Abstract

Alcohol abuse and hepatitis C virus (HCV) infection coexist with chronic liver disease in many patients. The mechanism of injury in these patients is probably multifactorial and involves, but is not limited to, a combination of diminished immune clearance of HCV, oxidative stress, emergence of HCV quasi-species, hepatic steatosis, increased iron stores, and increased rate of hepatocyte apoptosis. In patients with HCV infection, alcohol consumption is known to cause accelerated progression of liver fibrosis, higher frequency of cirrhosis, and increased incidence of hepatocellular carcinoma (HCC). These patients also have decreased survival as compared with patients with either alcohol abuse or HCV liver injury alone. Alcohol abuse causes decreased response to interferon treatment in HCV patients. It is therefore necessary for patients with HCV infection to abstain from alcohol consumption.

Introduction

Chronic hepatitis C infection and alcohol abuse account for 70 to 90% of all the cases of chronic liver diseases in the western world. About 20% of chronic alcoholics and patients with hepatitis C infection develop cirrhosis over a period of 20 to 30 years^[1,2] and a portion of these patients develop HCC.^[3] Hepatitis C-related cirrhosis now accounts for more than 50% of all liver transplants performed in the United States.^[4]

The progression to cirrhosis in patients with chronic hepatitis C is affected by several variables. Published data show that viral genotype and viral load, although important predictors of response to treatment with interferon,^[5] lack association with disease severity.^[6] Besides the genetic factors in the host,^[7] there are three other independent variables associated with disease progression in patients infected with hepatitis C. These are age at infection > 40 years, heavy ethanol abuse > 50 g/d, and male gender.^[8-10]