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Additional Evidence that Alcohol Consumption Negatively Impacts the Outcome of Hepatitis C Infection

Mary Rinella, MD University of Illinois at Chicago Medical Center Chicago, IL Journal: Liver Update: Vol. 10, No. 2, Winter 1996-1997

Retrospective regression analysis of histologic data from alcoholic and non-alcoholic patients with hepatitis C demonstrate that alcoholics with hepatitis C are three times more likely to have cirrhosis than non-alcoholics with hepatitis C. That is, alcohol abuse is an independent risk factor for advanced liver disease in patients with hepatitis C. What remains unclear is whether alcoholics with HCV are more likely to be cirrhotic than alcoholics without HCV. That is, is hepatitis C infection an independent risk factor for more advanced liver disease in alcoholic patients?

Chronic viral infection develops in 80% of the patients infected with the hepatitis C virus (HCV). In those infected patients, 30 to 40% develop cirrhosis over the following two to three decades. Antibody to hepatitis C virus is detected in 10 to 25% of chronic alcoholics as compared to 1 to 2% of healthy blood donors. The clinical, biochemical and viral variables that affect the development of cirrhosis in HCV infected patients have only been partially elucidated. Chronic alcohol ingestion appears to increase the incidence of cirrhosis in hepatitis C infected patients. However, the overall impact of alcohol ingestion on the rate and extent of histologic injury is unknown.

In the present retrospective study conducted at a liver referral center, we sought to determine whether liver injury from hepatitis C was accelerated by alcohol ingestion. Liver biopsies from 78 patients were analyzed for the presence of cirrhosis and graded for activity using the Histological Activity Index of Knodell (HAI). Forty-two patients were HCV positive without significant alcohol exposure and 38 patients had significant alcohol exposure, defined as daily intake of greater than 40 to 80g of alcohol for a period of at least five years.

Sixty-one percent of the alcohol group had cirrhosis, whereas only 21% of the non-alcoholic group had cirrhosis an average of 20 years after the HCV exposure. In the HCV alone group there was a significant linear relationship between the years of exposure to the hepatitis C virus and an increasing HAI score. In contrast, in the alcohol group a linear relationship could only be demonstrated for the first 15 years of HCV exposure. The HAI score plateaued after 15 years primarily due to the fact that the majority of patients had already become cirrhotic by 15 years. The HAI score was significantly greater in the alcohol group, averaging 13 vs. 8 in the non-alcohol group. The development of cirrhosis was independent of age, sex, or route of infection. (IVDA vs. PTH). Further, it appeared to be independent of viral load as the average ACV RNA level was 6.2 x 105 eq/ml in the non-alcohol group and 7.8 x 105 eq/ml in the alcohol group (not significant). The percent of patients infected with genotype 1a or 1b was similar in both groups (75%).

In conclusion, our results suggest that moderate to severe alcohol intake accelerates the rate of histologic progression of liver disease in HCV infected patients. This accelerated progression appears to develop independent of the presence of alcoholic hepatitis, viral load, source of exposure or viral genotype.

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