Kinetics of serum O‐glycosylated M‐hepatitis B surface antigen with hepatocellular carcinoma history and nucleos(t)ide analogue therapy in hepatitis B patients

  • Taiki Okumura
    Department of Medicine, Division of Gastroenterology and Hepatology Shinshu University School of Medicine Matsumoto Japan
  • Satoru Joshita
    Department of Medicine, Division of Gastroenterology and Hepatology Shinshu University School of Medicine Matsumoto Japan
  • Takanobu Iwadare
    Department of Medicine, Division of Gastroenterology and Hepatology Shinshu University School of Medicine Matsumoto Japan
  • Shun‐ichi Wakabayashi
    Department of Medicine, Division of Gastroenterology and Hepatology Shinshu University School of Medicine Matsumoto Japan
  • Hiroyuki Kobayashi
    Department of Medicine, Division of Gastroenterology and Hepatology Shinshu University School of Medicine Matsumoto Japan
  • Yuki Yamashita
    Department of Medicine, Division of Gastroenterology and Hepatology Shinshu University School of Medicine Matsumoto Japan
  • Ayumi Sugiura
    Department of Medicine, Division of Gastroenterology and Hepatology Shinshu University School of Medicine Matsumoto Japan
  • Takefumi Kimura
    Department of Medicine, Division of Gastroenterology and Hepatology Shinshu University School of Medicine Matsumoto Japan
  • Takeji Umemura
    Department of Medicine, Division of Gastroenterology and Hepatology Shinshu University School of Medicine Matsumoto Japan

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<jats:title>Abstract</jats:title><jats:p>A newly developed O‐glycosylated M‐hepatitis B surface antigen (HBsAgGi) measurement system can detect hepatitis B surface antigen (HBsAg) associated with infectious particles. We investigated the association of HBsAgGi levels with clinical parameters and a history of hepatocellular carcinoma (HCC) development in a cross‐sectional cohort analysis (Study 1) as well as the quantitative changes in HBsAgGi during nucleos(t)ide analogue (NA) therapy in a longitudinal cohort analysis (Study 2). A total of 124 patients with genotype C chronic HBV infection were analysed in Study 1 to evaluate correlations of HBsAgGi with conventional HBV markers and HCC history. Among those, 36 patients receiving NA therapy were enrolled in Study 2 for quantitative comparisons between pre‐treatment baseline and 48 weeks of NA therapy. In Study 1, serum HBsAgGi was significantly associated with HBsAg (<jats:italic>r</jats:italic> = .5857, <jats:italic>p</jats:italic> < .00001) and weakly but significantly correlated with HBV DNA (<jats:italic>r</jats:italic> = .2936, <jats:italic>p</jats:italic> = .001). Although HBsAgGi (<jats:italic>p</jats:italic> = .111) was comparable between HCC history (+) group and HCC history (−) group, the HBsAgGi/HBsAg ratio (<jats:italic>p</jats:italic> = .011) was significantly higher in HCC history (+) patients. In Study 2, HBsAgGi was significantly decreased after 48 weeks of NA therapy (<jats:italic>p</jats:italic> < .001). HBsAg findings were similar (<jats:italic>p</jats:italic> = .005) along with an HBV DNA reduction (<jats:italic>p</jats:italic> < .001). In the baseline hepatitis B e antigen (HBeAg) (+) subgroup, HBsAgGi decreased significantly between baseline and 48 weeks of NA (<jats:italic>p</jats:italic> = .005), while HBsAg was comparable (<jats:italic>p</jats:italic> = .051). Low HBsAg and high HBsAgGi were associated with a history of HCC development. HBsAgGi decreased significantly by 48‐week NA therapy.</jats:p>

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