Abstract
Autoimmune disorder is one of the important side effects of interferon-α therapy. Some polymyositis cases as complication of interferon-α therapy were reported, but dermatomyositis were rarely. We report a case of dermatomyositis as a complication of interferon-α therapy for hepatitis C. A 52-year-old Japanese man was treated by combination therapy with pegylated interferon-α-2b and ribavirin for hepatitis C. Three months after the initiation of therapy, he showed erythema in the posterior cervical to dorsal and anterior cervical to thoracic regions, weight loss, general malaise, muscle pain, and severe increase in levels of muscle enzymes. We made a diagnosis of dermatomyositis according to these clinical features, proximal muscle-predominant myogenic change on electromyography, and infiltration of monocytes and CD4+-dominant lymphocytes on skin biopsy, although myositis-associated antibodies were absent. He was successfully treated with intravenous immunoglobulin and tacrolimus in addition to glucocorticoid. This is a very rare case of dermatomyositis associated with interferon-α therapy. We reviewed several similar published cases and the association of dermatomyositis and type I interferon.
Highlights
Polymyositis (PM) and dermatomyositis (DM) are autoimmune muscle disorders that symmetrically affect primarily the proximal limbs, neck, and pharyngeal muscles
Inflammatory cytokines such as TNF-α, IL-1, IL-6, IL-15, and IL-18 are thought to play a crucial role in the pathogenesis of PM/DM [1]
Several studies reported that autoimmune diseases such as systemic lupus erythematosus and PM/DM can develop during treatment with IFN-α or IFN-β [3,4,5,6,7,8,9,10,11,12,13,14]
Summary
Polymyositis (PM) and dermatomyositis (DM) are autoimmune muscle disorders that symmetrically affect primarily the proximal limbs, neck, and pharyngeal muscles. CD4+ T cells, CD8+ T cells, macrophages, and dendritic cells infiltrate around muscular tissue and blood vessels with degeneration and regeneration of muscular fibers. Inflammatory cytokines such as TNF-α, IL-1, IL-6, IL-15, and IL-18 are thought to play a crucial role in the pathogenesis of PM/DM [1]. We report a patient who developed DM as a complication of IFN-α therapy for hepatitis C. In this patient, dermatomyositis was rapidly progressive and successfully treated with glucocorticoid therapy in addition to intravenous immunoglobulin (IVIG) and tacrolimus without reactivation of the hepatitis C virus
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