Severe Dermatomyositis Triggered by Interferon Beta-1a Therapy and Associated With Enhanced Type I Interferon Signaling

Abstract

Background: Type I interferons (IFNs) are common therapeutics for several diseases, including viral infections and multiple sclerosis (MS). Although numerous studies have implicated type I INFs with the production of autoantibodies and the development of certain autoimmune disorders, interferon beta has not previously been described in association with dermatomyositis, to our knowledge. Previous microarray studies of muscle biopsy specimens from patients with dermatomyositis disclosed a type I IFN-induced gene expression profile. The central role of plasmacytoid dendritic cell precursors, together with increased type I IFN production, suggests a pivotal role for type I IFNs in dermatomyositis. We report a case of dermatomyositis exacerbated or induced by interferon beta therapy for MS and provide evidence that demonstrates enhanced type I IFN signaling in this patient. Observations:We observed new-onset dermatomyositis in a 57-year-old patient treated with interferon beta Conclusions: To our knowledge, this is the first description of dermatomyositis exacerbated or induced by interferon beta treatment. Our results demonstrate enhanced type I IFN signaling following interferon beta treatment in our patient with dermatomyositis.

Cutaneous adverse events associated with disease-modifying treatment in multiple sclerosis: a systematic review

“…[93][94][95] Cutaneous events with an inflammatory pathogenesis that were described only once in association with DMTs include dermatomyositis, erythema nodosum, scleromyxedema, lupus erythematosus profundus, vitiligo, and Jessner-Kanof benign lymphocytic infiltrate. [96][97][98][99][100][101] …”

Role of cytokines and chemokines in idiopathic inflammatory myopathies

“…Gene expression microarrays have shown overexpression of many IFN-inducible genes in dermatomyositis patients [1,3]. Furthermore, administration of IFN-a [4] and IFN-b [5] in the treatment of autoimmune disease has been observed to induce dermatomyositis, and the development of IIM has been identified as a rare complication of IFN-a treatment in a series of case reports [6]. Up till now the cellular sources of IFNs have not readily been demonstrated.…”

Interferons as components of the complex web of reactions sustaining inflammation in idiopathic inflammatory myopathies

“…In contrast, IBM patients did not display high levels of muscle or blood IFN type 1-inducible transcripts [39]. Additional evidence of the importance of IFN-a b in DM pathology stems from the observation that administering IFN-a [5,6] and IFN-b [7] for treating autoimmune disease, can induce DM as a rare complication in a series of case reports. IFN type 1-inducible gene products have been shown upregulated in arterioles and capillaries in DM muscle tissues, possibly as components of the endothelial tubuloreticular inclusions [8].…”