The prevalence of eosinophilic esophagitis, a manifestation of food allergy, has increased in recent years for reasons that are not clear. The gastrointestinal mucosa is regularly exposed to food antigens with the potential to evoke immunological reactions. Studies have shown that some food allergens that ordinarily would be degraded by peptic digestion are not degraded when the pH of gastric fluid is raised to levels commonly found in the stomachs of patients treated with proton pump inhibitors (PPIs). Other studies have shown that PPIs increase gastrointestinal mucosal permeability, which might facilitate the uptake of undegraded peptide allergens. Mice treated with antisecretory medications while being fed a diet of caviar have been found to develop caviar-specific immunoglobulin E (IgE) antibodies, T-cell reactivity, and gastric eosinophilia. Adult patients treated with antisecretory medications for 3 months have been found to develop a rise in their IgE antibody levels and new, food-specific IgE antibodies. These data establish a plausible mechanism whereby acid-suppressive medications, by interfering with the peptic digestion of food allergens and increasing mucosal permeability, might lead to the development of food allergy. The time course of the introduction and subsequent widespread usage of PPIs with the emergence of eosinophilic esophagitis fits well with the hypothesis that PPIs may play an etiological role. Although the mere demonstration of a plausible association does not establish cause and effect, further studies on the role of acid suppression in the development of eosinophilic esophagitis clearly are warranted.
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