Serum Hepatitis B DNA level is a marker of viral replication and efficacy of antiviral treatment in individuals with chronic Hepatitis B.
Dr Chien-Jen Chen and colleagues from Taiwan evaluated the relationship between serum Hepatitis B DNA level and hepatocellular carcinoma risk.
The investigators conducted a cohort study of 3653 participants aged 30 to 65 years.
The patients were seropositive for the Hepatitis B surface antigen and seronegative for antibodies against the Hepatitis C virus.
The team recruited the patients at a community-based cancer screening program between 1991 and 1992.
|The risk by serum Hep B DNA levels was significant after adjusting for cigarette smoking|
|Journal of the American Medical Association|
The main outcome measure was the incidence of hepatocellular carcinoma during follow-up examination.
The incidence of hepatocellular carcinoma was also determined by data linkage with the national cancer registry and the death certification systems.
The team had 164 incident cases of hepatocellular carcinoma and 346 deaths during a mean follow-up of 11 years and 41,779 person-years of follow-up.
The incidence of hepatocellular carcinoma increased with serum Hepatitis B DNA level at study entry in a dose-response relationship.
The doses ranged from 108 per 100,000 person-years for a Hepatitis B DNA level of less than 300 copies/mL to 1152 per 100,000 person-years for a level of 1 million copies/mL or greater.
The investigators observed that the corresponding cumulative incidence rates of hepatocellular carcinoma for the above doses were 1% and 15%, respectively.
The biological gradient of hepatocellular carcinoma by serum Hepatitis B DNA levels remained significant after adjustment for sex, age, and cigarette smoking.
The biological gradient of hepatocellular carcinoma by serum Hepatitis B DNA was also significant after adjusting for alcohol consumption, and liver cirrhosis at study entry.
This remained significant when adjusting for serostatus for the Hepatitis B e antigen, and serum alanine aminotransferase levels.
The dose-response relationship was most prominent for participants who were seronegative for Hepatitis B e antigen.
These participants also had normal serum alanine aminotransferase levels and no liver cirrhosis at study entry.
Participants with persistent elevation of serum Hepatitis B DNA level during follow-up had the highest hepatocellular carcinoma risk.
Dr Chen's team commented, “Elevated serum Hepatitis B DNA level is a strong risk predictor of hepatocellular carcinoma independent of Hepatitis B e antigen, serum alanine aminotransferase level, and liver cirrhosis.”