Gastric Tissue Biomonitoring Identifies Tissue-Specific Metal Profiles Associated with Helicobacter pylori Infection

Background: Helicobacter pylori infection is a common chronic bacterial infection and an established cause of gastritis, peptic ulcer disease, and gastric cancer. Environmental and host metal status may interact with gastric inflammatory and microbial processes, and infection-related changes in gastric acidity, mucosal permeability, and metal handling may in turn alter local tissue concentrations. This study compared systemic and gastric tissue concentrations of seven elements in adults with histopathologically confirmed H. pylori infection and uninfected controls. Methods: This single-center case–control study included 110 adults undergoing upper gastrointestinal endoscopy (55 H. pylori-positive and 55 H. pylori-negative). H. pylori status was established by hematoxylin–eosin and modified Giemsa staining. Whole blood collected in purple-top K2EDTA tubes was analyzed for As, Pb, Cd, and Sn; serum obtained from yellow-top serum-separator tubes containing clot activator and separator gel was analyzed for Al, Co, and Ni. A separate fresh antral biopsy, not the formalin-fixed histology specimen, was used for ICP-MS; tissue concentrations were normalized to recorded dry weight. Between-group metal comparisons were corrected as one family of 14 tests using Benjamini–Hochberg FDR. Prespecified age- and sex-adjusted models and an exploratory multivariable model were supplemented by ROC, PCA, and internally cross-validated PLS-DA analyses. Results: The H. pylori-positive group was older than the negative group (55.65 ± 15.01 vs. 52.42 ± 12.53 years). Blood aluminum was nominally higher in the positive group (p = 0.032; q = 0.112). In gastric tissue, aluminum was higher [0.23 (0.13–13.40) vs. 0.13 (0.10–0.23) μg/g dry weight; p < 0.001; q = 0.002], whereas arsenic was lower [1.35 (0.54–2.02) vs. 1.92 (1.47–2.43) μg/g dry weight; p < 0.001; q = 0.003] in H. pylori-positive participants. Tissue cobalt and blood/tissue nickel differences did not remain significant after FDR correction. In prespecified age- and sex-adjusted models, tissue arsenic showed an inverse association (OR = 0.431, 95% CI 0.263–0.705; p = 0.0008), whereas tissue aluminum showed a positive association (OR = 4.957, 95% CI 1.629–15.085; p = 0.0048). In the exploratory joint model, only tissue aluminum remained significant (adjusted OR = 4.016, 95% CI 1.119–14.417; p = 0.033). The joint model had an apparent within-cohort AUC of 0.774; repeated five-fold cross-validated PLS-DA yielded an AUC of 0.707. Conclusions: Histopathologically confirmed H. pylori status was associated with compartment-specific metal concentration patterns, particularly higher tissue aluminum and lower tissue arsenic. Because the study was cross-sectional and measured total concentrations, these findings do not establish environmental exposure, temporal accumulation, toxicity, or a causal direction. The regression and multivariate findings are exploratory and require validation in independent cohorts with standardized tissue sampling, arsenic speciation, exposure assessment, and quantitative gastric pathology.