In HBeAg-negative patients, high surface antigen levels increase liver cancer risk

In a large study of HBeAg-negative patients, Taiwanese researchers were surprised to discover that high levels of HBsAg increased these patients' liver cancer risk more so than having high viral loads. The study was published in the May issue of the journal Gastroenterology 

—Christine. M. Kukka, Project Manager, HBV Advocate

Source: http://www.ncbi.nlm.nih.gov/pubmed/?term=High+Levels+of+Hepatitis+B+Surface+Antigen+Increase+Risk+of+Hepatocellular+Carcinoma+in+Patients+With+Low+HBV+Load

Abstract: High levels of hepatitis B surface antigen increase risk of hepatocellular carcinoma in patients with low HBV load.

Tseng TC, Liu CJ, Yang HC, Su TH, Wang CC, Chen CL, Kuo SF, Liu CH, Chen PJ, Chen DS, Kao JH.

Source
Division of Gastroenterology, Department of Internal Medicine, Buddhist Tzu Chi General Hospital Taipei Branch, Taipei, Taiwan.

BACKGROUND & AIMS:
Patients with chronic hepatitis B virus (HBV) infection have a high risk for developing hepatocellular carcinoma (HCC). Patients with lower levels of hepatitis B surface antigen (HBsAg) have higher chances of losing HBsAg than those with high levels. However, little is known about whether higher levels of HBsAg increase risk for HCC.

METHODS:
We followed 2688 Taiwanese HBsAg-positive patients without evidence of cirrhosis for a mean time period of 14.7 years. In addition to the known risk factors of HCC, we investigated the association between levels of HBsAg and development of HCC.

RESULTS:
Of the patients followed, 191 developed HCC, with an average annual incidence rate of 0.5%. Baseline levels of HBsAg and HBV were associated with development of HCC, and risk increased with level. Compared to HBsAg level, by receiver operating characteristic curve analysis, HBV DNA level better predicted the development of HCC during 10-year and 15-year periods (both, P < .001). However, when we evaluated hepatitis B e antigen-negative patients with levels of HBV DNA <2000 IU/mL, factors that determined HCC risk included sex, age, and levels of alanine aminotransferase and HBsAg (≥1000 IU/mL), but not level of HBV DNA. Multivariate analysis showed that the adjusted hazard ratio for HCC in patients with levels of HBsAg ≥1000 IU/mL versus <1000 IU/mL was 13.7 (95% confidence interval: 4.8-39.3).

CONCLUSIONS:
Among patients infected with HBV genotype B or C, determinants of HCC risk include their sex, age, hepatitis B e antigen status, HBV genotype, and levels of alanine aminotransferase and HBV DNA, but not level of HBsAg. Among hepatitis B e antigen-negative patients with low viral loads, HCC risk is determined by levels of HBsAg and alanine aminotransferase and age, but not HBV DNA.
Copyright © 2012 AGA Institute. Published by Elsevier Inc. All rights reserved.

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