Abstract

Purpose: Eosinophilic esophagitis (EoE) is an increasingly prevalent chronic disease which is thought to be an allergy/immune mediated process. Helicobacter pylori has been inversely associated with allergic diseases, but the relationship between H. pylori, EoE and esophageal eosinophilia is unknown. Our aim was to determine the association between esophageal eosinophilia and H. pylori. Methods: We performed a cross-sectional study of patients with esophageal biopsies in a United States national pathology database between 2008 and 2010. Patients with and without H. pylori on gastric biopsy were compared and odds of esophageal eosinophilia were determined. Results: Of 233,662 unique patients in the source population, 165,017 had both esophageal and gastric biopsies. Of these, 56,301 (34.1%) had normal esophageal biopsies, 5,767 (3.5%) had esophageal eosinophilia, and 11,170 (4.8%) had H. pylori. Overall, the presence of esophageal eosinophilia was inversely associated with H. pylori infection (OR: 0.77, 95% CI: 0.69-0.87). There was a dose-response trend noted as well, with lower odds of H. pylori as levels of esophageal eosinophilia increased (Figure). Specifically, compared to patients with normal esophageal biopsies, odds of H. pylori were progressively reduced among patients with ≥15 eosinophils per high-power field (eos/hpf) (OR 0.79; 95% CI 0.70-0.88), ≥45 eos/hpf (OR 0.75; 0.61-0.93), ≥75 eos/hpf (OR 0.72; 0.62-0.83), and ≥90 eos/hpf (OR 0.52; 0.31-0.87) (p for trend <0.001). A similar dose-response trend was observed for increasingly restrictive clinicopathologic definitions of EoE (requiring dysphagia symptoms or eosinophilic microabscesses on pathology) and decreasing prevalence of H pylori (Figure). Additionally, severity of histologic manifestation of H. pylori was inversely associated with esophageal eosinophilia. All trends held after multivariate analysis. Conclusion: There is a strong inverse association between H. pylori infection and esophageal eosinophilia in this large nationwide patient population. This association persists on several sensitivity analyses, and may have important implications for understanding the pathogenesis and evolving epidemiology of EoE. Disclosure: Robert M. Genta - employed by Caris Life Sciences, Irving, Texas; shareholder in the company. Richard H. Lash - employed by Caris Life Sciences, Irving, Texas; shareholder in the company. There are no other potential conflicts of interest for any of other the authors pertaining to this study.

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