IMPACT OF ALCOHOL ON THE HISTOLOGICAL AND CLINICAL PROGRESSION OF HEPATITIS-C INFECTION

Citation
Te. Wiley et al., IMPACT OF ALCOHOL ON THE HISTOLOGICAL AND CLINICAL PROGRESSION OF HEPATITIS-C INFECTION, Hepatology, 28(3), 1998, pp. 805-809
Citations number
30
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
28
Issue
3
Year of publication
1998
Pages
805 - 809
Database
ISI
SICI code
0270-9139(1998)28:3<805:IOAOTH>2.0.ZU;2-X
Abstract
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.