In patients infected with the hepatitis C virus (HCV), 20% to 30% will
progress to cirrhosis in over two to three decades. Viral and host fa
ctors that are important in the clinical and histologic progression of
HCV infection are not entirely certain. It has been suggested that li
ver disease is worse in alcoholics infected with HCV. In the present r
etrospective study, we examined the effect of moderate alcohol intake
on the histologic and clinical progression of HCV infection and assess
ed whether other variables such as gender, length of exposure, mode of
exposure, HCV RNA levels, and ferritin levels also independently impa
cted disease progression. Liver biopsies were analyzed for the degree
of fibrosis, presence of cirrhosis, and histologic activity by using t
he Histologic Activity Index of Knodell, Patients were divided into tw
o groups based on whether their alcohol intake was significant or not
significant. Significant alcohol intake was defined as >40 g alcohol/d
ay in women and >60 g of alcohol/day in men for >5 years. Groups were
further divided based on the decades of exposure to HCV. There was no
difference in the age or length of exposure to HCV in the alcohol and
the alcohol-free group. HCV RNA serum levels, ferritin levels, and vir
al genotypes were similar in both groups. There was a two- to threefol
d greater risk of liver cirrhosis and decompensated liver disease in t
he alcohol group. Also, the rate to which subjects developed cirrhosis
was faster in the alcohol group with 58% being cirrhotic by the secon
d decade as opposed to 10% being cirrhotic in the nonalcohol group by
the second decade. The histologic and clinical acceleration of liver d
isease was independent of the mode of exposure or sex. In summary, alc
ohol intake is an independent risk factor in the clinical and histolog
ic progression of HCV infection.