AKT · Gastroenterology/Oesophagus & stomach

Eosinophilic oesophagitis

Chronic Th2/eosinophil-mediated, food-antigen-driven immune inflammation of the oesophagus

Overview

A chronic immune/antigen-mediated oesophageal disease defined by symptoms of oesophageal dysfunction plus dense eosinophilic infiltration (≥15 eosinophils/high-power field) on biopsy, with other causes of oesophageal eosinophilia excluded. Typically affects young atopic men. The classic exam trap is recurrent solid-food dysphagia or a food-bolus obstruction with heartburn that does NOT respond to a PPI.

Recognise

Young man (often) with atopy (asthma, eczema, allergic rhinitis); dysphagia for SOLIDS and recurrent food-bolus impaction — frequently the first presentation
Heartburn/chest or epigastric pain that is unresponsive to acid suppression; slow, careful eating/food avoidance behaviours
OGD: fixed rings (trachealisation / 'feline' oesophagus), linear furrows, white exudates/plaques, oedema, narrow-calibre oesophagus/strictures

Red flags

Acute food-bolus impaction unable to swallow own saliva → urgent endoscopic disimpaction (do NOT push the bolus blindly — perforation risk)
Fibrostenotic strictures with progressive dysphagia/weight loss → dilatation + exclude malignancy

Differentials & how to tell them apart

GORDresponds to PPI; distal-predominant lower-grade eosinophilia; reflux symptoms — but PPI-responsiveness no longer excludes EoE

Achalasiadysphagia for solids AND liquids; bird-beak on barium, aperistalsis + failure of LOS relaxation on manometry

Peptic/Schatzki stricturemechanical ring/stricture without diffuse eosinophilia

Investigations

OGD with ≥6 biopsies (proximal AND distal) — diagnostic histology is ≥15 eosinophils/hpf; document endoscopic features (rings, furrows, exudates, strictures). Exclude other causes of oesophageal eosinophilia. PPI no longer needs to be trialled before biopsy (PPI-responsive oesophageal eosinophilia is now considered part of EoE).

Management

High-dose PPI and/or swallowed topical corticosteroid (budesonide orodispersible); dietary elimination; dilate strictures

1Confirm on biopsy (≥15 eos/hpf). Induce remission with high-dose PPI and/or a swallowed topical corticosteroid (budesonide orodispersible — Jorveza), or empirical dietary elimination. Reassess symptoms + repeat biopsy for histologic remission.Gate: If a food bolus is impacted and the patient cannot swallow their own saliva → urgent endoscopic disimpaction; never push the bolus blindly through (perforation).
2Maintenance therapy (relapse after stopping is high) — lowest effective topical steroid dose ± continued dietary control; endoscopic dilatation for fibrostenotic strictures. Dupilumab for refractory disease.

High-dose PPI — a substantial proportion achieve clinico-histologic remission; reasonable first-line

Swallowed topical corticosteroid — budesonide orodispersible (Jorveza) or swallowed fluticasone — first-line topical therapy (Jorveza is the only EU/UK-licensed drug for EoE); not systemically absorbed; candidiasis risk

Dietary elimination (empirical six-food / targeted) — effective alternative, especially where drug avoidance is preferred

Endoscopic dilatation — for fibrostenotic strictures; treats the mechanical narrowing, not the inflammation

Key points

Young atopic man + recurrent solid-food dysphagia / food-bolus obstruction + heartburn unresponsive to PPI + rings & linear furrows on OGD with ≥15 eosinophils/hpf = eosinophilic oesophagitis. Maintenance needed — it relapses off treatment.

Monitor & prognosis

Repeat OGD/biopsy to confirm histologic remission (symptoms correlate poorly); high relapse off therapy.

Chronic relapsing; untreated inflammation causes fibrostenotic remodelling and strictures.

Source: BSG/BSPGHAN 2022 EoE guideline