Dermatomyositis is an uncommon autoimmune disorder with distinctive cutaneous manifestations that are frequently challenging to manage. Although a number of therapies including hydroxychloroquine, methotrexate, mycophenolate mofetil, and intravenous immunoglobulin have demonstrated efficacy, few alternative treatments are available when these agents fail. Recently, tofacitinib, an oral Janus kinase (JAK)-1/3 inhibitor, was approved for use in rheumatoid arthritis and has demonstrated efficacy for treating inflammatory skin diseases including psoriasis, alopecia areata, vitiligo, and atopic dermatitis. 1,2 Studies suggest that tofacitinib suppresses interferon signaling, 3 a pathway that has been found to be abnormally upregulated in dermatomyositis. 4 With this context in mind, we sought to evaluate the utility of tofacitinib for treating cutaneous dermatomyositis.
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