Association of Helicobacter pylori Seropositivity with Liver Enzyme Alterations and Antioxidant Defense Status

Helicobacter pylori (H. pylori) represents a highly prevalent Gram-negative bacterium primarily associated with chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Increasing evidence, however, suggests that its biological effects may extend beyond the stomach through systemic inflammation, metabolic perturbation, and oxidative stress. The present study investigated the association between H. pylori seropositivity, serum liver enzymes, and selected antioxidant and oxidative-stress biomarkers. A comparative cross-sectional design comprising 200 adults was adopted. Participants were classified into H. pylori-seropositive (n = 100) and seronegative (n = 100) groups according to serum anti-H. pylori IgG measured by enzyme-linked immunosorbent assay. This study revealed that H. pylori-seropositive participants were shown significantly higher mean ALT (34.8±12.7 U/L), AST (31.6±10.2 U/L), GGT (27.5±11.8 U/L), and MDA (4.63±1.21 µmol/L) concentrations than seronegative participants (27.1±9.6 U/L, 25.8±8.3 U/L, 27.5±11.8 U/L, and 3.38±0.94 µmol/L, respectively). On the other hand, the difference in ALP concentration between the positively (91.4±24.6 U/L) and negatively (85.2±22.1 U/L) infected individuals was comparatively modest. Antioxidant homeostasis was altered, with reduced GPx (42.3±9.8 U/L) and GSH (4.12±0.91 µmol/L) accompanied by increased SOD (14.8±3.6 U/mL) and CAT (58.7±14.9 U/mL) activities among the positively infected individuals. Anti-H. pylori IgG concentration correlated positively with MDA (+0.47), SOD (+0.38), ALT (+0.34), AST (+0.31), CAT (+0.29), and GGT (+0.22); but negatively with GSH (−0.36) and GPx (−0.30). Multivariable analysis indicated that H. pylori seropositivity remained associated with selected biochemical alterations after adjustment for demographic and metabolic covariates. These findings support a possible association between H. pylori exposure, subtle hepatic biochemical abnormalities, and systemic redox imbalance. Nevertheless, the cross-sectional and serological design precludes causal inference and cannot reliably distinguish active from previous infection. Prospective studies employing active-infection diagnostics and longitudinal assessment before and after eradication are warranted.