Original article—liver, pancreas, and biliary tract
Fibrosis Progression in African Americans and Caucasian Americans With Chronic Hepatitis C

https://doi.org/10.1016/j.cgh.2008.08.006Get rights and content

Background & Aims

Prior studies suggest the rate of liver fibrosis progression is slower in African Americans (AAs) than Caucasian Americans (CAs) with chronic HCV infection.

Methods

With a multi-state Markov model, fibrosis progression was evaluated in a well-characterized cohort of 143 AA and 157 CA adults with untreated chronic HCV genotype 1 infection. In subjects with a history of injection drug use, duration of infection was imputed from a fitted risk model rather than assumed to be the reported first year of use.

Results

The distribution of Ishak fibrosis stages was 0 (8.7%), 1/2 (55.7%), 3/4 (29.3%), and 5/6 (6.3%) and was similar in AAs and CAs (P = .22). After adjusting for biopsy adequacy, AAs had a 10% lower rate of fibrosis progression than did CAs, but the difference was not statistically significant (hazard ratio, 0.90; 95% confidence interval, 0.72–1.12). The overall 20-year estimates of probabilities of progression from stage 0 to stages 1/2, 3/4, and 5/6 were 59.3%, 28.8%, and 4.7%, respectively. The estimated median time from no fibrosis to cirrhosis was 79 years for the entire cohort and 74 and 83 years for CAs and AAs, respectively. In 3-variable models including race and biopsy adequacy, the factors significantly associated with fibrosis progression were age when infected, steatosis, ALT level, and necroinflammatory score.

Conclusions

The rates of fibrosis progression were slow and did not appear to differ substantially between AAs and CAs.

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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    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.

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