Hepatitis B virus infection and decreased risk of nonalcoholic fatty liver disease: A cohort study
Journal
Hepatology
Journal Volume
66
Journal Issue
2
Date Issued
2017
Author(s)
Wang C.-C.
Abstract
Potential conflict of interest: Nothing to report. TO THE EDITOR: We read with great interest the article by Joo et al.1 In this study involving 83,339 participants without nonalcoholic fatty liver disease (NAFLD) at baseline, 20,200 incident NAFLD cases were identified during a median follow‐up period of 6.6 years. The adjusted hazard ratio of hepatitis B surface antigen (HBsAg)‐positive participants for incident NAFLD was 0.83 compared with HBsAg‐negative participants. After adjustment for confounders, the association between hepatitis B virus (HBV) infection and decreased risk of incident NAFLD remained, suggesting HBV infection may have a protective effect on the development of NAFLD. Although this large‐scale cohort study improves our understanding about the relationship between HBV infection and the development of NAFLD, several issues deserve discussion and further investigation. First, this study showed a decreased risk of incident NAFLD in HBsAg‐positive participants, even having larger body mass index and higher percentage of obesity at baseline compared with HBsAg‐negative participants. Furthermore, the favorable lipid profiles in HBsAg‐positive subjects such as lower triglyceride, cholesterol, and low‐density lipoprotein, as well as higher high‐density lipoprotein, may explain the decreased risk of NAFLD development. These results were consistent with our previous observations, suggesting chronic HBV infection protects against the development of NAFLD possibly due to a lower frequency of dyslipidemia profiles.2 However, the mechanisms involved in altered lipid metabolism by persistent HBV infection remain largely unclear and require additional study. Second, NAFLD is considered to be the liver manifestation of metabolic syndrome, which is associated with insulin resistance. Although chronic hepatitis C virus infection is known to be associated with insulin resistance, the relationship between HBV infection and insulin resistance has been inconclusive.3 In this study, baseline insulin resistance using homeostatic model assessment‐insulin resistance (HOMA‐IR) was comparable between HBsAg‐positive and HBsAg‐negative subjects. To clarify the complex interaction between HBV infection, NAFLD, and insulin resistance, the authors may compare HOMA‐IR between HBsAg‐positive and HBsAg‐negative subjects at the last visit to see whether chronic HBV infection affects insulin resistance. Third, because metabolic syndrome and its components can accelerate the progression of liver disease to cirrhosis and even hepatocellular carcinoma in patients with chronic HBV infection, it is imperative to realize which factors could predict the development of NAFLD in these patients.3 The authors may perform a subgroup analysis to identify the risk factors associated with the incident NAFLD in HBsAg‐positive subjects and then modify them with lifestyle modification or medications to reduce the progression of liver damage.
SDGs
Other Subjects
cholesterol; lipid; low density lipoprotein; triacylglycerol; body mass; cohort analysis; hepatitis B; hepatitis C; homeostasis model assessment; human; insulin resistance; Letter; nonalcoholic fatty liver; priority journal; risk reduction; chronic hepatitis B; hepatitis B; Hepatitis B virus; virology; Cohort Studies; Hepatitis B; Hepatitis B virus; Hepatitis B, Chronic; Humans; Non-alcoholic Fatty Liver Disease
Publisher
John Wiley and Sons Inc.
Type
letter