Recovery of hepatitis C specific T‐cell responses after rituximab therapy in hepatitis C mixed cryoglobulinemic vasculitis

Recovery of hepatitis C specific T‐cell responses after rituximab therapy in hepatitis C mixed... 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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Medical Virology Wiley

Recovery of hepatitis C specific T‐cell responses after rituximab therapy in hepatitis C mixed cryoglobulinemic vasculitis

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Publisher
Wiley Subscription Services, Inc., A Wiley Company
Copyright
© 2018 Wiley Periodicals, Inc.
ISSN
0146-6615
eISSN
1096-9071
D.O.I.
10.1002/jmv.25002
Publisher site
See Article on Publisher Site

Abstract

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

Journal of Medical VirologyWiley

Published: Jan 1, 2018

Keywords: ; ; ; ;

References

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