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Alopecia areata is characterized by single or multiple well demarcated patches of hair loss, typically on the scalp and occasionally in the beard, eyebrows, eyelashes, or other hair-bearing areas of the body. Patterns of hair loss due to alopecia areata include the following^1,4:

Less common forms of alopecia areata include alopecia totalis (complete loss of hair on the scalp) and alopecia universalis (a generalized pattern of total body hair loss).

Patients with alopecia areata usually present with massive shedding of hair within a short period. The lesions are typically round or oval well demarcated smooth patches on hair-bearing areas.⁴ The hair cycle has three sequential stages: anagen, catagen, and telogen. In early alopecia areata, the hair follicles enter the late catagen and telogen phases prematurely, resulting in malformation of the hair shaft and subsequent distal fracturing.² As a result, short “exclamation point” hairs that taper proximally form and are visible at the margins of the hairless lesions; these hairs are considered pathognomonic of alopecia areata. Positive results of a hair-pull test at the margins of the lesion indicate an active disease process. Most patients are asymptomatic; a few describe mild-to-moderate pruritus, pain, or a burning sensation before a patch of alopecia appears.^2,4

Nail dystrophy can be seen in 10% to 66% of patients on careful inspection.^2,4 The most common nail change appears as an irregular pattern of pitting, sometimes described as “hammered silver” or “sandpaper.” Other presentations include opacification; longitudinal ridging; superficial splitting, thinning or thickening of the nail matrix; and onycholysis with nail loss. A few patients also have associated autoimmune disorders, such as atopic dermatitis, vitiligo, autoimmune diseases (eg, pernicious anemia, lupus erythematosus, rheumatoid arthritis, ulcerative colitis), and endocrine abnormalities (eg, thyroid disease, diabetes).^1,2,4,5

Although the etiology and pathophysiology of alopecia areata are unknown, genetic predisposition and environmental factors are thought to be responsible. About 40% of patients with early-onset alopecia areata have an affected family member.⁵ The current hypothesis from animal models attributes alopecia areata to a T lymphocyte autoimmune reaction to hair follicles. A detailed medical history can rule out hair loss from recent stressful life events or severe illness (ie, telogen effluvium) or self-inflicted hair loss secondary to psychiatric conditions (ie, trichotillomania).⁶ Diagnosis is most often made clinically, but a skin biopsy of the affected area can be useful in difficult cases to differentiate alopecia areata from androgenetic alopecia, telogen effluvium, and trichotillomania.

Treatment for alopecia areata aims to suppress the autoimmune process and promote regrowth of hair. Wiseman and Shapiro⁷ have recommended a useful treatment plan. For patients older than 10 years with less than 50% scalp involvement, first-line therapy consists of intralesional corticosteroids every 4 to 6 weeks for up to 6 months. This can be combined with topical therapies, including 5% minoxidil and potent corticosteroids or short-contact anthralin in isolation. For patients younger than 10 years with more than 50% scalp involvement, therapy could commence with topical immunomodulatory agents that act as contact sensitizers, including diphenylcyclopropenone, squaric acid dibutyl ester, and dinitrochlorobenzene, followed by the aforementioned topical therapies. Other therapies recommended for children younger than 10 years include topical 5% minoxidil solution with potent corticosteroids or short-contact anthralin in isolation.^3,4,8