Successful Treatment of Refractory Discoid Lupus Erythematosus with Deucravacitinib

Main Article Content

Alice Sohn
Nicole Bouché
George Michael Lewitt
Eingun James Song

Keywords

general dermatology, medical dermatology, immunodermatology, biologics, drug response, clinical research

Abstract

Discoid lupus erythematosus (DLE) is the most common subtype of chronic cutaneous lupus erythematosus (CLE) that may present with or without systemic lupus erythematosus (SLE). Treatment for DLE remains limited, as there are no medications specifically approved to treat DLE. Deucravacitinib, an oral, selective, allosteric tyrosine kinase 2 (TYK2) inhibitor, is currently being studied for adults with moderate-to-severe discoid and/or subacute CLE. We report a case of successful treatment of refractory DLE with deucravacitinib.


A 65-year-old female with a longstanding history of systemic lupus erythematosus presented with prominent discoid lesions involving the nose, cheeks, and mid upper cutaneous lip. Having tried topical medications, multiple courses of systemic steroids were attempted, but the patient flared shortly after the tapers. Despite the patient experiencing some improvement on mycophenolate mofetil and prednisone, the decision to switch to deucravacitinib was made due to the patient developing multiple infections while on the former regimen. Three months after starting deucravacitinib, the patient returned with their skin completely clear.


A better understanding of the molecular pathogenesis of CLE is informing the development of more targeted therapeutic strategies. TYK2 and Janus Kinases (JAKs) both mediate the signaling of cytokines, some of which play a role in the pathogenesis of SLE. Deucravacitinib binds to TYK2 at the regulatory domain, which is unique to its respective kinase unlike conventional Janus Kinase (JAK) inhibitors that bind to the active domain conserved across all JAKs. Deucravacitinib offers more targeted inhibition with a potentially improved safety profile compared to conventional JAK inhibitors.

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