Effect of alcohol on the progress of hepatitis B cirrhosis

Hepatitis B virus (HBV) and alcohol are primary causes of cirrhosis. Alcohol can result in replication of HBV, an increase in oxidative stress, a compromised immune response to the virus and an increase in liver inflammation, all of which can result in progression of cirrhosis. The aim was to explore the interaction of alcohol with HBV and to show the effect of different levels of alcohol intake on liver fibrosis and cirrhosis.

We selected 90 patients with hepatitis B cirrhosis and divided them into three groups: non-drinking, moderate drinking and excessive drinking. Indicators of fibrosis (type III procollagen, type IV collagen, laminin, hyaluronic acid), HBV-DNA load, transaminases, quantitative detection of hepatitis B surface antigen (HBsAg), Child-Pugh scoring system rating and the number of complications were tested at three time points: 0, 3 and 6 months after quitting drinking and after medical treatment.

We found that all indicators of fibrosis, HBV-DNA load, alanine (ALT) and aspartate (AST) transaminases in the excessive drinking group were highest among the three groups at any time. There were almost no differences between the moderate drinking and non-drinking groups at 0, 3 and 6 months after quitting drinking and treatment. We also found no difference among the three groups in quantitative detection of HBsAg at any time. It was observed that there are more patients with excessive drinking were in Child-Pugh C class and had more complications compared with the other two groups.

Patients with chronic HBV infection and an excessive drinking habit activate HBV-DNA which increases liver inflammation, thus accelerating the progress of liver cirrhosis. Moderate drinking had no significant effect on the progress of liver cirrhosis. Hepatitis B cirrhosis patients with excessive drinking had more complications and were more likely to be in Child-Pugh C class compared with the other groups.