Hepatitis B surface antigen glycan isomer is a predictor of the development of hepatocellular carcinoma during nucleoside/nucleotide analog therapy.

Abstract

A recombinant monoclonal antibody against the hepatitis B surface antigen glycan isomer (HBsAgGi) was newly developed using the O-glycosylated PreS2 peptide in M-HBsAg of hepatitis B virus (HBV) genotype C. However, the association between HBsAgGi and the development of hepatocellular carcinoma (HCC) during nucleoside/nucleotide analog (NA) therapy remains unknown. A total of 112 HBV genotype C-infected patients who were treated with NA were included in this study. We assessed the association between HBV markers, including HBsAgGi and other conventional markers, and the development of HCC during NA therapy. Ten patients developed HCC during the follow-up period. Of the HBV markers, HBsAg (≤3.53logIU/mL; p=0.047), HBsAgGi/HBsAg ratio (≥1.10; p=0.035), and HBV DNA (≤6.3logcopies/mL; p=0.012) at baseline and HBsAg (≤3.19logIU/mL; p=0.033) and HBsAgGi/HBsAg ratio (≥1.09; p=0.003) at 48weeks after NA therapy were significantly associated with the development of HCC according to the log rank test. In contrast, no significant association was observed between HBsAgGi and the development of HCC. Multivariate analysis revealed that a platelet count at baseline ≤88×103 /mm3 (p=0.026; hazard ratio [HR], 10.577) and an HBsAgGi/HBsAg ratio at 48weeks after NA therapy ≥1.09 (p=0.040; HR, 10.099) were independently and significantly associated with the development of HCC. Our findings suggest that a combination of on-treatment HBsAgGi and HBsAg predicts the development of HCC during NA therapy.