Excessive Hair: Expert Guide To Hirsutism And Hypertrichosis

Excessive hair growth, encompassing

hirsutism

and

hypertrichosis

, represents a common dermatological concern affecting individuals across genders, ages, and ethnicities. Hirsutism specifically refers to a male-pattern hair growth in women, typically post-puberty, while hypertrichosis denotes hair growth exceeding normal limits for age, sex, and race, independent of androgen influence. These conditions can cause significant psychosocial distress, prompting extensive efforts for hair removal. This article delineates the distinctions, etiologies, clinical evaluation, management strategies, and prognosis of excessive hair.

What is excessive hair?

Excessive hair comprises two primary entities:

hirsutism

and

hypertrichosis

. Hirsutism manifests as a male pattern of secondary or post-pubertal hair growth in women, emerging in areas such as the moustache, beard, chest, and abdomen at puberty, alongside normal underarm and pubic hair development in non-hirsute women. Hirsute women often exhibit thicker, longer hair on limbs and trunk compared to typical norms.

Hypertrichosis, by contrast, is non-androgenic excessive hair growth surpassing normal expectations for the individual’s age, sex, and race. It may involve unpigmented vellus hair or darker terminal hair and can be generalised across the body or localised to specific regions. Perceptions of excess vary culturally and ethnically, as normal secondary hair growth differs by race; modern societal norms of hairlessness in women further amplify subjective complaints.

Genetic variability in hair follicle response to androgens underscores individual differences. What constitutes ‘excessive’ remains subjective, influenced by grooming practices and cultural expectations.

Who gets excessive hair? (Epidemiology)

Hirsutism affects approximately 5-10% of women of reproductive age, with higher prevalence in Mediterranean, South Asian, and Middle Eastern populations due to genetic predispositions. It typically onset in late teenage years, progressively worsening with age. Risk factors include polycystic ovary syndrome (PCOS), affecting up to 70% of hirsute women, obesity, and insulin resistance.

Hypertrichosis is rarer, particularly congenital forms. Congenital hypertrichosis lanuginosa, dubbed ‘werewolf syndrome’, has fewer than 50 reported cases worldwide since the Middle Ages. Acquired hypertrichosis occurs sporadically across all demographics, often linked to medications, malignancies, or malnutrition. Localised forms associate with specific dermatoses or trauma.

What causes excessive hair?

Hirsutism predominantly stems from

hyperandrogenism

, elevated male hormones (androgens) like testosterone stimulating androgen-sensitive follicles. Common causes include:

• Polycystic ovary syndrome (PCOS): The leading etiology, featuring ovarian androgen overproduction, insulin resistance, and obesity.
• Idiopathic hirsutism: Normal androgen levels but heightened follicle sensitivity.
• Non-classical congenital adrenal hyperplasia (CAH): Enzyme deficiencies (e.g., 21-hydroxylase) causing adrenal androgen excess.
• Androgen-secreting tumours: Rare ovarian or adrenal neoplasms.
• Medications: Phenytoin, minoxidil, anabolic steroids, progestins.

Rare associations encompass Cushing syndrome, acromegaly, and hyperprolactinaemia.

Hypertrichosis arises from non-hormonal mechanisms, driven by genetic mutations, cytokines, or external stimuli. Congenital hypertrichosis results from prolonged lanugo persistence or nevoid conditions. Acquired generalised hypertrichosis links to:

• Drugs: Phenylbutazone, diazoxide, ciclosporin, interferon, EGFR inhibitors.
• Malignancies: Lung cancer, colonic polyps (as a paraneoplastic phenomenon).
• Malnutrition: Anorexia nervosa, HIV-associated wasting.
• Autoimmune: Dermatomyositis, systemic sclerosis.

Localised acquired hypertrichosis associates with repeated trauma (e.g., cast sites), irritant dermatitis, viral exanthems, or naevi (e.g., Becker melanosis, congenital melanocytic naevi).

Clinical features

Hirsutism first appears in late adolescence, intensifying gradually. Sites include upper lip, chin, sideburns, chest, abdomen (midline ‘male escape’), thighs, and back. Accompanying hyperandrogenism signs: acne, androgenetic alopecia, acanthosis nigricans (insulin resistance marker).

Hypertrichosis varies: congenital forms present at birth with lanugo-like hair covering the body, persisting lifelong. Acquired types emerge anytime, featuring fine vellus or terminal hair. Localised patches occur over melanocytic naevi, vascular malformations, or friction sites. Severe generalised cases (‘malignant down’) signal underlying malignancy.

Areas affected depend on type: hirsutism targets androgen-dependent zones; hypertrichosis spares none, potentially involving face, trunk, limbs diffusely.

