common inherited adrenal cause in adults. It is due to 21-hydroxylase deficiency, which shunts precursors into the androgen pathway, raising androstenedione and testosterone. ^[3] Screen in hirsute patients with elevated testosterone or a high clinical risk (positive family history, or membership of a high-risk ethnic group) by measuring 17-OHP between 7 and 9 a.m.:

• A level above 500 ng/dL makes the diagnosis.
• A level of 200 to 500 ng/dL requires a stimulated 17-OHP 60 minutes after 250 micrograms of cosyntropin; a level of 1500 ng/mL or above confirms. ^[3]
• The source values use ng/dL for the baseline and ng/mL for the stimulated threshold; do not confuse the units. ^[3]

Unlike classic CAH, NCCAH rarely causes cortisol deficiency, so glucocorticoids are not needed for safety, only optionally for ovulation induction. ^[3]

These are rare but must not be missed. They are suggested by rapid progression (over months rather than years; in one study a mean of 12 months for tumours versus 42 months for PCOS), severe hirsutism and signs of virilisation: deepening of the voice, clitoromegaly (clitoral length above 10 mm, or a clitoral index above 35 mm2) and increased muscle mass. ^[3] Severe biochemical excess (total testosterone at least 150 ng/dL premenopausal, or at least 64 ng/dL postmenopausal, on LC-MS/MS) should prompt pelvic imaging; the source is ovarian in about 80% of cases. ^[3] Further clues to other endocrine disease include features of Cushing syndrome (purple striae, supraclavicular fullness, facial plethora, easy bruising) or acromegaly (enlarged jaw, macroglossia, swollen hands or feet). ^[3]

Ovarian hyperthecosis is a histological diagnosis in which nests of luteinized theca cells sit throughout the ovarian stroma, causing slow, progressive hyperandrogenism with insulin resistance (acanthosis nigricans, skin tags, central obesity) and sometimes virilisation and postmenopausal bleeding from endometrial hyperplasia. Testosterone (and oestradiol) are raised, but LH and FSH are inappropriately low for a postmenopausal woman. ^[3]

This is the diagnosis of exclusion in a woman under 40 with unwanted hair, no menstrual disturbance, normal androgens and normal ovaries on ultrasound, who is not on hormonal contraception. ^[3] Treatment is cosmetic and antiandrogenic and directed at her concerns.

Always take a drug history. Implicated agents include danazol, valproic acid, oxcarbazepine, oral minoxidil, anabolic steroids, exogenous androgens (including a partner's topical testosterone transferring accidentally) and supplements such as DHEA, "bioidentical" hormone preparations and "anti-ageing" cocktails from wellness clinics. ^[3]

Hirsutism is usually the presenting symptom. The woman's own report and her perceived areas of concern matter as much as the score: self-reported hair growth is often higher than the clinician's score and has high validity. ^[2][3] Hair distribution should be documented (including sideburns, lower buttocks and facial areas that formal scores miss), with any onset after hair removal procedures noted, since previous plucking or waxing limits scoring. ^[3]

Associated features of androgen excess include acne and male-pattern hair loss (vertex thinning). Hormonal treatment takes over 6 months to show on hair, so follow-up should be planned accordingly.

Red flags for a serious underlying endocrine disorder are:

• Sudden onset or rapid progression of hirsutism
• Menstrual irregularity or infertility
• Galactorrhoea, acanthosis nigricans, central obesity
• Features of Cushing syndrome or acromegaly
• Clitoromegaly or any virilisation
• Hirsutism in a child or new hirsutism in a postmenopausal woman ^[1][3]

Examine the nine androgen-sensitive sites and score each from 0 (no terminal hair) to 4 (full coverage): upper lip, chin, chest, upper abdomen, lower abdomen, upper arms, thighs, upper back and lower back. ^[1][3] The original FG score covers nine androgen-sensitive sites. In the US general population a normal score is below 8, mild is 8 to 15 and severe is above 15. ^[1] Inter-observer variability is substantial and previous cosmetic removal makes scoring unreliable. ^[3]

Ethnic cut-offs for a positive (abnormal) score differ between sources, which is worth being honest about in clinic and in exams:

