Eosinophilic Esophagitis and Celiac Disease: A True Association or Coincidence?

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Although the possible relationship between eosinophilic esophagitis (EoE) and celiac disease (CD) has been previously suggested, they are 2 clinically and histologically distinct disorders of upper gastrointestinal tract involving different anatomy and physiology (1). Immunologically, CD is a TH1-mediated response, triggered by gluten-derived peptides, that is activated in genetically susceptible individuals, whereas EoE has been shown to be a TH2-mediated disorder that is associated with immunoglobulin E– and non–immunoglobulin E-mediated food allergies. Traditionally, TH1 and TH2 immune responses have been considered mutually antagonistic, but recent molecular studies have suggested that autoimmune and atopic diseases share risk factors that increase the propensity of the immune system to generate both TH1- and TH2-mediated inappropriate responses to nonpathological antigens. These findings seem to suggest a more generalized defect of immune regulation than a casual association between CD and EoE (2,3).
According to one theory, increased intestinal permeability secondary to CD may facilitate the exposure of the intestinal immune system to various antigens and an upregulated immune response, which, in turn, causes intestinal inflammation and damage (4,5). There are several food antigens that have been implicated in EoE, similar to the role gluten plays in CD, which is why the question exists of whether these 2 conditions are associated. And, because wheat can also trigger EoE, several studies have investigated the relationship between these 2 disease entities (6). It has been suggested that eosinophilic infiltration of the esophagus may be a manifestation associated with gluten exposure in a small population of patients with CD and could also be caused by CD itself (7). Reported observations of an association have been based on the increased prevalence of EoE in those with CD. It is not clear whether this is secondary to an increasing awareness and detection of the disease or whether it is a true phenomenon (8). In a study by Jensen et al, (9) children with CD who were treated with a gluten-free diet (GFD) exhibited symptomatic and histologic improvement of their EoE, suggesting a possible shared pathogenic trigger between the 2 diseases. A study by Lucendo et al (10), did not find an increased human leukocyte antigen (HLA) DQ2 and DQ8 in those with EoE when compared with controls.
Shah et al first described the coexistence of EoE and CD in the same patient in 2006. Since then, several case reports and cohort studies have suggested an association between EoE and CD (11). Although this association was initially reported for pediatric patients, it has since been reiterated in adult patients, but not universally confirmed in large population-based studies (10). A systematic review of studies showed the prevalence of CD in EoE varied between 0.16% and 57.1%, whereas the prevalence of EoE in CD ranged from 0% to 10.7%. A significant bias exists in favor of short studies reporting positive associations, whereas large cohorts show no support for any relation between CD and EoE (10,12,13).
Hommeida et al retrospectively reviewed 10,201 children who underwent endoscopic evaluation and found that the prevalence of EoE in children with CD was 1.83% compared with 5.83% in all children who had EoE. They also concluded that there was no increased risk of EoE in children with CD supporting other published large cohorts (14). Le Fevre et al concluded that tissue transglutaminase (tTG) antibody was elevated in 23% of their EoE cohort. They examined total tTG antibody level rather than separate tTG IgA and IgG. Only 3 patients had lymphocytic inflammation in the duodenum and no concomitant villous atrophy. The tTG level in 1 patient improved even without an intervening elimination diet. A second patient had a negative HLA DQ2/DQ8 status.

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