A case of refractory dermatomyositis responsive to tofacitinib

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    The JAK inhibitor CP-690,550 (tofacitinib) inhibits TNF-induced chemokine expression in fibroblast-like synoviocytes: autocrine role of type I interferon

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    Janus kinase reduces interferon signaling, which has been shown to be up-regulated in DM. Tofacitinib has been shown in case reports and small series to be beneficial in the management of refractory skin lesions of DM as well as in refractory myositis and ILD.26–28 Other biologic agents, including tocilizumab and abatacept, have shown promise in small series and larger trials are ongoing to better define their use in management of myositis.29,30

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