Abstract

Background Hepatitis C (HCV) infects 1-3% of the United States population. African Americans(AA)are disproportionately infected with this virus (5%) and predominately infected with genotype 1 HCV. The natural history of this disease in AA has not been analyzed in a large number of HCV infected patients. Aim To analyze demographic, virolgical, biochemical and histological data in order to determine the natural history of liver disease in AA versus non-African Americans (non-AA). Methods We retrospectively reviewed the records of 289 patients with HCV seen at our institution from 1996 through 1999. We included patients who had adequate histological data to assess HAl and the degree of hepatic fibrosis. The following data were collected: age, gender, race, weight, baseline ALT, genotype, HCV RNA levels, mode and duration of infection. The duration of infection was estimated from earliest potential exposure to the virus. Liver biopsies were reviewed (blindly) and graded for histologic activity using the Knodell scoring system (HAl). Results There were 93 AA and 196 non-AA patients. There were no significant differences in mean baseline HCV RNA and weight. Although not significant, only 23% of AA's compared to 31% of non-Ax's were cirrhotic. There was a significant difference between AA and non-AA patients in piecemeal necrosis (PN)(2.5 vs. 3.1, p=.04), mean baseline ALT(86.55 vs. 112.41, p=.Ol), age (49 vs. 45, p=.OOI), and duration of infection(27 vs. 23, p=.(02). AA patients were more often infected with genotype 1 HCV (87.7% vs. 70.9%, p=.02) No AA patients were infected with genotype 3 HCV. When analyzing the data according to the duration of infection, AA patients had a lower ALT(56 vs. 134, p=.03), total HAI(3.1 vs. 4.8, p=.05), as well as portal inflammation(1.4 vs. 2.4,p=.02), PN(.8 vs. 3.1, p=.05), and HAl without fibrosis(3.5 vs. 6.6, p= .04) during the second decade of exposure (years 10-19). There were no AA patients with cirrhosis by the second decade compared to 26% of non-AA patients with cirrhosis, although this was not statistically significant. By the third decade (years 20-29), 18% of AA patients vs. 31% of non-Ax's were cirrhotic. The degree of fibrosis was significantly greater in non-AA patients (2.1 vs. 2.6, p=.04). Summary AA's are more likely to be infected with genotype 1 HCV and tend to progress more slowly to cirrhosis. In addtition, early in their exposure, AA's had lower HAl, baseline ALT, and percentage of cirrhosis, although mean baseline HCV RNA levels and weight were not significantly different.

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