• 2018 Endocrine Society hirsutism guideline: a positive score is 8 or greater in white and black women, 2 to 7 or greater (depending on ethnicity) in Asian women, and 9 to 10 or greater in Hispanic and Middle Eastern women. ^[1]
• 2023 international PCOS guideline: a modified FG score of 4 to 6, depending on ethnicity. ^[2]
• Practical review cut-offs: 9 or greater in Middle Eastern, Mediterranean, South Asian and Hispanic women; 8 or greater in Black and European Caucasian women; 7 or greater in Southern Chinese women; 6 or greater in South American women; 2 or greater in Han Chinese women. ^[3]

These differences reflect ethnicity, the definition of "positive" versus "screening" and the scorer; they are not an invitation to chase a single number. A useful operational rule is to score it, note the ethnicity and treat the woman's distress (patient-important hirsutism) together with any abnormal result and a menstrual history, which raises suspicion more than the score alone. ^[1][2]

Most routine immunoassays (RIA and enzyme-linked assays) were designed for men and have poor precision at the low concentrations found in women, so they miss the mild elevations typical of PCOS and give falsely reassuring results. ^[1][3] LC-MS/MS is the most reliable method for total testosterone, and where LC-MS/MS is unavailable an extraction/chromatography immunoassay is the acceptable alternative. ^[2][3]

Free testosterone is most accurately measured by equilibrium dialysis, which is rarely available; in practice, measure SHBG and calculate the free androgen index or free testosterone. ^[1][3] Obesity, hypothyroidism, inflammation, SHBG polymorphisms and mutations all lower SHBG. ^[3]

Do not measure androgens in women with normal menses and a normal hirsutism score. ^[1] When a woman is on any hormonal contraception, stop it for at least 3 months before testing (with non-hormonal contraception in the interim), because hormones suppress the values you are trying to measure. ^[2][3]

1. Pregnancy test first in any premenopausal woman. ^[3]
2. Random total testosterone in all women with an abnormal hirsutism score. ^[1] If it is normal but sexual hair growth is moderate or severe, or mild but associated with a menstrual or endocrine abnormality, repeat total plus free testosterone on an early-morning sample (between 7 and 9 a.m.). ^[1]
3. If suspicion is higher (oligomenorrhoea or moderate-to-severe hirsutism with an FG score above 15), measure both morning total and free testosterone. ^[1]
4. Confirmatory total and free testosterone on an early-morning sample on days 4 to 10 of the menstrual cycle, when levels peak, plus SHBG. ^[1]
5. Early-morning 17-OHP (7 to 9 a.m.) in all women with elevated testosterone, and in hirsute women at high risk of CAH (positive family history or high-risk ethnicity), even if testosterone is normal. ^[1]
6. DHEAS if an adrenal source is suspected. It can be raised in both PCOS and adrenal tumours; a level above 700 micrograms/dL mandates exclusion of an adrenal tumour. ^[3]
7. Prolactin, FSH, TSH and an early-morning 17-OHP, plus screening for Cushing syndrome and acromegaly on clinical grounds. ^[3]

Women with PCOS are also screened for cardiometabolic problems, including lipids and blood pressure. ^[2]

Image only when a tumour is plausible: virilisation on examination, or severe biochemical excess (total testosterone at least 150 ng/dL premenopausal, or at least 64 ng/dL postmenopausal on LC-MS/MS). ^[3] Start with transvaginal ultrasound (colour Doppler) because ovarian tumours are often small and isoechoic; MRI is the next step if ultrasound is negative. ^[3] If DHEAS is above 700 micrograms/dL or pelvic imaging is negative, adrenal CT (with and without contrast) is next. ^[3] Remember that an adrenal incidentaloma, especially after menopause, may be irrelevant; imaging is only pursued when clinically indicated. ^[3]

For PCOS itself, polycystic morphology is defined as 20 or more antral follicles in at least one ovary, or an ovarian volume above 10 mL; an AMH level can be used instead of ultrasound in adults, but not in adolescents. ^[2] An ultrasound is unnecessary when cycles are irregular and hyperandrogenism is already present. ^[2]

Surgery is curative for androgen-secreting tumours: complete resection for adrenal or ovarian tumours, and bilateral oophorectomy for ovarian hyperthecosis (cytoreductive, fertility-sparing surgery in premenopausal women). ^[3] In selected cases of functional adrenal adenoma where surgery is unsafe or declined, radiofrequency ablation or CT-guided cryoablation have been used with outcomes similar to surgery. ^[3] Treat Cushing syndrome on its merits.

