Helicobacter pylori infection and liver function alterations in individuals undergoing gastric cancer screening: a cohort study

Helicobacter pylori is a major cause of gastric disease, but recent evidence suggests it may also contribute to liver dysfunction. We analyzed 16,855 participants from the Ardabil gastric cancer prevention cohort. H. pylori infection was diagnosed by stool antigen testing. Associations with liver enzymes, lipid profile, and fasting blood sugar were assessed using multivariable logistic and linear regression. The prevalence of H. pylori infection was 70.5%. Logistic regression showed that infection was independently associated with liver disease (OR = 1.91, 95% CI: 1.27–2.88, P = 0.002), representing a moderate effect size. The AST/ALT ratio was the strongest predictor of ALD versus NAFLD (OR = 9.52, 95% CI: 6.91–13.12, P < 0.001). In linear regression, H. pylori infection was positively associated with AST (β = 0.017, P = 0.026) but not with ALT, GGT, or ALP. Conversely, metabolic factors including BMI, triglycerides, and FBS showed strong and broad associations with ALT, GGT, ALP, and glycemic control. Higher triglycerides and total cholesterol were inversely associated with liver disease risk. H. pylori infection is associated with subtle AST elevation, which may reflect systemic or metabolic stress rather than direct hepatocellular injury, given the absence of associations with liver-specific enzymes. Metabolic factors play a more dominant role in liver enzyme alterations. The AST/ALT ratio remains a robust diagnostic marker for distinguishing ALD from NAFLD. These findings highlight the complex interplay between infectious and metabolic determinants of liver function and warrant confirmation in longitudinal and interventional studies.