Introduction
Hirsutism is defined as excessive, male-pattern hair growth in women, typically involving the face (chin, upper lip), chest, abdomen, back, and thighs. Unlike generalized hypertrichosis (excess hair growth anywhere on the body, not necessarily androgen-dependent), hirsutism reflects increased androgen activity.
It affects up to 5–10% of women of reproductive age, with significant psychosocial impact including low self-esteem, anxiety, and depression. While often benign (e.g., familial tendency, mild PCOS), it may rarely indicate serious conditions such as androgen-secreting tumors.
Pathophysiology
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Androgens (testosterone, androstenedione, dehydroepiandrosterone sulfate – DHEAS) stimulate transformation of vellus (fine) hair into terminal (thick, pigmented) hair in androgen-sensitive areas.
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Hirsutism may result from:
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Increased androgen production (ovarian or adrenal).
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Increased peripheral sensitivity of hair follicles to androgens.
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Reduced sex hormone-binding globulin (SHBG), leading to higher free testosterone.
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Causes of Hirsutism
1. Polycystic Ovary Syndrome (PCOS) – most common
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Features: irregular menses, infertility, obesity, acne, insulin resistance.
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Elevated LH:FSH ratio, increased androgens, polycystic ovaries on ultrasound.
2. Idiopathic/Familial Hirsutism
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Normal ovulatory cycles, androgen levels often normal.
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Likely due to increased skin sensitivity to androgens.
3. Endocrine Disorders
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Congenital adrenal hyperplasia (CAH): Excess adrenal androgens due to enzyme deficiency (commonly 21-hydroxylase).
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Cushing’s syndrome: Cortisol excess with associated androgen overproduction.
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Hyperprolactinemia: May coexist with PCOS.
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Hypothyroidism: Rare cause, can worsen androgen effects.
4. Androgen-Secreting Tumors (Ovarian or Adrenal)
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Rapid onset, severe hirsutism, virilization (deep voice, clitoromegaly, muscle mass).
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Require urgent evaluation.
5. Medications
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Anabolic steroids, danazol, minoxidil, phenytoin, cyclosporine.
Clinical Features
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Hair growth in male-pattern distribution: upper lip, chin, chest, abdomen, back, thighs.
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Acne, oily skin.
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Menstrual irregularities (oligomenorrhea, amenorrhea).
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Signs of virilization (severe cases): deepening of voice, clitoromegaly, male-pattern baldness.
Diagnostic Approach
1. History
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Age at onset, progression rate.
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Menstrual/obstetric history.
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Drug history.
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Family history.
2. Physical Examination
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Distribution and severity of hair (Ferriman–Gallwey scoring system).
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Signs of virilization.
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BMI, waist circumference, signs of insulin resistance.
3. Laboratory Tests
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Total and free testosterone (elevated in ovarian causes).
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DHEAS (elevated in adrenal causes).
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LH/FSH ratio (in PCOS).
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17-hydroxyprogesterone (for CAH).
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Cortisol tests (dexamethasone suppression, 24-h urinary cortisol for Cushing’s).
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Prolactin, TSH if menstrual disturbance present.
4. Imaging
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Pelvic ultrasound (PCOS, ovarian tumor).
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CT/MRI abdomen (adrenal tumor).
Management and Treatment
Treatment depends on severity, underlying cause, and patient preference (cosmetic vs. fertility concerns).
A. General and Cosmetic Measures
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Weight loss & exercise: In obese women with PCOS, reduces insulin resistance and lowers androgen levels.
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Cosmetic options:
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Shaving, waxing, depilatory creams.
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Bleaching (for mild facial hair).
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Laser hair removal or electrolysis (long-term reduction).
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B. Pharmacological Therapy
1. Combined Oral Contraceptives (COCs) – first-line in PCOS-related hirsutism
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Mechanism: Suppress ovarian androgen production and increase SHBG.
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Common formulations:
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Ethinylestradiol 30–35 mcg + Levonorgestrel 150 mcg orally once daily
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Ethinylestradiol 30 mcg + Drospirenone 3 mg orally once daily
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Drospirenone has anti-androgenic effect, beneficial in hirsutism.
2. Anti-Androgens (used when COCs insufficient, often in combination)
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Spironolactone:
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50–100 mg orally twice daily.
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Blocks androgen receptors and inhibits androgen synthesis.
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Side effects: hyperkalemia, menstrual irregularities (use with contraception).
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Cyproterone acetate:
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50–100 mg orally once daily (not available everywhere).
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Strong anti-androgenic activity.
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Flutamide:
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250 mg orally once daily.
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Potent androgen receptor blocker, but risk of hepatotoxicity → monitor liver function.
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Finasteride:
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5 mg orally once daily.
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Inhibits 5-alpha reductase, reducing dihydrotestosterone (DHT).
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Teratogenic (must use contraception).
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3. Insulin-Sensitizing Agents
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For PCOS with insulin resistance.
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Metformin:
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500 mg orally two to three times daily with meals.
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Improves ovulation and reduces androgen levels.
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4. Corticosteroids (for congenital adrenal hyperplasia)
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Hydrocortisone: 15–25 mg/day orally in divided doses.
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Dexamethasone: 0.25–0.5 mg orally at bedtime.
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Suppresses adrenal androgen overproduction.
5. Gonadotropin-Releasing Hormone (GnRH) Analogues
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Reserved for resistant cases.
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Leuprolide depot: 3.75 mg intramuscular monthly.
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Suppresses ovarian androgen production.
C. Treatment of Secondary Causes
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Cushing’s syndrome: Surgical removal of adrenal/pituitary tumor.
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Androgen-secreting tumors: Surgical resection (urgent).
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Hypothyroidism: Levothyroxine replacement (starting 25–50 mcg daily, titrated).
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Hyperprolactinemia: Dopamine agonists (e.g., Cabergoline 0.25 mg orally twice weekly).
Prognosis
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PCOS/idiopathic hirsutism: Good response to long-term therapy (6–12 months).
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Adrenal/ovarian tumors: Curable if detected early.
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CAH: Requires lifelong corticosteroid therapy, prognosis good with compliance.
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Cushing’s: Prognosis depends on cause and success of treatment.
Complications
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Psychological distress, depression, social isolation.
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Infertility (in PCOS).
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Increased risk of metabolic syndrome, diabetes, endometrial hyperplasia (in PCOS).
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Drug side effects (hepatotoxicity, teratogenicity, hormonal disturbances).
Patient Education
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Hirsutism often requires long-term treatment (6–12 months) for visible improvement.
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Contraception is essential when using anti-androgens.
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Lifestyle changes (diet, weight reduction) are crucial in PCOS.
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Cosmetic procedures can complement medical therapy.
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Sudden severe hirsutism with virilization = urgent evaluation for tumor.
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