Eosinophilic Esophagitis
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Basics
Description
Epidemiology
- All ages, most common in 20s to 30s; male > female, 3:1
- Leading cause of dysphagia and food impaction in children and young adults
Incidence
Incidence in general population is ~1 to 20/10,000 per year.
Prevalence
Gradually increasing, perhaps due to better case finding; 45 to 55/100,000
- Increased prevalence in patients with celiac disease
Etiology and Pathophysiology
- An atopic inflammatory disease; pathogenesis is an aberrant immune response to antigenic stimulation.
- Like eczema and asthma, T-helper 2 (TH2) lymphocytes play a role, as do mixed IgE and non–IgE-mediated allergic responses to food and environmental allergens.
- Although not well understood, the pathophysiology of EoE is postulated to be due to increased recruitment and activation of eosinophils in the esophagus by the eosinophil chemoattractants eotaxin-3, IL-5, and IL-13, which are ultimately responsible for inflammation and fibrotic change.
Genetics
- EoE susceptibility may be caused by polymorphisms in thymic stromal lymphopoietin protein (TSLP).
- Potential new subphenotype of EoE (may also overlap with GERD): proton pump inhibitor (PPI)–responsive esophageal eosinophilia (REE), where PPIs may act to decrease the inflammatory response in EoE
Risk Factors
- High rate of associated food and aero antigen allergies/anaphylaxis
-- To view the remaining sections of this topic, please log in or purchase a subscription --
Basics
Description
Epidemiology
- All ages, most common in 20s to 30s; male > female, 3:1
- Leading cause of dysphagia and food impaction in children and young adults
Incidence
Incidence in general population is ~1 to 20/10,000 per year.
Prevalence
Gradually increasing, perhaps due to better case finding; 45 to 55/100,000
- Increased prevalence in patients with celiac disease
Etiology and Pathophysiology
- An atopic inflammatory disease; pathogenesis is an aberrant immune response to antigenic stimulation.
- Like eczema and asthma, T-helper 2 (TH2) lymphocytes play a role, as do mixed IgE and non–IgE-mediated allergic responses to food and environmental allergens.
- Although not well understood, the pathophysiology of EoE is postulated to be due to increased recruitment and activation of eosinophils in the esophagus by the eosinophil chemoattractants eotaxin-3, IL-5, and IL-13, which are ultimately responsible for inflammation and fibrotic change.
Genetics
- EoE susceptibility may be caused by polymorphisms in thymic stromal lymphopoietin protein (TSLP).
- Potential new subphenotype of EoE (may also overlap with GERD): proton pump inhibitor (PPI)–responsive esophageal eosinophilia (REE), where PPIs may act to decrease the inflammatory response in EoE
Risk Factors
- High rate of associated food and aero antigen allergies/anaphylaxis
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