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Does suppression of HBV replication by antiviral therapy confer the same benefit as host immune control of HBV?
  1. Suna Yapali,
  2. Anna S Lok
  1. Division of Gastroenterology and Hepatology, University of Michigan Health System, Ann Arbor, Michigan, USA
  1. Correspondence to Dr Anna S Lok, Division of Gastroenterology, University of Michigan Health System, 3912 Taubman Center, SPC 5362, Ann Arbor, MI 48109, USA; aslok{at}

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Approximately 50% of hepatocellular carcinoma (HCC) worldwide is attributed to chronic HBV infection.1 Data from the population-based Risk Evaluation of Viral Load Elevation and Associated Liver Disease/Cancer-HBV REVEAL-HBV study showed that high levels of serum HBV DNA are associated with increased risk of cirrhosis, HCC and liver-related mortality.2 The REVEAL-HBV study also demonstrated that among hepatitis B surface antigen positive persons with high levels of HBV DNA at enrolment, the risk of HCC was lower in those who had decline in HBV DNA levels during follow-up compared with those with persistently high levels of HBV DNA. These data suggest that antiviral therapy may decrease the risk of HCC through suppression of HBV replication.

There has been only one randomised controlled trial of nucleos(t)ide analogue (NUC) treatment in patients with chronic hepatitis B (CHB) with HCC as one of the predefined outcomes.3 This study comparing lamivudine versus placebo was terminated after a median of 32.4 months (range 1–42 months) because a significant difference in the composite outcome of disease progression which included HCC was observed between the two groups. At the time of study termination, HCC had occurred in 3.9% of the lamivudine-treated group and 7.4% of the placebo group with a HR of 0.49, and 95% CI 0.25 to 0.99 (p=0.047); however, this difference was no longer significant when the five cases of HCC diagnosed during the 1st year were excluded (p=0.052). …

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  • Contributors SY and ASL: conception and design, drafting of the article and final approval of the version to be published.

  • Competing interests SY received support from the Turkish Association for The Study of the Liver. SY and ASL received support from the Tuktawa Foundation through the Alice Lohrman Andrews Professorship. ASL is partially supported by NIH grant U01 DK082863. SY has no conflicts of interests to disclose. ASL had received research grants from Bristol-Myers Squibb, Gilead and Merck, and had served as advisor for Gilead, GlaxoSmithKline and Merck.

  • Provenance and peer review Commissioned; internally peer reviewed.

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