The impact of certain skin diseases on the lives of those affected tends to be underestimated or even dismissed as simply a “cosmetic problem.” Alopecia areata exemplifies such a condition, owing to its substantial disease burden and its often devastating effects on the patient’s quality of life and self-esteem. The latest review article from our Medical Progress series synthesizes relevant information about hair-follicle biology and pathobiology and summarizes the clinical presentation and management of this common condition.
• What is the epidemiology of alopecia areata?
Alopecia areata is the most frequent cause of inflammation-induced hair loss, affecting an estimated 4.5 million people in the United States. Depending on ethnic background and area of the world, the prevalence of alopecia areata is 0.1 to 0.2%, with a calculated lifetime risk of 2%. Alopecia areata affects both children and adults and hair of all colors. Although the disorder is uncommon in children under 3 years of age, most patients are relatively young: up to 66% are younger than 30 years of age, and only 20% are older than 40 years of age. There is generally no sex predilection, but more men were found to be affected in one study involving patients who were 21 to 30 years of age.
• What is the association between alopecia areata and autoimmune disease?
Alopecia areata is associated with an increased overall risk of other autoimmune disorders (16%). For example, it is accompanied by lupus erythematosus in 0.6% of patients, vitiligo in 4%, and autoimmune thyroid disease in 8 to 28%.
Morning Report Questions
Q: What is the clinical presentation of alopecia areata?
A: Alopecia areata manifests as the loss of hair in well-circumscribed patches of normal-appearing skin, most commonly on the scalp and in the region of the beard. The onset is typically rapid, and the disease can progress to the point that all scalp hair is lost (alopecia areata totalis) or even that all body hair is lost (alopecia areata universalis). Variants of this disorder include ophiasis, in which hair loss affects the occipital scalp; diffuse forms of alopecia; and demasking, which results in the loss of pigment and sudden “graying.” These presentations, together with telltale clinical signs, such as exclamation-mark hairs, cadaver hairs, nail pitting, and the growth of white hair in formerly alopecic lesions, often render the diagnosis straightforward.
Q: What treatment options exist for alopecia areata?
A: Curative therapy does not exist. Some clinicians rely on the high rate of spontaneous remission and recommend a wig if remission does not occur. Clinicians have two principal management options — use of an immunosuppressive regimen (preferable for patients with acute and rapidly progressing alopecia areata) or an immune-deviation strategy that manipulates the intracutaneous inflammatory milieu (favored for patients with the chronic, relapsing form). The best-tested immunosuppressive treatment consists of intradermal injections of triamcinolone acetonide (5 to 10 mg per milliliter) given every 2 to 6 weeks. This agent stimulates localized regrowth in 60 to 67% of cases. High- otency topical glucocorticoids with occlusive dressings lead to improvement in more than 25% of affected patients. The most effective form of immunotherapy is topical sensitization with diphenylcyclopropenone or squaric acid dibutylester. Diphencyprone can now be considered first-line therapy for alopecia areata totalis.