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H. pylori Infection Linked to Reduced Risk for Eosinophilic Esophagitis
Although the etiology of eosinophilic esophagitis is still unknown, Helicobacter pylori infection may play a protective role in the development of the disease.
“Helicobacter pylori infection is inversely associated with EoE,” the researchers wrote. “Our results may contribute to further understanding the pathogenesis and evolving etiology of EoE.”
In a case-control study, researchers examined H. pylori infection in relation to risk for developing EoE. They evaluated H. pylori infection serology in 58 patients with a clinically and histologically proven diagnosis of EoE (81% men; median age, 36.5 years). Also included in the study were 116 age- and sex-matched controls, giving two controls to each case of EoE.
Three of the 58 EoE patients had serological evidence of current H. pylori infection and five of the 58 patients had prior infection that was treated with therapy. A significantly higher seroprevalence of H. pylori was found in the control group compared with patients with EoE (37.9% vs. 5.17%; P < .0001).
“We found a low serological and histological prevalence of H. pylori in EoE patients compared to our matched controls, which was not due to younger age of EoE cases, because interference of age could be eliminated by almost 1:1 matching conditions (3.7 days age difference),” the researchers wrote.
Both current and former H. pylori infection was found to be inversely associated with EoE (OR = 0.24; 95% CI; 0.11-0.5).
“In the present study we made use of a large local H. pylori serology database to assess the association between EoE and H. pylori infection compared to a well matched control population,” the researchers wrote. “We showed a remarkable inversed relationship between H. pylori infection and EoE, and the reported OR 0.24 allocates a protective role of H. pylori in developing EoE.” – by Suzanne Reist
Disclosures: von Arnim reports serving as speaker and/or advisory board member for AbbVie GmbH, Dr. Falk Pharma, MSD and Takeda. Please see the study for a full list of all other researchers’ relevant financial disclosures.
Perspective
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Since its initial recognition over two decades ago, the incidence of eosinophilic esophagitis (EoE) has been steadily increasing. This increase is faster than can be accounted for by changes in diagnosis or endoscopy and biopsy practices, and raises a key question: Why is EoE being so commonly detected?
Investigators have postulated whether this evolving epidemiology may be due to environmental factors such as increasing pollution, changing food supply, climate, or population density. However, another possible factor is Helicobacter pylori. Since its discovery and association with peptic ulcer disease and gastric malignancy, there have been extensive efforts at eradicating this microorganism when it is detected. Therefore, over the past several decades, the prevalence of H. pylori has plummeted at the same time EoE has been increasing. Could the two be linked?
The study by von Arnim et al. provides additional patient level data to support this ecological association. In a rigorously designed and conducted case-control study, they found that the odds of EoE are markedly lower in patients who are H. pylori seronegative as compared to those who are seropositive. This study joins four prior publications that found a similar association — patients with esophageal eosinophilia or EoE are less likely to have H. pylori than control groups without EoE. The consistency of these results across different populations and study designs suggests that the association is real, but causality has yet not been established.
It is possible that the inverse association between EoE and H. pylori may be a reflection of the hygiene hypothesis. In fact, other atopic disorders such as asthma and atopic dermatitis are also inversely associated with H. pylori infection. However, the proximity of the infection in the stomach to the esophagus is appealing, and it has been hypothesized that the presence of H. pylori polarizes the immune system to a Th1 response, whereas its absence may be associated with a Th2 response, the predominant immune response seen in EoE. Ultimately, mechanistic studies, perhaps in animal models, are needed to elucidate whether H. pylori and EoE are merely associated, or whether the decrease in H. pylori prevalence might be the explanation for the rise of EoE.