Original article—liver, pancreas, and biliary tractFibrosis Progression in African Americans and Caucasian Americans With Chronic Hepatitis C
Section snippets
Study Population
The Virahep-C study cohort included adult patients from 8 clinical centers in the United States who self-identified as either Black/African American or White/Caucasian American. All but 7 patients had a pretreatment liver biopsy within 18 months of the study enrollment, and those with cirrhosis or transition to cirrhosis (ie, Ishak stage 5 or 6) were required to have compensated liver disease and no evidence of hepatocellular carcinoma. Patients with detectable hepatitis B surface antigen,
Baseline Characteristics of the Cohort
The clinical and demographic features of the AA (n = 143) and CA (n = 157) subjects are shown in Table 1. The groups were comparable in age, sex, alcohol use, adequacy of liver biopsy, presumed sources of hepatitis C, and physician-estimated duration of disease. The physician-estimated age of onset of HCV was significantly older in AAs than in CAs. AAs also had a significantly higher body mass index than CAs, but the prevalence of hepatic steatosis was similar. The participants included in this
Discussion
African Americans had an estimated 10% lower risk of fibrosis progression than did CAs, but this difference was not statistically significant. Race-specific fibrosis progression rates for AAs and CAs, adjusting for biopsy adequacy and the uncertain time of infection, were developed. In these models, the probability of progressing from no fibrosis to mild fibrosis (fibrosis stage 0 to 1/2) was the most rapid transition, with subsequent transitions occurring more slowly. These models provide less
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Limited Fibrosis Progression but Significant Mortality in Patients Ineligible for Interferon-Based Hepatitis C Therapy
2016, Journal of Clinical and Experimental HepatologyViral Hepatitis
2014, Mandell, Douglas, and Bennett's Principles and Practice of Infectious DiseasesHepatitis B and C in African Americans: Current status and continued challenges
2014, Clinical Gastroenterology and HepatologyCitation Excerpt :In addition, most studies found a lower alanine aminotransferase level and less piecemeal necrosis and hepatic fibrosis in African Americans.56,57 In contrast, a more recent study that used mathematical modeling of disease progression suggested that there is little difference on the basis of race in progression of hepatic fibrosis in HCV infection.60 Hence, data on racial differences in hepatic fibrosis remain inconclusive.
Fatigue before, during and after antiviral therapy of chronic hepatitis C: Results from the Virahep-C study
2012, Journal of HepatologyCitation Excerpt :The aim of this study was to assess whether fatigue was associated with disease severity and whether fatigue improved with successful treatment. Virahep-C was a prospective clinical study conducted at 8 U.S. medical centers between 2002 and 2005 in which 196 AAs and 205 CAs patients with chronic hepatitis C, genotype 1, were treated with the standard antiviral regimen of peginterferon alfa-2a (Pegasus, Roche Pharmaceuticals; Nutley, NJ) and ribavirin (Copegus, Roche) while undergoing extensive studies of HCV viral kinetics, immune function, genetics, and interferon signaling pathways [21–24,33]. The major aims of Virahep-C were to define response rates to conventional therapy among AA versus CA patients and investigate factors associated with non-response in the two racial groups.
Prevalence and challenges of liver diseases in patients with chronic hepatitis C virus infection
2010, Clinical Gastroenterology and HepatologyCitation Excerpt :Among 485 plasma donors infected during the early 1970s, 34% had stage F3/F4 fibrosis (bridging fibrosis), cirrhosis, or HCC after 31 years; their 35-year cumulative survival was 84% versus 91%–95% for the general population.53 Similarly, a study of 300 black and white Americans with untreated HCV infection found that 29% of patients had stage F3/F4 fibrosis after 20 years, and 4.7% had confirmed cirrhosis.54 It should be noted, however, that these studies could have selected patients with severe disease.
The authors disclose the following: The clinical study was a cooperative agreement funded by the NIDDK and co-funded by the National Center on Minority Health and Health Disparities (NCMHD), with a Cooperative Research and Development Agreement (CRADA) with Roche Laboratories, Inc. Grant numbers: U01DK60329, U01 DK 60340, U01 DK60324, U01 DK60344, U01 DK60327, U01 DK60335, U01 DK60352, U01 DK60342, U01 DK60345, U01 DK60309, U01 DK60346, U01 DK60349, U01 DK60341. Other support provided by National Center for Research Resources (NCRR) General Clinical Research Centers Program grants M01 RR00645 (New York Presbyterian), M02 RR000079 (University of California, San Francisco), M01 RR16500 (University of Maryland), M01 RR000042 (University of Michigan), and M01 RR00046 (University of North Carolina). The study was also funded by R01 AI069952 from the National Institutes of Health and was supported in part by the Intramural Research Program of the National Cancer Institute.