Eosinophilic Esophagitis
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Basics
Description
- Eosinophilic esophagitis (EoE) is a chronic immune-mediated esophageal disease characterized clinically by variable symptoms of esophageal dysfunction and pathologically by localized eosinophilic inflammation.
- The diagnosis is established in symptomatic patients who have the following:
- At least 15 eosinophils/HPF isolated to the esophagus on endoscopic biopsies
- Persistent eosinophilic infiltrate in esophageal biopsies after a trial of proton pump inhibitor (PPI) therapy
Epidemiology
- Incidence rates range from 0.7 to 10 per 100,000 person-years, and prevalence from 0.2 to 43 per 100,000.
- 3:1 male-to-female ratio
- Peaks of onset in childhood and 3rd–4th decade
Pathophysiology
- The exact pathophysiology of EoE is unknown but likely involves an immune response to environmental antigens in genetically predisposed individuals.
- Environmental factors (food and possibly aeroallergens) trigger inflammatory response mediated by type 2 T-helper (Th2) cells.
- Genetic polymorphisms which predispose to EoE include eotaxin-3, thymic stromal lymphopoietin, and filaggrin.
-- To view the remaining sections of this topic, please log in or purchase a subscription --
Basics
Description
- Eosinophilic esophagitis (EoE) is a chronic immune-mediated esophageal disease characterized clinically by variable symptoms of esophageal dysfunction and pathologically by localized eosinophilic inflammation.
- The diagnosis is established in symptomatic patients who have the following:
- At least 15 eosinophils/HPF isolated to the esophagus on endoscopic biopsies
- Persistent eosinophilic infiltrate in esophageal biopsies after a trial of proton pump inhibitor (PPI) therapy
Epidemiology
- Incidence rates range from 0.7 to 10 per 100,000 person-years, and prevalence from 0.2 to 43 per 100,000.
- 3:1 male-to-female ratio
- Peaks of onset in childhood and 3rd–4th decade
Pathophysiology
- The exact pathophysiology of EoE is unknown but likely involves an immune response to environmental antigens in genetically predisposed individuals.
- Environmental factors (food and possibly aeroallergens) trigger inflammatory response mediated by type 2 T-helper (Th2) cells.
- Genetic polymorphisms which predispose to EoE include eotaxin-3, thymic stromal lymphopoietin, and filaggrin.
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