Helicobacter pylori infection, hyperuricemia, and serum uric acid levels: The role of metabolic, renal, and inflammatory factors in a large health examination population.

Abstract

Helicobacter pylori (H. pylori) infection has been linked to several extragastric metabolic disorders. However, its cross-sectional association with hyperuricemia remains uncertain, partly because previous studies have often been limited by small sample sizes and incomplete adjustment for metabolic and renal factors. This large-scale cross-sectional study used data from a health examination database. The main regression analyses included 67,826 participants with valid H. pylori status, serum uric acid measurements, hyperuricemia classification, age, sex, and BMI. Modified Poisson regression with a log link and HC0 robust sandwich variance was used to estimate prevalence ratios for hyperuricemia, while linear regression with HC3 heteroscedasticity-robust standard errors was used for continuous serum uric acid. Sex-stratified and robustness analyses were also performed. In the unadjusted model, H. pylori infection was associated with higher prevalence of hyperuricemia (PR = 1.27, 95% CI: 1.22-1.32, p < 0.001). This association was progressively attenuated after sequential adjustment and was small in the extended clinical model (PR = 1.02, 95% CI: 0.98-1.06, p = 0.269). For continuous serum uric acid, H. pylori positivity remained associated with a small increase after full adjustment (β = 2.14 μmol/L, 95% CI: 0.80-3.49, p = 0.002). Functional-form sensitivity analyses yielded similarly small effect estimates for hyperuricemia, although statistical significance varied across model specifications. Sex-stratified and robustness analyses were generally consistent with these findings. In this large health examination population, any remaining association between H. pylori positivity and hyperuricemia after comprehensive adjustment was small and sensitive to model specification. H. pylori positivity was also associated with a statistically detectable but clinically modest difference in continuous serum uric acid levels. Given the cross-sectional design, these findings should not be interpreted causally.