Weight loss in obese women with PCOS produces a small fall in free androgen (mean difference about 1.1 units of free androgen index) and a mild improvement in hirsutism (mean difference about 1.1 FG points), but it is not sufficient as sole treatment for clinically important hirsutism. ^[3] Weight management still matters for overall health, but it changes hair only modestly.

Most women have already used shaving, plucking or waxing before presenting. ^[1] Direct methods are recommended as an add-on rather than a substitute for pharmacologic treatment when hirsutism is patient-important:

• Photoepilation (laser or light) for auburn, brown or black hair; photoepilation is recommended for darker hair. ^[1]
• Electrolysis for white or blonde hair.
• Topical eflornithine can be added to photoepilation for a faster initial response.
• Women with known hyperandrogenaemia benefit from pharmacologic therapy alongside hair removal to limit regrowth. ^[1][3]

A pharmacologic response takes at least 6 months because of the hair cycle, so align expectations and follow-up.

• For the majority of women with patient-important hirsutism who are not seeking fertility, the Endocrine Society suggests combined oral contraceptive pills (OCPs) as initial therapy. ^[1] OCPs suppress LH and raise SHBG, lowering ovarian androgen production and free testosterone. ^[3]
• Either an OCP or an antiandrogen is acceptable as initial therapy in women who are not sexually active, have been permanently sterilised, or use long-acting reversible contraception. ^[1]
• All OCPs appear equally effective for hirsutism and side-effect risk is low; no single OCP is preferred over another. ^[1]
• If VTE risk is higher (obesity or age above 39 years), choose an OCP with the lowest effective ethinyl oestradiol dose, usually 20 micrograms, and a low-risk progestin. ^{[1] [3]}
• Either an OCP or an antiandrogen may be used first line; the choice depends on preferences about efficacy, side effects and cost. ^[1]
• OCPs improve biochemical markers within cycles but hair improvement is assessed after 6 months. ^[1][3]

• Antiandrogens are contraindicated in pregnancy because they disrupt external genital development; use reliable contraception unless abstinence applies. ^[1][3]
• Do not use antiandrogen monotherapy as initial treatment unless adequate contraception is guaranteed. ^[1]
• If hirsutism persists after 6 months of OCP monotherapy, add an antiandrogen. ^[1]
• One antiandrogen is not clearly better than another, but flutamide is contraindicated because of hepatotoxicity. ^[1]
• Available options (off-label in women):
  • Spironolactone 100 to 200 mg/day, a competitive androgen receptor antagonist that is also a potassium-sparing diuretic; monitor potassium, avoid in renal impairment and warn about hypotension, dizziness and hyperkalaemia. ^[3]
  • Finasteride 2.5 to 5 mg/day (a type 2 5-alpha reductase inhibitor); hirsutism scores fall similarly at 2.5 and 5 mg and slightly more at 7.5 mg. Side effects include low libido, depression or asthenia and orthostatic hypotension. ^[3]
  • Dutasteride (type 1 and 2 5-alpha reductase inhibitor) has limited data in women. ^[3]
  • Cyproterone acetate, commonly used outside the USA, is equivalent at 2 mg to 50 mg of spironolactone; combined cyproterone-containing OCPs give a mildly lower mFG score but carry a 50% to 100% higher VTE risk than levonorgestrel-containing OCPs and are not preferred. ^[3]
• Reassess pharmacologic outcomes after at least 6 months before changing dose, switching or adding. ^[3]

