Eosinophilic Oesophagitis
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Direct answer
Fifteen eosinophils per high-power field in oesophageal biopsies, in a patient with oesophageal symptoms and after excluding other causes of oesophageal eosinophilia — principally GERD, drug reaction and infection — defines eosinophilic oesophagitis. Management is no longer a proton-pump inhibitor trial followed by nothing: current guidance treats EoE as a chronic allergen-driven inflammatory disease managed with elimination diet, swallowed topical corticosteroids or the biologic dupilumab, with endoscopic dilatation reserved for fibrostenotic strictures once inflammation is controlled. Histological remission (under 15 eosinophils per high-power field) plus symptom resolution is the treatment target, reassessed by endoscopy with biopsies after roughly 8–12 weeks of therapy. Untreated disease progresses from inflammatory to fibrostenotic pathology, which is the argument for early, maintained therapy rather than intermittent rescue courses.
What you must remember
- Diagnostic numbers: peak count of 15 or more eosinophils/HPF in at least one biopsy site (report the maximum, not the average), taken from distal and proximal oesophagus; proximal biopsies help separate EoE from GERD-predominant distal eosinophilia.
- Clinical signature: dysphagia and food impaction in a young atopic patient (asthma, eczema, allergic rhinitis, food allergy); over half of adult food impactions presenting to endoscopy have EoE.
- Endoscopic findings — the EREFS score: oedema (loss of vascular markings), rings (trachealisation), exudates (white plaques), furrows (vertical lines) and strictures; a normal-looking oesophagus never excuses the biopsy.
- Proton-pump inhibitors are now a therapy, not a diagnostic sieve: PPI-responsive oesophageal eosinophilia is no longer a separate disease; PPIs carry anti-eosinophil action and are a legitimate first-line option.
- Diet therapy: the six-food elimination diet removes milk, wheat, egg, soy, nuts and fish/shellfish, then reintroduces sequentially; targeted elimination guided by allergy testing performs less well than the empirical approach; milk is the commonest adult trigger.
- Topical steroids: swallowed fluticasone (880 micrograms twice daily, swallowed not inhaled) or budesonide viscous slurry/orodispersible tablet 1 mg twice daily; systemic absorption is minimal; candidiasis is the main adverse effect; maintenance dosing prevents relapse.
- Dupilumab: anti-interleukin-4 receptor alpha antibody, the approved biologic for EoE, improving dysphagia and histology in adults and children.
- Dilatation rule: dilate strictures for symptom relief, ideally after medical suppression of inflammation; direct visualisation with a starting dilator size of 15 mm or less for narrow strictures reduces perforation risk; mucosal tears are expected, chest pain is common.
A worked clinic case
A 24-year-old man with childhood asthma attends after his second food impaction — both released in the emergency department. Endoscopy shows a narrowed, ringed oesophagus with linear furrows; biopsies from proximal and distal oesophagus show 60 eosinophils/HPF. The plan: start swallowed budesonide 1 mg twice daily, verify histological response at 8–12 weeks with repeat endoscopy and biopsies, and only then decide on dilatation — his dysphagia often improves substantially once inflammation settles, and dilating an inflamed oesophagus raises perforation risk. If he relapses on stopping, options are maintenance low-dose steroid, a six-food elimination diet (milk first to re-challenge, since it is the usual adult culprit), or dupilumab for steroid-refractory or steroid-dependent disease. This sequencing — diagnose histologically, suppress inflammation, prove remission, then mechanically remodel — is the framework examiners build scenario questions around.
How the exam frames it
Stems contrast EoE with three mimics: GERD (distal eosinophilia, response to PPI, no atopy), achalasia (dysphagia to liquids as well as solids, manometry abnormal, biopsy normal) and idiopathic oesophageal strictures. The favourite traps: giving systemic corticosteroids (wrong — topical swallowed steroid is standard), dilating first in an inflamed oesophagus, and forgetting that the eosinophil count must persist after an adequate PPI trial before the label sticks. A viva favourite is why an inhaled-then-swallowed fluticasone technique matters: the drug must coat the oesophageal mucosa, not the lungs — rinse nothing, spit nothing, no eating for 30 minutes.
Frequently asked questions
What histological threshold diagnoses eosinophilic oesophagitis?
At least 15 eosinophils per high-power field in at least one oesophageal biopsy site, in a patient with oesophageal symptoms, after excluding GERD and other causes of eosinophilia.
Why take proximal and distal biopsies?
Proximal eosinophilia supports EoE over GERD, whose eosinophilia is characteristically distal; two levels also guard against patchy disease producing a false-negative single-site biopsy.
When is endoscopic dilatation indicated?
For fibrostenotic disease — strictures and narrow-calibre oesophagus causing dysphagia — preferably after medical control of inflammation; repeated sessions with gradual sizes are safer than aggressive single dilatation.
What is the role of the six-food elimination diet?
Empirical removal of milk, wheat, egg, soy, nuts and fish/shellfish with structured reintroduction; it achieves remission in a substantial minority and identifies a dietary trigger worth maintaining, milk being the commonest adult culprit.
Which biologic is approved for eosinophilic oesophagitis?
Dupilumab, an anti-IL-4 receptor alpha antibody that blocks IL-4 and IL-13 signalling, used for steroid-refractory or severe disease.