Eosinophilic Esophagitis

Eosinophilic oesophagitis (EoE) is a chronic, immune mediated oesophageal disease defined clinically by oesophageal dysfunction and histologically by eosinophil predominant inflammation (15 or more eosinophils per high power field).

• Prevalence about 30 to 60 per 100,000, more in men (3:1), young adults, atopic individuals (asthma, eczema, food allergy).
• Pathogenesis: antigen driven Th2 inflammation (IL 4, IL 5, IL 13), epithelial barrier dysfunction, eotaxin 3, TSLP, CAPN14; food antigens (milk, wheat, egg, soy) are the main triggers.
• Natural history: inflammatory then fibrostenotic phenotype (rings, strictures, narrow calibre oesophagus), with diagnostic delay of 4 to 7 years associated with stricture risk.
• Complications: food impaction, oesophageal perforation (rare), strictures, malnutrition (children).

• Adults: dysphagia for solids (most common), food impaction requiring endoscopic removal, chest pain, heartburn unresponsive to PPI, regurgitation.
• Children: feeding difficulty, vomiting, abdominal pain, failure to thrive.
• Patients adapt by eating slowly, drinking with meals, avoiding hard textures.
• Associated atopic disease. Examination normal.

• Upper endoscopy: rings (trachealisation, felinisation), furrows, white exudates, oedema, strictures, narrow calibre oesophagus, crepe paper mucosa; may be normal (10 to 25%).
• Biopsy: at least 6 biopsies from the proximal and distal oesophagus targeting abnormal areas, showing 15 or more eosinophils per high power field (peak count), eosinophilic microabscesses, basal zone hyperplasia, dilated intercellular spaces, lamina propria fibrosis. Biopsy mid and distal oesophagus for any dysphagia.
• Exclude other causes of oesophageal eosinophilia: reflux disease, achalasia, infection (fungal, herpes), drug hypersensitivity, connective tissue disease, hypereosinophilic syndrome, Crohn disease.
• PPI responsive oesophageal eosinophilia is considered part of the EoE spectrum.
• Scoring: EREFS, EoE histology scoring system. Allergy testing is not reliable for diet selection.

First line options

• Proton pump inhibitor: omeprazole 20 mg twice daily (or esomeprazole 20 to 40 mg) for 8 weeks, with response in about 40 to 50%.
• Topical corticosteroids: swallowed fluticasone propionate 880 micrograms twice daily from a metered dose inhaler (no spacer, swallow, no food or drink for 30 minutes), or orodispersible budesonide 1 mg twice daily for 12 weeks (histological remission in 85%).
• Dietary therapy: six food elimination diet for 6 to 8 weeks with reintroduction and repeat biopsies (remission 70%), or two or four food elimination (milk, wheat), elemental diet in children.
• Biologic: dupilumab 300 mg SC weekly (adults and children over 12 years, 40 kg or more), improves dysphagia and histology, especially refractory disease and in atopic comorbidities.
• Oesophageal dilation (balloon or bougie) for strictures, with gradual dilation and risk of chest pain, tear; ensure inflammation is treated.
• Maintenance therapy: lifelong topical steroids at lowest effective dose (relapse in over 90% after stopping), or maintained diet avoidance.
• Management of food impaction: endoscopic removal within 24 hours (glucagon is not effective); avoid blind pushing.
• Monitor with endoscopy and biopsy at 8 to 12 weeks after treatment change, then every 1 to 3 years. Candidal oesophagitis is a common adverse effect of steroids.
• Treat atopic disease and consider allergen immunotherapy.