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A chronic, local, immune-mediated, esophageal disease characterized clinically in adults by dysphagia, food impaction, and heartburn and in children with nonspecific abdominal complaints, abdominal pain, and failure to thrive. Histologically, EoE is characterized by an eosinophil-predominate inflammation (1)[A].
- 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 in general population is ~1 to 20/10,000 per year.
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.
- 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