This content has not yet been reviewed and may contain errors.

eosinophilic oesophagitis

in review 4 min read Updated 2026-08-19
Contents
eosinophilic oesophagitis

Chronic immune-mediated oesophageal disease defined by symptoms of oesophageal dysfunction + ≥15 eosinophils/hpf on biopsy. Most common cause of food impaction and dysphagia in young adults. Three treatment pillars: PPI (first-line), topical swallowed corticosteroids, and elimination diet. Dupilumab (Dupixent) for PPI-refractory disease. Untreated EoE progresses from inflammatory to fibrostenotic phenotype — early treatment prevents stricture formation.


diagnosis

Both required:

  1. Symptoms of oesophageal dysfunction (dysphagia, food impaction, chest pain, heartburn unresponsive to PPI in adults; feeding difficulty, vomiting, abdominal pain in children)
  2. ≥15 eosinophils/hpf on oesophageal biopsy

biopsy protocol

  • ≥6 biopsies from at least 2 oesophageal levels (proximal and distal) — eosinophilic infiltration is patchy
  • Biopsy any visible abnormalities (rings, furrows, exudates) AND normal-appearing mucosa
  • PPI no longer needs to be trialled before biopsy — PPI-responsive oesophageal eosinophilia is now considered part of the EoE spectrum

EREFS endoscopic scoring

featureappearance
Edemaloss of vascular pattern, mucosal pallor
Ringsconcentric mucosal rings (“trachealization”)
Exudateswhite punctate plaques
Furrowslongitudinal linear grooves
Stricturesfixed luminal narrowing
normal-looking oesophagus does not exclude EoE

Up to 10% of EoE patients have grossly normal endoscopy. Always biopsy if clinical suspicion — especially young males with dysphagia, food impaction, or atopic history.


treatment

Goal: histological remission (<15 eos/hpf, ideally <6) + symptom improvement. Symptom resolution alone is insufficient — subclinical inflammation drives fibrostenotic remodelling.

first-line: PPI

  • Standard or high-dose PPI × 8 weeks → repeat EGD with biopsies
  • Achieves histological remission in ~50%
  • If remission: continue maintenance PPI at the lowest effective dose

second-line: topical swallowed corticosteroids

For PPI non-responders or as initial therapy in centres that prefer this approach.

agentdoseformulation
budesonide oral suspension (Jorveza-type)1 mg twice dailypurpose-made orodispersible tablet (where available)
budesonide nebuliser solution (swallowed)1 mg twice dailymix with sucralose, swallow — do not inhale
fluticasone MDI (swallowed)880–1760 µg/day in divided dosesactuate into mouth without spacer, swallow; do not rinse
  • No eating or drinking for 30 minutes after dosing
  • Repeat EGD at 8–12 weeks to confirm histological remission
  • Maintenance: reduce to lowest effective dose; relapse is nearly universal off therapy
  • Oesophageal candidiasis risk (~5–10%) — counsel on symptoms

dietary therapy: step-up elimination

Effective alternative, particularly if patient prefers non-pharmacological approach.

stepfoods eliminatedhistological response
2-fooddairy, wheat~40–50%
4-food+ egg, legumes/soy~55–65%
6-food+ seafood, nuts~70–75%
  • Start with 2-food elimination × 6 weeks → EGD with biopsies
  • If no remission, step up to 4-food, then 6-food
  • Once remission achieved, reintroduce one food group every 6 weeks with EGD to identify the trigger
  • Requires motivated patient and dietician support

biologic therapy: dupilumab

  • Indication: PPI-refractory EoE in adults and adolescents ≥12 years weighing ≥40 kg
  • LIBERTY EoE TREET (2022) — 60% histological remission vs 5% placebo at 24 weeks
  • Dose: 300 mg SC weekly
  • Also addresses concurrent atopic comorbidities (asthma, atopic dermatitis)

dilation

  • For established fibrostenotic strictures causing mechanical dysphagia despite anti-inflammatory therapy
  • Through-the-scope balloon or Savary bougie — gradual dilation, not aggressive single-session
  • Does not treat underlying inflammation — always combine with medical or dietary therapy
  • Perforation risk is low (~0.3%) with modern graded technique — the historical fear of “fragile EoE oesophagus” is overstated

monitoring

  • Repeat EGD with biopsies is the only reliable way to assess remission — symptoms correlate poorly with histology
  • After achieving remission: EGD at 1 year, then as clinically indicated
  • Assess for fibrostenotic progression at each endoscopy (EREFS scoring)

common traps

  • Relying on symptoms alone to assess treatment response — subclinical eosinophilic inflammation persists in up to 40% of asymptomatic patients; repeat biopsies are mandatory
  • Forgetting to biopsy after food impaction — EoE is the underlying cause in the majority of young adults with food bolus impaction
  • Insufficient biopsies — <6 biopsies miss patchy disease; biopsy proximal and distal oesophagus
  • Stopping topical steroids after remission without a maintenance plan — relapse rate approaches 90% within 1 year off therapy
  • Dilating without treating inflammation — strictures recur rapidly without concurrent anti-inflammatory therapy

related: gastro-oesophageal reflux disease · dysphagia · Barrett’s oesophagus

Key references

+1 more source