• Glucocorticoids are effective for classic 21-hydroxylase CAH. In NCCAH they should not be first line for hirsutism except for ovulation induction; OCPs improve hirsutism more than dexamethasone. ^[3]
• GnRH agonists are as effective as OCPs at reducing hirsutism but cause hypoestrogenism, bone loss and hot flushes; reserve for severe virilisation unresponsive to other therapy. ^[3]
• Metformin and other insulin-sensitising drugs are no more effective than placebo for hirsutism and should be reserved for prediabetes or type 2 diabetes in PCOS; do not use them to treat hair. ^[1][3]
• Topical antiandrogens have limited efficacy; acne and alopecia should be managed jointly with dermatology, with topical minoxidil first line for alopecia. ^[3]

Arrange review at 6 months to assess hair score, patient-reported distress, cycle control, blood pressure and tolerance. ^[1][3] Monitor clinical signs of hyperandrogenism for response and adjust therapy accordingly. ^[2] Psychological support, which is often overlooked, should be offered in proportion to the woman's distress. ^[2]

A sudden or rapidly progressive onset, virilisation, or hirsutism beginning in childhood or after menopause is a red flag that should be investigated promptly for a tumour or Cushing syndrome. ^[1][3] Refer women with an identified androgen-secreting tumour to gynaecologic or endocrine surgery; refer Cushing syndrome or acromegaly to the appropriate specialist service; and involve dermatology when direct hair removal or acne management is central to care.

• A modified Ferriman-Gallwey score needs no laboratory equipment; use ethnicity-adjusted thresholds but always consider local hair norms and the woman's distress. ^[2][3]
• Where LC-MS/MS is unavailable, use the most accurate local assay and interpret it cautiously; immunoassays miss mild hyperandrogenism. ^[1][2]
• A single early-morning 17-OHP screen is cheap and high-yield for NCCAH in high-risk groups. ^[1]
• OCPs and spironolactone are widely available and remain first-line pharmacologic care; flutamide should be avoided. ^[1][3]
• When photoepilation and electrolysis are unavailable, shaving, waxing and depilatory creams remain effective adjuncts; topical eflornithine may be prohibitively expensive in some settings. ^[1]
• If surgical capacity is limited, refer tumours early to a centre that can operate.

• Adolescents. Both hyperandrogenism and ovulatory dysfunction are required for a PCOS diagnosis; ultrasound and AMH are not used in adolescents. ^[2] Severe acne and hirsutism are the relevant hyperandrogenic signs. ^[2] Set realistic expectations that hair therapies take months.
• Pregnancy. Androgens rise physiologically in pregnancy; rare causes include pregnancy luteoma, placental aromatase deficiency and fetal CAH. Antiandrogens are contraindicated; use cosmetic measures only and refer when indicated. ^[3]
• Postmenopausal women. New hirsutism needs exclusion of ovarian hyperthecosis or an androgen-secreting tumour; biochemical thresholds differ from those used premenopausally. ^[3]
• Family. First-degree relatives of women with PCOS have an increased risk of metabolic syndrome, type 2 diabetes and hypertension in some studies, and the dermatologic impact of hirsutism warrants attention to quality of life. ^[2]

Hirsutism is common, visible and frequently minimised, yet it has a measurable negative psychosocial impact on women. ^[2] Recording it carefully is therefore part of good care, not just bureaucracy. A comprehensive history and examination should include acne, female-pattern hair loss and hirsutism in adults, and severe acne and hirsutism in adolescents. ^[2] Standardized visual scales such as the mFG scale, preferably with a photographic atlas, are preferred. ^[2] Recall that only terminal hairs count: they can reach greater than 5 mm if untreated, vary in shape and texture, and are generally pigmented; vellus hair must be ignored. ^[2]

Patient-reported (self) assessment of unwanted excess hair growth has a high degree of validity and merits close evaluation, even when overt clinical signs are not readily evident on examination. ^[2] Clinicians should be aware that women commonly treat clinical hyperandrogenism cosmetically, which diminishes its apparent severity, so the absence of a high score does not exclude significant androgen excess. ^[2] In PCOS, the presence of hirsutism alone is considered predictive of biochemical hyperandrogenism in adults; in contrast, female-pattern hair loss or acne in isolation are relatively weak predictors. ^[2]

Severity of hirsutism may vary by ethnicity, but its prevalence appears similar across ethnicities. ^[2] When pharmacologic or hair-removal treatment is chosen, clinical signs should be monitored for improvement and therapy adjusted. ^[2]

For every woman diagnosed with PCOS, assess cardiovascular risk factors (including lipids and blood pressure) and glycaemic status with an oral glucose tolerance test at diagnosis and during pregnancy planning, because insulin resistance is a key feature even though insulin assays have limited routine use. ^[2] These assessments are part of the hirsutism work-up when PCOS underlies the hair growth, because treating hair alone misses the long-term risks.

