Treatment of Persistent Erythema Multiforme With Janus Kinase Inhibition and the Role of Interferon Gamma and Interleukin 15 in Its Pathogenesis
In case series study, 4 patients with persistent erythema multiforme treated with JAK inhibitor experienced marked clinical improvement; RNA sequencing & proteomic evaluation suggest cytotoxic responses may be promoted by IFN-γ & IL-15 and may be controlled with JAK inhibition.
Source:
JAMA Dermatology
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SPS commentary:
This is one of two studies in JAMA Dermatology that describe the effectiveness of two unique treatments for chronic erythema multiforme (CEM), each targeting a separate immunologic pathway. The other study of the use of thalidomide, an inhibitor of tumor necrosis factor synthesis reports that 6 months of treatment was linked to complete remission in two-thirds of the 35 patients, however, adverse events were a common cause of thalidomide withdrawal (5 [14%] stopped treatment; 7 [20%] experienced ≥1 flare).
An editorial notes that although future studies are needed, these studies show that the pathophysiology of CEM is complex, likely with contributions from numerous pathways involving TNF, IFN-γ, and IL-15 signalling, and thalidomide and JAK inhibition are promising treatment options for patients with CEM, historically a mysterious and difficult to treat disease.