INTRODUCTIONChronic hepatitis C virus (HCV) infection is one of the most prevalent viral infections in the United States (US) with an estimated 2.7 million individuals living with HCV. The natural history of untreated chronic HCV is characterized by a gradual progression to fibrosis and cirrhosis, hepatocellular carcinoma, liver failure, and mortality. HCV remains the leading cause of chronic liver disease, hepatocellular carcinoma, and liver transplantation in US, and Western countries. Extra‐hepatic manifestations (EHM) occur in approximately 40–74% of HCV‐infected patients. EHM include mixed cryoglobulinemic (MC) vasculitis, B cell lymphomas, rheumatic disorders, autoimmune thyroiditis, hypothyroidism, papillary thyroid cancer, and type 2 diabetes mellitus. While most EHM are provisionally associated with chronic HCV infection, Type II MC vasculitis is perhaps the most strongly associated with HCV, as 70‐86% of symptomatic patients have HCV viremia.Pathogenesis of HCV‐associated MC vasculitis is categorized by preferential expansion of monoclonal B cells, probably triggered by HCV neoantigens/epitopes, which produce soluble IgM with rheumatoid factor activity capable of forming immune complexes that fix complement, resulting in glomerulonephritis, and small vessel vasculitis. Clinical signs of HCV‐associated MC vasculitis include classic manifestations of systemic immune complex diseases, such as cutaneous vasculitis (non‐healing ulcers), arthralgia/arthritis, peripheral neuropathy, and membranoproliferative glomerulonephritis.The
Journal of Medical Virology – Wiley
Published: Jan 1, 2018
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