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Secondary analysis shows H. pylori infection fails to significantly impact metabolic scores in morbidly obese individuals.
Background: The interplay between Helicobacter pylori (H. pylori) infection and metabolic dysfunction-associated steatotic liver disease (MASLD) in patients with morbid obesity remains unclear. This study aimed to investigate associations between H. pylori infection, surrogate markers of insulin resistance, and MASLD in a well-characterized cohort. Methods: In this secondary analysis of 444 adults with morbid obesity, H. pylori status was determined histologically from gastric biopsies. MASLD was assessed via liver biopsy in 93 patients. Metabolic indices, including TyG, TyG-BMI, Atherogenic Index of Plasma (AIP), and METS-IR, were calculated from fasting laboratory data. Statistical analyses included correlation analyses and restricted cubic spline (RCS) modeling. Results: Among participants, 343 subjects were included in the analysis, where 30% had type-2 diabetes, and 18% had MASLD. No significant differences in TyG, TyG-BMI, AIP, or METS-IR were observed between H. pylori-positive and -negative groups, or between MASLD subgroups stratified by H. pylori status. Correlation analyses showed negligible associations between infection status and metabolic scores. RCS analyses suggested non-linear trends, with higher TyG and TyG-BMI values modestly increasing MASLD probability in H. pylori-positive patients, though these did not reach statistical significance. Discussion: H. pylori infection may modestly increase MASLD risk, acting as a cofactor that amplifies metabolic dysfunction, particularly in obesity. However, evidence is heterogeneous, causality remains unproven, and effect sizes are small. Future mechanistic and interventional studies are needed to clarify its role and potential for targeted therapy. Conclusion: In adults with morbid obesity, H. pylori infection was not significantly associated with surrogate markers of insulin resistance.
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Hoseini et al. (2026) studied this question.
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