Abstract

Chronic hepatitis C-virus (HCV) infection is frequently associated with a variety of autoimmune phenomenons. Mixed cryoglobulins appear in up to 50% of chronic HCV-infected patients, mostly asymptomatic. Cryoprecipitates present IgM with rheumatoid factor activity and development of immunocomplexes deposited in small vessels responsible for resulting vasculitis. MANIFESTATIONS: Characteristic clinical findings are weakness, arthralgia and purpura with further complications including glomerulonephritis and neuropathic lesions. Several mechanisms for HCV-induced clinical lymphoproliferation are discussed, such as chronic B-cell stimulation and activation of the antiapoptotic oncogene bcl-2 leading to immunoglobulin synthesis and eventually evolving into B-cell non-Hodgkin's lymphoma (NHL). Conventional treatment of HCV-associated mixed cryoglobulinemia aimes at reducing circulating immunocomplexes and causal therapy with interferon (IFN) and ribavirin. New approaches using the anti-CD20 antibody rituximab have been described recently.

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