Helicobacter pylori (H. pylori) infects approximately 50% of the global population, with a wide variation between regions and countries. Prevalence is highest in Africa, Latin America, and Asia, but lowest in Northern Europe and Northern America, preciselly the regions with a highest prevalence of EoE. Therefore, an inverse association between… Read More
Helicobacter pylori (H. pylori) infects approximately 50% of the global population, with a wide variation between regions and countries. Prevalence is highest in Africa, Latin America, and Asia, but lowest in Northern Europe and Northern America, preciselly the regions with a highest prevalence of EoE. Therefore, an inverse association between rising EoE and declining H. pylori patterns has been repeatedly reported in literature over the past five years, to suggest a protective role of H. pylori infection against the development of EoE. However, the limited number of studies and potential methodological issues (retrospective design, small sample size, inadequate H. pylori diagnostic methods), contituted a reason to develop prospective large-scale multicenter studies in order to clarify the proposed association between H. pylori and EoE.
A group of international researches under the leadership of the Spanish Asociation of Gastroenterology (or AEG) recently conducted a prospective multicenter case-control study involving multiple centers in Spain (16 centers), Italy (5 centers), France (1 center), and Colombia (1 center). Consecutive patients with EoE aged over 2 years old were recruited from outpatient gastroenterology clinics or endoscopy suites. Controls were required to be individuals who also were undergoing upper endoscopy, mostly due to suspicion of EoE, in whom esophageal biopsies were obtained and EoE were excluded.
All included individuals, both cases and controls, were required to be naïve for H. pylori eradication therapy. EoE patients and controls with previous eradication regimens for H. pylori were excluded. The diagnosis of H. pylori infection was based on positivity to non-invasive tests [13C-urea breath test (UBT), monoclonal stool antigen test] or invasive tests (rapid urease test or histology) during endoscopic procedures. Serology was not accepted as a diagnostic test. All tests were performed with patients off antibiotics or bismuth for 4 weeks and off proton pump inhibitor (PPI) therapy for 2 weeks.
Overall, the authors recruited a large series of 404 adult and 404 children. Among them, 312 individuals (38%) were diagnosed with H. pylori infection at baseline. H. pylori prevalence was significantly higher in children than in adults [77/170 (45%) vs. 235/638 (37%), p 0.009]. No significant differences in H. pylori infection prevalence were identified between cases and controls in an overall analysis [cases 151/404 (37%) vs. controls 161/404 (40%), p 0.3], in children [cases 36/85 (42%) vs. controls 39/85 (46%), p 0.1], and adult population [cases (115/319 (36%) vs. controls 122/319 (38%), p 0.3].
Contrary to all previous reports, H. pylori infection was present in a similar proportion of cases and controls recruited in this study, questioning the inverse protective association of H. pylori against EoE suggested in previous literature. After this research data showing parallel declining H. pylori infection and rising incidence of EoE merely reflect a coincidental divergent trend between diseases, rather than a causal relationship.
In conclusion, no inverse relationship was observed between H. pylori infection and EoE in a large prospective multicenter case-control study. In line with recent evidence, this findings question a true protective role of H. pylori infection against allergic disorders. Therefore, H. pylori infection may merely act as a weak surrogate for socio-economic status and hygiene, rather than modulate the immune host response.
Read the full paper at: https://www.ncbi.nlm.nih.gov/pubmed/29545632