INTRODUCTION
Alopecia areata (AA) is an autoimmune condition which affects roughly 2% of the population globally and is characterized by non-scarring hair loss.1 AA presents as patchy hair loss on the scalp or beard which, in <10% of AA patients, can expand to alopecia totalis (AT) resulting in complete hair loss on the scalp and often the eyebrows and eyelashes.2,3 AA pathogenesis involves the loss of immune privilege of the hair follicle because of downregulated proteins that prevent self-antigens from binding with CD8+ T Cells during follicular growth.1 T helper type 1 cells (Th1) and the induction of IFN-γ are major contributors to AA.1,2
AA's effect on pediatric patients, especially adolescents, is associated with concurrent atopic dermatitis (AD).2,3 Dupilumab is an antagonist to interleukin (IL)-4 and IL-13 receptors that is approved for treatment of AD and asthma in pediatric and adult populations. In recent years, dupilumab has shown potential for use in treating AA.1 This report highlights the use of dupilumab in managing AT in an adolescent male.
AA's effect on pediatric patients, especially adolescents, is associated with concurrent atopic dermatitis (AD).2,3 Dupilumab is an antagonist to interleukin (IL)-4 and IL-13 receptors that is approved for treatment of AD and asthma in pediatric and adult populations. In recent years, dupilumab has shown potential for use in treating AA.1 This report highlights the use of dupilumab in managing AT in an adolescent male.
CASE REPORT
A 13-year-old male with a history of AD and food atopy presented with two months of progressive scalp hair loss. Examination revealed discrete, non-scarring patches of hair loss on the mid scalp, crown, and parietal regions meeting the criteria for alopecia areata (Figure 1A). The patient was referred to an endocrinologist, and laboratory work-up was within normal limits (Table 1). Initial treatment for the hair loss included topical, oral, and intralesional corticosteroids, among other pharmacologic therapies (Table 1). Despite topical management, nine months after the initial diagnosis, the chronic AA progressed to AT with complete non-scarring hair loss of the scalp and eyebrows (Figure 1B). The patient's concurrent AD had also progressed in severity, failing treatment with oral and topical steroids and calcineurin inhibitors. Dupilumab was initiated for AD, and at the one-month follow-up, signs of patchy hair growth on the scalp were noted. Hair growth continued over the following months with eventual complete hair regrowth on the scalp and eyebrows. This regeneration was sustained on evaluation 17 months post dupilumab initiation (Figure 1C).





