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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