Helicobacter pylori infection does not protect against eosinophilic esophagitis: results from a large multicenter case-control study.

Am J Gastroenterol

Department of Gastroenterology, Hospital Universitario San Pedro de Alcantara, Caceres, Spain. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Madrid, Spain. Department of Pediatrics, Pediatric Gastroenterology Unit, Hospital Universitario Puerta de Hierro-Majadahonda, Madrid, Spain. Department of Surgery, Division of Gastroenterology, Oncology and Gastroenterology, University of Padua, Padua, Italy. Gastroenterology and Endoscopy Unit, Università degli Studi di Milano, Milan, Italy. Department of Gastroenterology, Consorci Sanitari Terrassa, Barcelona, Spain. Department of Allergy, Hospital Universitario Gregorio Marañon, Madrid, Spain. Department of Gastroenterology, Hospital Universitario Miguel Servet, Zaragoza, Spain. Department of Gastroenterology, Hospital de Viladecans, Barcelona, Spain. Department of Gastroenterology, Hospital de la Santa Creu I Sant Pau, Barcelona, Spain. Department of Gastroenterology, Hospital Clinico Universitario, Valladolid, Spain. Clinical Analysis and Pediatrics, Hospital Universitario Río Hortega, Valladolid, Spain. Department of Pediatrics, Hospital Universitario San Pedro de Alcantara, Caceres, Spain. Department of Gastroenterology, Hospital Quirón, Marbella, Spain. Departement of Gastroenterology, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa (IIS-IP), and CIBEREHD, Madrid, Spain. Department of Gastroenterology, Hospital General de Tomelloso, Tomelloso, and CIBEREHD, Ciudad Real, Spain.

Published: July 2018

Objectives: Rising trends in eosinophilic esophagitis (EoE) have been repeatedly linked to declining Helicobacter pylori (H. pylori) infection, mostly in retrospective studies. We aimed to prospectively evaluate this inverse association.

Methods: Prospective case-control study conducted in 23 centers. Children and adults naïve to eradication therapy for H. pylori were included. Cases were EoE patients, whereas controls were defined by esophageal symptoms and <5 eos/HPF on esophageal biopsies. H. pylori status was diagnosed by non-invasive (excluding serology) or invasive testing off proton pump inhibitor (PPI) therapy for 2 weeks. Atopy was defined by the presence of IgE-mediated conditions diagnosed by an allergist.

Results: 808 individuals, including 404 cases and 404 controls (170 children) were enrolled. Overall H. pylori prevalence was 38% (45% children vs. 37% adults, p 0.009) and was not different between cases and controls (37% vs. 40%, p 0.3; odds ratio (OR) 0.97; 95% confidence interval (CI) 0.73-1.30), neither in children (42% vs. 46%, p 0.1) nor in adults (36% vs. 38%, p 0.4). Atopy (OR 0.85; 95%CI 0.75-0.98) and allergic rhinitis (OR 0.81; 95%CI 0.68-0.98) showed a borderline inverse association with H. pylori infection in EoE patients. This trend was not confirmed for asthma or food allergy.

Conclusions: H. pylori infection was not inversely associated with EoE, neither in children nor in adults. A borderline inverse association was confirmed for atopy and allergic rhinitis, but not asthma of food allergy. Our findings question a true protective role of H. pylori infection against allergic disorders, including EoE.

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Source
http://dx.doi.org/10.1038/s41395-018-0035-6DOI Listing

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