Gastrointestinal Helicobacter pylori infection is associated with reproductive tract HPV prevalence in a propensity score-matched cross-sectional study of 7734 women.

Helicobacter pylori (H. pylori) and human papillomavirus (HPV) are common mucosal pathogens, but population-level evidence on their co-occurrence at distant anatomical sites is limited. We examined whether gastrointestinal H. pylori status was associated with cervical HPV positivity, genotype distribution, and detection of multiple HPV genotypes, and explored whether fasting glucose statistically mediated this association. We conducted a cross-sectional analysis of 7734 asymptomatic women who underwent concurrent H. pylori screening by 13C-urea breath testing and cervical HPV genotyping during routine health examinations. We used 1:1 propensity score matching (PSM) to balance measured demographic and metabolic covariates. An exploratory mediation analysis evaluated fasting glucose as a potential statistical mediator. In the overall cohort, H. pylori positivity was associated with HPV positivity after adjustment for age, body mass index, systolic blood pressure, fasting glucose, total cholesterol, and triglycerides (adjusted odds ratio [aOR] = 1.228, 95% CI 1.082-1.393, p = 0.001). After PSM (N = 6770), the association remained (OR = 1.182, 95% CI 1.035-1.350, p = 0.014). Among HPV-positive participants in the matched cohort, multiple genotype detection (≥ 2 genotypes) was more frequent in H. pylori-positive than H. pylori-negative women (26.4% vs. 19.9%, p = 0.031). H. pylori status was not associated with cervical cytological abnormalities (p = 0.395). In the exploratory mediation model, the estimated indirect association through fasting glucose was small and not statistically significant (proportion mediated = 1.23%, p = 0.132). Gastrointestinal H. pylori positivity was modestly associated with concurrent cervical HPV positivity and with detection of multiple HPV genotypes in this cross-sectional screening cohort. The findings are hypothesis-generating and do not establish temporality, viral persistence, or an immunological mechanism. The absence of an association with cytological abnormalities also argues against interpreting H. pylori as a marker of cervical lesion progression.