674 - Association Between Helicobacter Pylori Infection and Risk of Eosinophilic Esophagitis, Inflammatory Bowel Disease, and Celiac Disease in Adolescents
Monday, April 27, 2026
8:00am - 10:00am ET
Publication Number: 4659.674
Mahnoor Memon, State University of New York Downstate Medical Center College of Medicine, Bronx, NY, United States; Thomas Wallach, State University of New York Downstate Medical Center College of Medicine, Brooklyn, NY, United States
Medical Student State University of New York Downstate Medical Center College of Medicine Bronx, New York, United States
Background: Helicobacter pylori (H. pylori), a gram-negative, urease-positive bacterium transmitted via person-to-person or fecal–oral routes, survives stomach acid and often causes gastric and peptic ulcers. Infection activates innate immunity and Th1/Th17 responses, releasing TNF-α and IFN-γ. Similar immune pathways drive Eosinophilic Esophagitis, Crohn’s disease, Ulcerative Colitis, and Celiac disease, with regulatory T cells modulating inflammation. Objective: To evaluate whether adolescents aged 12–18 years with a diagnosis of H.Pylori infection have a different risk of developing Eosinophilic Esophagitis, Crohn’s disease, Ulcerative Colitis, or Celiac Disease compared to adolescents without an H. pylori diagnosis Design/Methods: A comparative design done on the TriNetX platform evaluated hazard risk for Eosinophilic Esophagitis (ICD-10-CM: K20.0), Celiac Disease (K90.0), Crohn’s Disease (K50), and Ulcerative Colitis (K51) in adolescents aged 12–18 diagnosed with H. pylori (B96.81, K29.60) versus those without. Neisseria meningitidis serotype A vaccination (RxNorm: 797629) anchored the cohort timeline. Cohorts were propensity score-matched for age, sex, race/ethnicity (Hispanic/Latino, Not Hispanic/Latino, Black/African American, Asian), and obesity to minimize confounding. Kaplan-Meier analysis was used to calculate hazard ratios and assess significant subsequent diagnoses Results: Hazard ratios from highest to lowest are Crohn’s disease 21.086 (95% CI 14.578–30.499), Eosinophilic Esophagitis (EoE) 20.230 (95% CI 13.137–31.153), Ulcerative Colitis (UC) 15.619 (95% CI 10.376–23.510), and Celiac Disease 8.206 (95% CI 5.677–11.859). All CIs exclude 1, indicating statistical significance. Crohn’s disease and EoE show wider CIs, reflecting greater variability.
Conclusion(s): Adolescents diagnosed with H. pylori have an increased risk of gastrointestinal disorders. Early exposure may involve antibiotic use, acid suppression, and other microbiome-altering interventions that raise the risk of Eosinophilic Esophagitis (EoE). For individuals with IBD, including Crohn’s disease and Ulcerative Colitis, a prior H. pylori infection can disrupt the gut microbiota and alter gastric and intestinal permeability. H. pylori eradication therapy, typically using antibiotics and proton pump inhibitors, may further dysregulate the gut microbiome. While some studies suggest H. pylori may be protective, timing is critical.
Hazard Ratio H.Pylori and GI Figure 1- Forest Plot .pdfFigure 1: Forest Plot shows the Hazard Ratio and 95% CI with the Gastrointestinal Diseases explored.