No influence of hepatic steatosis on the 3-year outcomes of patients with quiescent chronic hepatitis B

Jin Won Chang, Jae Seung Lee, Hye Won Lee, Beom Kyung Kim, Jun Yong Park, Do Young Kim, Sang Hoon Ahn, Seung Up Kim

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4 Citations (Scopus)

Abstract

The influence of hepatic steatosis on the natural history of chronic hepatitis B (CHB) virus is unclear. Therefore, we investigated whether concurrent steatosis in patients with CHB influences the probability of hepatitis B surface antigen (HBsAg) loss, fibrosis progression and hepatocellular carcinoma (HCC) development. This study enrolled treatment-naïve patients with virologically (HBV DNA <2,000 IU/ml) and biochemically (alanine aminotransferase level <40 IU/L) quiescent CHB who underwent transient elastography between January 2004 and December 2015 and completed 3 years of follow-up. Results: The mean age of the study population (n = 720) was 52.0 years, and there were more men than women (n = 419, 58.2%). The mean HBV DNA level was 321.6 IU/ml. During the 3-year period, 74 (10.3%) patients achieved HBsAg seroclearance. Lower HBV DNA levels (hazard ratio = 0.995, p <.05) were independently associated with HBsAg seroclearance, while hepatic steatosis was not (p >.05). Fibrosis progressed in 89 (12.4%) patients. Male gender (odds ratio [OR] = 1.720) and higher body mass index (OR = 1.083) were independently associated with an increased probability of fibrosis progression (all p <.05), while higher total cholesterol levels (OR = 0.991) and higher liver stiffness values (OR = 0.862) were independently associated with a decreased probability of fibrosis progression (all p <.05). HCC developed in 46 (6.4%) patients. Male gender (OR = 3.917) and higher AST levels (OR = 1.036) were independently associated with an increased probability of HCC development (p <.05). Hepatic steatosis was not associated with the probability of HBsAg seroclearance, fibrosis progression or HCC development in patients quiescent CHB in our study. Further studies with longer follow-up periods are required to validate our findings.

Original languageEnglish
Pages (from-to)1545-1553
Number of pages9
JournalJournal of Viral Hepatitis
Volume28
Issue number11
DOIs
Publication statusPublished - 2021 Nov

Bibliographical note

Funding Information:
This study was supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT and Future Planning (2019R1A2C4070136). The funders had no role in the study design, data collection and analysis, decision to publish or preparation of the manuscript.

Publisher Copyright:
© 2021 John Wiley & Sons Ltd

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Infectious Diseases
  • Virology

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