CASE #1: Alopecia areata

Alopecia areata (AA) is a nonscarring hair loss that most commonly occurs over the scalp but can occur over any hair-bearing portion of the body. AA is an autoimmune condition in which activated T-lymphocytes target hair follicles. Some evidence points to follicular melanocytes as being the target in this disease.1 Many patients report a positive family history of the condition, and there are reports of twins with AA.1

The most common presentation of AA is rapid and complete hair loss in one or more round or oval patches over the scalp, eyebrows, eyelashes, beard area, or other hairy areas of the body.1 A characteristic feature that may be present in these patches is the presence of “exclamation mark” hairs, especially at the periphery of the lesion.2 These short hairs are tapered toward the scalp end with thickening of the distal portion.3

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Other presentations of AA include alopecia totalis (loss of all scalp hair), alopecia universalis (loss of all scalp and body hair), ophiasis pattern of AA (bandlike hair loss along the periphery of the temporal and occipital scalp), and the reticular variant of AA (widespread thinning).2 Gray or white hairs may initially be spared in the autoimmune process, and patients with salt-and-pepper hair may report rapid graying over the site of alopecia or generalized rapid graying in more diffuse forms. Likewise, early hair regrowth in affected lesions is often depigmented.1

One clue to the diagnosis of AA is nail changes. Nails are affected in approximately 10% of patients with AA, especially in cases that are extensive or long-standing. The most commonly noted change is uniform pitting, but other changes can occur.1

Multiple conditions and autoimmune diseases have been reported in association with AA including atopic dermatitis, Down syndrome, lichen planus, vitiligo, thyroiditis, systemic lupus erythematosus, diabetes mellitus, and myasthenia gravis; however, most cases of AA are not associated with other diseases. Screening for associated conditions is generally not performed unless the patient presents with associated signs or symptoms.1

The differential diagnosis of AA includes trichotillomania, tinea capitis, temporal triangular alopecia, traction alopecia, secondary syphilis, and loose anagen syndrome.2 Clues that the condition is AA include a history of periodic regrowth, nail pitting, and the presence of “exclamation point” hairs.1 If the type of alopecia cannot be differentiated on the basis of history, a scalp biopsy may need to be performed.2

The characteristic pathologic feature of AA is a dense peribulbar lymphocytic inflammation affecting anagen hair follicles. This infiltrate has been likened to a swarm of bees in appearance. The immune attack on anagen follicles leads to a premature conversion to catagen follicles, and the number of catagen and telogen follicles seen histologically is greatly increased.4

The course of AA is unpredictable, and many cases may improve with no intervention. The treatment of choice for localized, cosmetically conspicuous patches of alopecia is intralesional injections of triamcinolone, 2 to 10 mg/mL, given intradermally or in the superficial subcutaneous tissue.1 The optimal concentration when injecting the scalp may be 10 mg/mL, and response rates of 64%-97% have been reported.3 Potent topical steroids, such as clobetasol propionate 0.05% ointment, may also be used as a first-line therapy; however, results have been less reliable than injections. Unlike injections, topical treatment is not painful and may be preferred for young children. Minoxidil has been tried with some success to promote hair growth. Multiple substances have been used to try to stimulate hair regrowth by initiating either an irritant (anthralin) or an allergic (dinitrochlorobenzene, squaric acid dibutyl ester, diphenylcyclopropenone) contact dermatitis over sites of hair loss. Light therapy has also been used in certain patients.3

The patient in this case had already experienced regrowth of some patches of alopecia over his scalp. He was prescribed clobetasol propionate 0.05% to be used twice daily for two weeks out of each month to minimize cutaneous side effects. He was seen for a three-month follow-up examination and had almost complete regrowth of hair over lesion. No new patches of alopecia had developed, but the patient was counseled that new patches could develop in the future.