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Published on: September 26, 2013
EoE behaves as a unique Th2 disease: a narrative review.
Simon S Rabinowitz1, Liwei Yu1, Patrick Geraghty2,3
1Division of Pediatric Gastroenterology, Children's Hospital at Downstate, Downstate Health Sciences University, Brooklyn, NY, USA.
Eosinophilic esophagitis (EoE) lacks serologic markers and does not respond to biological therapies, unlike asthma, atopic dermatitis, and chronic rhinosinusitis. This suggests a unique Th2 pathway mechanism in EoE.
Area of Science:
- Immunology
- Gastroenterology
- Allergy
Background:
- Eosinophilic esophagitis (EoE) is a type 2 helper cell (Th2) mediated disease.
- EoE shares inflammatory pathways with asthma, atopic dermatitis (AD), and chronic rhinosinusitis (CRS).
- Distinct characteristics of EoE suggest a unique pathophysiologic mechanism.
Purpose of the Study:
- To compare serologic markers and response to biological therapies in EoE versus other Th2 diseases.
- To highlight key differences in EoE's Th2 pathway activation and therapeutic response.
- To propose and summarize evidence for a novel EoE pathophysiology.
Main Methods:
- Conducted four narrative reviews combining PubMed and Google searches.
- Reviewed studies on serologic markers in EoE compared to asthma, AD, and CRS.
- Compared responses to parenteral biological therapies in EoE and other Th2 diseases.
Main Results:
- EoE lacks identifiable serologic markers, unlike asthma, AD, and CRS.
- EoE does not respond to parenteral biological therapies, whereas other Th2 diseases show significant therapeutic benefit.
- Literature supports a novel pathophysiology for EoE.
Conclusions:
- EoE's unique presentation may stem from a distinct application of the Th2 pathway.
- A potential mechanism involves exclusive activation of the Th2 cascade by esophageal mucosal constituents.
- This localized pathway activation may lead to fibrostenotic changes characteristic of EoE.
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