A 15-year-old white male presented with a 3-week history of hair loss affecting his entire scalp (Figure 1). His past medical history was significant for atopic dermatitis. There was no family history of hair loss. On physical examination, he had complete alopecia of his entire scalp, eyebrows, eyelashes, and truncal hair. The follicular ostia were intact. His nails were normal. Based on his history and examination findings, the patient was diagnosed with alopecia universalis. Immunotherapy with squaric acid was felt to be an appropriate treatment, given the extensive scalp involvement and associated discomfort of intralesional steroids and risks of immunosuppressant medications.
The patient was sensitized to squaric acid by applying a 2% solution in acetone to an outlined 2 Ã— 2 cm area on his hip. He kept the area dry and removed the bandage after 24 hours. He was warned of the potential eczematous reaction and was given a class I topical steroid. He returned in 2 to 3 weeks to check the site for the expected inflammatory reaction. Approximately 2% to 3% of patients cannot be made allergic to the compound, and the sensitization process can be repeated if there is no reaction. After he manifested an eczematous response, squaric acid in acetone in dilute solutions of 0.001%, 0.01%, 0.1%, and 1% were applied to 4 sites on the volar aspects of the arms (Figure 2). The goal is to identify the concentration of squaric acid that produces a mild eczematous reaction, evidenced by lowgrade erythema and mild pruritus. This concentration is then applied to the areas of alopecia weekly. If there is no regrowth after 24 weeks, the treatment should be discontinued.
Our patient had an excellent response and recovered completely (Figure 3). He stopped applying squaric acid after about 9 months and had no relapse for 1 year, after which he was lost to follow-up.
Alopecia areata (AA) is a common cause of nonscarring alopecia. Although the exact pathogenesis of AA is unknown, it is considered a T-cellâ€“mediated autoimmune condition due to the loss of immune privilege in the hair follicle.1 It is also associated with an increased risk in other autoimmune disorders, including thyroid disease, vitiligo, and lupus erythematosus.1,2
Management of AA is often more challenging than the diagnosis. Management is based on either an immunosuppressive or immunomodulatory approach. Immunosuppression with corticosteroids is a common therapeutic approach. Topical and intralesional injections are utilized for localized disease. Systemic corticosteroids can be used for acute and rapidly progressing patients; however, its utility is limited by the side-effect profile.1