Literature DB >> 21397729

A sustained virologic response reduces risk of all-cause mortality in patients with hepatitis C.

Lisa I Backus1, Derek B Boothroyd, Barbara R Phillips, Pamela Belperio, James Halloran, Larry A Mole.   

Abstract

BACKGROUND & AIMS: The effectiveness of hepatitis C virus (HCV) treatment with pegylated interferon and ribavirin usually is evaluated by the surrogate end point of sustained virologic response (SVR), although the ultimate goal of antiviral treatment is to reduce mortality. The impact of SVR on all-cause mortality is not well documented by HCV genotype or in populations in routine medical practice with substantial comorbidities.
METHODS: From the US Department of Veterans Affairs (VA), we identified all patients infected with HCV genotypes 1, 2, or 3, without human immunodeficiency virus co-infection or hepatocellular carcinoma before HCV treatment with pegylated interferon and ribavirin, who started HCV treatment from January 2001 to June 2007, stopped treatment by June 2008, and had a posttreatment HCV RNA test result of SVR or no SVR. Mortality data from VA and non-VA sources were available through 2009.
RESULTS: HCV genotypes 1, 2, or 3 cohorts consisted of 12,166, 2904, and 1794 patients, respectively, with SVR rates of 35%, 72%, and 62%, respectively. Each cohort had high rates of comorbidities. During a median follow-up period of approximately 3.8 years, 1119 genotype-1, 220 genotype-2, and 196 genotype-3 patients died. In genotype-specific multivariate survival models that controlled for demographic factors, comorbidities, laboratory characteristics, and treatment characteristics, an SVR was associated with substantially reduced mortality risk for each genotype (genotype-1 hazard ratio, 0.70; P < .0001; genotype-2 hazard ratio, 0.64; P = .006; genotype-3 hazard ratio, 0.51; P = .0002).
CONCLUSIONS: An SVR reduced mortality among patients infected with HCV of genotypes 1, 2, or 3 who were being treated by routine medical practice and had substantial comorbidities.
Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.

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Year:  2011        PMID: 21397729     DOI: 10.1016/j.cgh.2011.03.004

Source DB:  PubMed          Journal:  Clin Gastroenterol Hepatol        ISSN: 1542-3565            Impact factor:   11.382


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