A woman presents with increasing chin and lower abdominal hair. Her periods are irregular. She has used threading on her face, which makes scoring difficult; the clinician documents that terminal hairs are present at the lip, chin, chest and lower abdomen and that she rates herself more severely than the score suggests. Examination shows no virilisation and no stigmata of Cushing or acromegaly. A pregnancy test is negative; testosterone and SHBG are requested if she stopped hormonal contraception at least 3 months ago, together with an early-morning 17-OHP and DHEAS if indicated. Given irregular cycles and clinical hyperandrogenism, a PCOS diagnosis can be made without ultrasound. ^[2] First-line management is a combined oral contraceptive with review at 6 months, plus advice on weight and direct hair removal for cosmetic benefit. If hirsutism persists at 6 months, an antiandrogen is added, with contraception. At follow-up she should have blood pressure, lipids and glucose assessed. ^[1][2][3]

• Hirsutism is a sign of androgen action, not a diagnosis: terminal hair in a male pattern, distinguished from hypertrichosis.
• It affects 5% to 10% of women worldwide; patient-important hirsutism is a valid treatment indication at any score.
• PCOS causes 75% to 80% of hirsutism; idiopathic hirsutism 5% to 20%; NCCAH, tumours, Cushing syndrome and drugs together less than 5%. ^[1]
• Score with Ferriman-Gallwey (0 to 4 at 9 sites) but use ethnicity-adjusted thresholds and remember scorer variability. ^[1]
• Test testosterone properly: LC-MS/MS where possible, random then early-morning on days 4 to 10 of the cycle, with SHBG; do not test on hormonal contraception without stopping it first for 3 months; stop testing when menses and the score are both normal.
• Screen for NCCAH with 17-OHP and for adrenal tumours with DHEAS above 700 micrograms/dL.
• Red flags (rapid onset, virilisation, postmenopausal or paediatric onset) demand tumour and Cushing work-up first.
• First-line pharmacologic therapy is a combined oral contraceptive, with antiandrogen added after 6 months; reassess all therapy after at least 6 months.
• Spironolactone 100 to 200 mg/day and finasteride 2.5 to 5 mg/day are the usual antiandrogens; flutamide is avoided. ^[3]
• Photoepilation for darker hair, electrolysis for light hair, topical eflornithine for faster response, combined with systemic therapy in women with biochemical hyperandrogenism.
• Metformin does not treat hirsutism; reserve for metabolic indications. Surgery cures androgen-secreting tumours.

• Do not tell a woman that her hair is "just cosmetic". Her distress is the indication. ^[1][2]
• Do not stop at the score: a normal Ferriman-Gallwey score does not rule out hyperandrogenism, and an abnormal one does not reveal the cause.
• Do not forget to ask about transfer of a partner's topical testosterone and about wellness supplements; these are easy to miss and fully reversible. ^[3]
• Do not order platelet or routine hormone panels at every visit: androgen levels need not be repeated for PCOS once the diagnosis is established. ^[2]
• Do not start antiandrogens without contraception, and do not promise improvement before 6 months.
• Do not image everyone: reserve imaging for virilisation, extreme biochemical values or clinical suspicion of a tumour. ^[3]
• Do not rely on acne or female-pattern baldness alone as proof of hyperandrogenism; they are relatively weak predictors compared with hirsutism. ^[2]

Polycystic ovary syndrome; nonclassic congenital adrenal hyperplasia; Cushing syndrome; acromegaly; acne and male-pattern hair loss; obesity and metabolic syndrome; anovulatory infertility; insulin resistance; adolescent health.