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Eosinophilic oesophagitis (EoE)

Written and medically reviewed by Bahir Hadi, specialist in surgery, PhD

Profile, experience and publications

Eosinophilic oesophagitis (EoE): the allergic oesophageal disease

Eosinophilic oesophagitis (EoE) is a chronic, immune-mediated inflammatory disease of the oesophagus in which allergic inflammatory cells (eosinophils) accumulate in the mucosa. EoE is an important cause of chronic dysphagia and must be distinguished from GERD. Prevalence has risen sharply over the past 20 years and is now estimated at about 0.5-1 case per 1,000 people in Western countries [1]. It most commonly affects men in their 20s-40s with concurrent asthma, eczema or hay fever.


Symptoms

EoE is a chronic condition, and symptoms often develop over years. The course varies from person to person. In a retrospective cohort study, stricture formation became more common the longer the diagnosis was delayed (Schoepfer AM et al., Gastroenterology 2013;145(6):1230-6):

  • Dysphagia - especially for solid food
  • Food bolus impaction - food stuck in the oesophagus (classic acute presentation in young men)
  • Chest pain - may mimic cardiac pain
  • Heartburn - often PPI-refractory
  • Vomiting, regurgitation
  • Adaptive eating behaviour - patients eat slowly, chew thoroughly, drink much water with meals

In children: failure to thrive, vomiting, food aversion.


Why does EoE occur?

EoE is a type 2 immune reaction against food antigens (milk, wheat, egg, soy, nuts, fish) or aeroallergens. Genetic factors (TSLP, CAPN14, CCL26) predispose. Eosinophilic inflammation leads to:

  • Acute phase: oedema, mucosal furrows, white exudates
  • Chronic phase: tracheal rings ("feline oesophagus"), strictures, fibrosis

Diagnosis

EoE is diagnosed by three concurrent criteria [2]:

  1. Symptoms of oesophageal dysfunction
  2. At least 15 eosinophils per high-power field on oesophageal biopsy (roughly 60 eosinophils per mm², depending on the microscope field size)
  3. Assessment and exclusion of other causes of oesophageal eosinophilia

All three criteria must be met. The cell count on its own is not a diagnosis, and the biopsy result is interpreted by the doctor alongside the symptoms and the other findings.

The former requirement of failure to respond to PPI is no longer a diagnostic criterion. PPI-responsive eosinophilia is now regarded as EoE, and PPI is a treatment option, not a test [4].

Gastroscopy with targeted biopsies is mandatory. The recommended protocol is six biopsies from at least two levels of the oesophagus, typically proximal and distal, because the inflammation is patchy [4].

A relatively normal endoscopic mucosa does not rule out EoE. Some patients have an almost normal-looking oesophagus, and the diagnosis rests on the biopsies, not on the appearance of the lining.

Pausing a PPI, an elimination diet or a prescribed nasal or inhaled steroid before the diagnostic gastroscopy can change the biopsy result. It must only be done in agreement with the treating doctor - never stop prescribed medication on your own.

Typical endoscopic findings:

  • Concentric rings
  • Longitudinal furrows
  • White exudates (eosinophil microabscesses)
  • Strictures
  • "Crepe paper" mucosa

Differential diagnoses

Condition Distinction
GERD Responds to PPI; eosinophilia usually distal
PPI-responsive oesophageal eosinophilia EoE responding to PPI (now considered a subgroup of EoE)
Achalasia Abnormal manometry; dysphagia to both liquids and solids
Candida oesophagitis White plaques, usually immunosuppressed
Crohn's with oesophageal involvement Rare; biopsy shows granulomas

Treatment - the 3 Ds

1. Drugs:

There is no single fixed first choice. PPI, swallowed topical steroid (fluticasone from an inhaler or orodispersible budesonide) and a structured elimination diet are all possible first-line options, and the choice is made with the patient based on severity, age, comorbidity and what is realistic to sustain [4]. Dupilumab (IL-4/IL-13 blocker) is an option when the others are insufficient.

2. Diet:

  • Empirical elimination diets in several variants, from milk elimination alone to broader 4- or 6-food elimination. The broader the diet, the higher the chance of remission, but the harder it is to live with.
  • Reintroduction of one food at a time with check gastroscopy and biopsies along the way. Diets should be planned with a clinical dietitian.

3. Dilatation:

  • Endoscopic dilatation for symptomatic strictures relieves the swallowing difficulty.
  • Dilatation treats the narrowing, not the underlying inflammation, so it must always be combined with medical or dietary therapy.

Follow-up

  • Repeat gastroscopy with biopsies 8-12 weeks after starting therapy. Response cannot be judged reliably from symptoms alone - inflammation can persist even when swallowing feels better, so endoscopy and biopsies form part of the assessment [4].
  • EoE is a chronic disease. Once remission is achieved, maintenance treatment and planned follow-up are usually relevant, because symptoms and inflammation return when treatment stops [4]. What to maintain with, and for how long, is decided individually.

Treatment at Kirurgen.dk

We investigate chronic dysphagia, heartburn and food impaction with oral or nasal gastroscopy and routine biopsies from proximal and distal oesophagus when EoE is suspected. See also: Dysphagia, GERD, Peptic ulcer, Nasal vs. oral gastroscopy.


References

  1. Dellon ES, Hirano I. Epidemiology and natural history of eosinophilic esophagitis. Gastroenterology 2018;154(2):319-32.
  2. Lucendo AJ, Molina-Infante J, Arias Á, et al. Guidelines on eosinophilic esophagitis. United European Gastroenterol J 2017;5(3):335-58.
  3. Laserna-Mendieta EJ, Casabona S, Savarino E, et al. Efficacy of therapy for eosinophilic esophagitis in real-world practice. Clin Gastroenterol Hepatol 2020;18(13):2903-11.
  4. Dellon ES, et al. ACG Clinical Guideline: Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol 2025.
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