Morphea induced by treatment with Interferon β-1α.

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ID: 4291
2019
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Abstract
The etiology of morphea is poorly understood, but small vessel endothelial damage, T-cell recruitment, immune dysregulation, and the release of profibrotic cytokines likely contribute to pathogenesis. Biologic agents such as interferon (IFN)-β1α influence the development of systemic sclerosis (SSc) in patients with multiple sclerosis (MS). Treatment with type I interferons, such as IFN-β1α, may activate shared pathogenic pathways of autoimmunity and promote the development of morphea. We present the case of a 55-year-old female who developed morphea secondary to IFN-β1α therapy for multiple sclerosis. This article is protected by copyright. All rights reserved.
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peterson2019morpheathe Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Peterson, E;Steuer, A;Franco, L;Nolan, M A;Lo Sicco, K;Franks, A G;
Journal the british journal of dermatology
Year 2019
DOI
10.1111/bjd.18357
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Keywords Keywords not found

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