Assessment and diagnosis

Diagnosis is clinical, predicated on history and examination. Hirsutism severity employs the

Ferriman-Gallwey (FG) score

, evaluating 9 androgen-sensitive sites (upper lip, chin, sideburns, chest, upper back, lower back, upper abdomen, lower abdomen, thighs) from 0 (none) to 4 (frankly virile), total >8 indicating mild, >15 moderate-to-severe.

General examination seeks hyperandrogenism clues: clitoromegaly, balding, obesity. For hypertrichosis, inspect for lanugo persistence, naevi, or systemic signs (e.g., cachexia).

Investigations if FG >15 or rapid onset/virilisation:

• Blood tests: Total/free testosterone, DHEAS, SHBG, 17-hydroxyprogesterone (for CAH), prolactin, TSH.
• PCOS suspicion: Transvaginal ultrasound (≥12 ovarian follicles 2-9mm or ovarian volume >10mL), exclude hyperandrogenism other causes.
• Skin fragility/sun blisters: Porphyria cutanea tarda screen.
• Faun tail (sacral hypertrichosis): Spinal MRI for spina bifida occulta.

Hypertrichosis probes medications, nutrition, malignancy (e.g., chest X-ray, colonoscopy if paraneoplastic).

Complications

Psychosocial repercussions dominate: embarrassment, anxiety, depression from visible hair, especially facial. Affected individuals incur substantial time, cost, and pain for removal. Women with hirsutism report reduced self-esteem and intimacy issues.

Underlying conditions pose risks: PCOS links to infertility, diabetes, cardiovascular disease; adrenal tumours to malignancy; paraneoplastic hypertrichosis signals poor cancer prognosis. Mechanical removal risks folliculitis, scarring, dermatitis.

Management

Treatment targets cosmesis and underlying causes. Mechanical/physical methods provide symptomatic relief; pharmacological addresses hirsutism/hyperandrogenism.

Cosmetic measures

• Bleaching: Hydrogen peroxide lightens dark hair, rendering it less conspicuous.
• Depilatories: Thioglycolate creams dissolve hair shaft (15-30min application); risk irritation/dermatitis. Test patch advised.
• Shaving: Quick, painless; myth of coarser regrowth debunked—does not alter follicle.
• Waxing/Plucking/Threading: Epilate roots; lasts 4-6 weeks; risks folliculitis, ingrown hairs, scarring.
• Sugaring: Natural paste alternative to waxing.
• Laser/IPL: Gold standard for dark hair on light skin (targets melanin); multiple sessions (months-years); effective long-term reduction. Nd:YAG for darker skin.

Topical pharmacological

• Eflornithine (Vaniqa®): Prescription cream inhibits ornithine decarboxylase, slowing facial hair growth (twice daily); 4-8 weeks for effect; combine with removal. Side effects: stinging, folliculitis.

Systemic pharmacological (hirsutism)

Antiandrogens slow growth, thin hair (6-12 months onset, continue 1-2 years):

• Combined oral contraceptive pill (COCP): Suppresses ovarian androgens, raises SHBG; first-line with PCOS.
• Spironolactone: 50-200mg daily; aldosterone antagonist with antiandrogen effects. Combine COCP; sides: breast tenderness, menstrual irregularity, hyperkalaemia (monitor).
• Cyproterone acetate: Potent antiandrogen (2-100mg cycles with oestrogen).
• Flutamide/Finasteride: Alternatives; hepatotoxicity risk (flutamide).

Not for hypertrichosis. Pregnancy contraception mandatory (teratogenic).

Treatment of cause

• Weight loss/diet improves insulin sensitivity in PCOS/obesity.
• Discontinue offending drugs.
• Cancer treatment for paraneoplastic.

Hypertrichosis management mirrors cosmetic; laser preferred for permanence.

Prevention

Genetically predetermined growth unpreventable. Mitigate modifiable risks: weight management reduces insulin-driven hyperandrogenism; avoid inducing drugs.

Prognosis

Hirsutism persists lifelong, often worsening with age perimenopausally. Effective management controls appearance. Hypertrichosis outlook hinges on cause—benign genetic forms lifelong; acquired resolves with underlying treatment (e.g., drug cessation).

Frequently Asked Questions (FAQs)

Q: Does shaving make hair grow back thicker?

A: No, shaving shears hair at skin level without affecting follicle size or growth rate; perceived coarseness is stubble illusion.

Q: How effective is laser hair removal for hirsutism?

A: Highly effective for dark terminal hair on light skin, reducing growth 50-90% after 6-8 sessions; maintenance yearly.

Q: Can hirsutism be cured?

A: Not cured, but managed excellently with antiandrogens and removal; address PCOS for best outcomes.

Q: Is hypertrichosis always genetic?

A: No, congenital is genetic; acquired often drug-induced, paraneoplastic, or metabolic.

Q: When should I see a doctor for excessive hair?

A: If rapid onset, virilisation (deep voice, muscle bulk), FG score >15, or associated symptoms (infertility, weight gain).