Faculty Bibliography

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).¹ 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.

Cutaneous T cell lymphoma (CTCL) represents a heterogeneous group of extranodal non-Hodgkin lymphomas in which monoclonal T lymphocytes infiltrate the skin. The mechanism of CTCL development is not fully understood, but likely involves dysregulation of various genes and signaling pathways. A variety of treatment modalities are available, and although they can induce remission in most patients, the disease may recur after treatment cessation. Owing to relatively low incidence and significant chronicity of disease, and the high morbidity of some therapeutic regimens, further clinical trials are warranted to better define the ideal treatment option for each subtype of CTCL.