Systemic lupus erythematosus arising during interferon-alpha therapy for cryoglobulinemic vasculitis associated with hepatitis C

• Published in: Clinical rheumatology Vol. 24; no. 2; pp. 178 - 181
• Main Authors: Niewold, Timothy B, Swedler, William I
• Format: Journal Article
• Language: English
• Published: Germany Springer Nature B.V 01.04.2005
• Subjects: Autoantibodies; Autoimmune diseases; Blood diseases; Case reports; Cryoglobulinemia - drug therapy; Cryoglobulinemia - virology; Female; Hepatitis; Hepatitis C; Hepatitis C, Chronic - complications; Humans; Hydroxychloroquine; Immunologic Factors - adverse effects; Immunologic Factors - immunology; Immunomodulation; Interferon-alpha - adverse effects; Interferon-alpha - immunology; Lupus; Lupus Erythematosus, Systemic - chemically induced; Lupus Erythematosus, Systemic - diagnosis; Lupus Erythematosus, Systemic - immunology; Lymphopenia; Middle Aged; Prednisone; Systemic lupus erythematosus; Ulcers; Vasculitis; Vasculitis - drug therapy; Vasculitis - virology; α-Interferon
• ISSN: 0770-3198; 1434-9949
• DOI: 10.1007/s10067-004-1024-2

We present the case of a 53-year-old woman who developed systemic lupus erythematosus (SLE) after being treated with interferon-alpha (IFN-alpha) for cryoglobulinemic vasculitis associated with hepatitis C virus (HCV) infection. Her cryoglobulinemic vasculitis resolved rapidly with IFN-alpha treatment. However, after 10 months of IFN-alpha therapy, she developed a photosensitive malar rash, oral ulcers, arthralgias, lymphopenia, and anti-SSA autoantibodies. She was diagnosed with SLE induced by IFN-alpha therapy. IFN-alpha was discontinued, she was treated with a short course of prednisone and hydroxychloroquine, and she improved rapidly. This is the first report of IFN-alpha-induced SLE complicating treatment of cryoglobulinemic vasculitis associated with HCV infection. The development of SLE during therapy with IFN-alpha could be due to direct immunomodulation by IFN-alpha, and review of experimental data and prior case reports suggests a pathogenic role for IFN-alpha in SLE.