Concomitant Diseases and Co-contribution on Progression of Liver Stiffness in Patients with Hepatitis B Virus

Chang-Hai Liu1,2, Wei Jiang1,2, Dong-Bo Wu1,2

  • 1Center of Infectious Diseases, West China Hospital of Sichuan University, Chengdu, China.

Insights

Hepatitis B (HBV) infection is linked to lower risks of fatty liver and metabolic syndrome but higher risks of type 2 diabetes (T2DM) and H. pylori infection. T2DM may worsen liver issues in HBV patients.

Area of Science:

  • Hepatology
  • Infectious Diseases
  • Metabolic Disorders

Background:

  • The interplay between Hepatitis B virus (HBV) infection and common comorbidities like fatty liver, type 2 diabetes mellitus (T2DM), metabolic syndrome (MetS), and Helicobacter pylori (Hp) infection is not well understood.
  • Clarifying these associations is crucial for comprehensive patient management.

Purpose of the Study:

  • To investigate the associations between Hepatitis B surface antigen (HBsAg) positivity and the prevalence of fatty liver, T2DM, MetS, and Hp infection.
  • To explore the co-contribution of HBV and T2DM to abnormal liver transaminase levels and liver stiffness progression.

Main Methods:

  • Analysis of HBsAg screening data from 95,998 participants at West China Hospital (2014-2017).
  • Utilized multivariable logistic regression to calculate adjusted odds ratios for various associations.

Main Results:

  • HBsAg positivity was associated with a decreased risk of fatty liver (OR 0.71) and MetS (OR 0.74), but an increased risk of Hp infection (OR 1.09) and T2DM (OR 1.18).
  • HBsAg-positive patients with T2DM exhibited significantly higher risks of elevated ALT and AST compared to HBV-alone patients.
  • T2DM, in conjunction with HBV, was also linked to increased risks of liver fibrosis (OR 3.23) and cirrhosis (OR 4.31).

Conclusions:

  • Hepatitis B patients demonstrate a reduced likelihood of fatty liver and metabolic syndrome but an elevated risk for T2DM and Hp infection.
  • Type 2 diabetes mellitus may be a significant contributing factor to abnormal liver enzyme levels and the progression of liver fibrosis in HBsAg-positive individuals.
Abstract