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Review
. 2017;26(7):258-266.
doi: 10.1007/s40629-017-0037-8. Epub 2017 Sep 13.

Current concepts in eosinophilic esophagitis

Dagmar Simon  1 , Alex Straumann  2 , Alain M Schoepfer  3 , Hans-Uwe Simon  4
Affiliations
Review

Current concepts in eosinophilic esophagitis

Dagmar Simon et al. Allergo J Int. 2017.

Abstract

Background: Eosinophilic esophagitis (EoE) is a disease entity first described in the 1990s, but showing an increasing incidence that is characterized clinically by esophageal dysfunction and histologically by a striking eosinophil infiltration.

Methods: This article discusses new aspects of the pathogenesis, symptoms, diagnosis, and treatment of EoE.

Results: EoE affects both children and adults and is frequently associated with atopic disease and IgE sensitization. Barrier dysfunction and T‑helper 2 inflammation are considered to be pathogenetically important factors. Recently, a proton pump inhibitor (PPI)-sensitive EoE subtype as well as an EoE-like disorder have been described.

Conclusion: Research in recent years has contributed to a better understanding of the disease spectrum and pathogenesis of EoE, including genetic dispositions, thereby laying the foundation for innovative treatment approaches.

Keywords: Barrier dysfunction; Diet; Eosinophilic esophagitis; Eosinophils; T‑helper 2 inflammation.

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Conflict of interest statement

D. Simon, A. Straumann, A.M. Schoepfer, and H.-U. Simon declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Endoscopic findings in eosinophilic esophagitis (EoE). a Acute inflammatory EoE with edema, white exudate, and furrows; b rings; c strictures in a chronic course
Fig. 2
Fig. 2
Pathomechanisms of eosinophilic esophagitis (EoE). Epithelial barrier impairment develops due to genetic predisposition and in consequence of reflux and food intake. Invading allergens and microbial antigens cause activation of the innate and acquired immune system. Eosinophils degranulate, release toxic proteins, and generate extracellular DNA traps, which serve as a defense system but also cause tissue damage. By releasing cytokines, eosinophils modulate inflammation and promote its chronification, ultimately with fibrosis, all of which, in turn, have negative effects on skin barrier function. PAR-2 protease-activated receptor 2, TLR toll-like receptor, DC dendritic cell, IL interleukin, TSLP thymic stromal lymphopoietin, TGF-β transforming growth factor-beta, IgE immunoglobulin E
See this image and copyright information in PMC

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