Eosinophilic Oesophagitis

Condition

A chronic inflammatory condition of the oesophagus related to a non-IgE-mediated form of food allergy, rather than a true acid reflux disorder. Most patients have comorbid atopic conditions such as asthma, allergic rhinitis and atopic dermatitis. The six most common food triggers are animal milk proteins, wheat, eggs, soy, nuts and seafood — most patients have only one trigger, though some have several.

Prevalence has quadrupled over the last 30 years and it is now the second most commonest oesophageal disease after GORD. It usually presents in childhood or early adulthood with a 3:1 male predominance, though it can be first diagnosed in older adults.

Presentation and when to refer

The most common symptoms in adults are dysphagia and food bolus impaction; other symptoms include chest pain and heartburn. In young children, symptoms are nonspecific — failure to thrive, fussy eating, irritability, vomiting and abdominal pain.

Refer any patient presenting with food bolus impaction, or a history of dysphagia with or without atopy, to a gastroenterologist. Other red flags warranting referral: odynophagia, unexplained weight loss, or persistent reflux despite treatment. Early diagnosis and referral limits progression of fibrosis and stricture formation and reduces the (rare) risk of oesophageal perforation.

Differentiating from GORD

Both conditions can cause oesophageal eosinophilia and share some symptoms (heartburn, regurgitation, chest pain), but dysphagia and food bolus impaction do not occur in GORD. Patients with eosinophilic oesophagitis are typically symptomatic at the time of eating, whereas GORD symptoms usually occur after eating and at night. A response (or lack of response) to a PPI trial does not reliably distinguish the two conditions, since either may respond. Eosinophilic oesophagitis has a 3:1 male predominance compared with GORD’s 1:1 gender ratio, and a history of atopy increases the likelihood of eosinophilic oesophagitis over GORD.

Diagnosis

Diagnosis (2017 AGREE consensus criteria) requires all of:

• Symptoms of oesophageal dysfunction (dysphagia, food bolus impaction, food refusal, heartburn, regurgitation, vomiting, odynophagia, chest pain), and
• Oesophageal biopsies showing at least 15 eosinophils (60/mm²) per high-power field, and
• Exclusion of other causes of oesophageal eosinophilia — GORD, eosinophilic gastrointestinal disease, achalasia, hypereosinophilic syndrome, connective tissue disease, Crohn disease, infection, pill-induced oesophagitis, graft-versus-host disease.

Biopsies should be taken from at least two oesophageal sites at least 5cm apart — ideally tri-level (lower, middle and upper oesophagus) — because the eosinophilic infiltrate is patchy. Gastric and duodenal biopsies should also be taken at the first endoscopy to exclude eosinophilic gastroenteritis. By contrast, GORD-related eosinophilia is usually under 5 eosinophils/hpf and confined to the lower oesophagus.

Macroscopic endoscopic features (rings/trachealisation, furrows, white exudates, strictures) are graded using the EREFS score (0–9) to assess severity and guide management, though they aren’t always present. Serum eosinophil count, skin testing and serum IgE do not correlate with disease activity or reliably identify food triggers, and are not useful for diagnosis or management.

Management

Overview

All patients require treatment, generally continued lifelong. No specific pharmacological treatment is considered first-line — the choice between dietary and pharmacological approaches is largely based on patient preference rather than disease severity, though orodispersible budesonide tablets may be preferred for their high efficacy. Response should be confirmed on repeat oesophageal biopsy, as symptoms alone are not a reliable guide.

Dietary elimination

Two approaches are used, both requiring dietitian input and repeat endoscopy to confirm response:

• Step-down (more appropriate for severe disease) — exclude all six common triggers at once, with endoscopy after 4–6 weeks; if remission is achieved, foods are reintroduced one at a time with repeat endoscopy after each. Histological remission in up to 68% of patients, but requires multiple endoscopies, has poorer adherence given the extreme restriction, and carries a higher risk of nutritional deficiency.
• Step-up (best for mild-to-moderate symptoms) — exclude only animal milk proteins and wheat first; if remission is demonstrated at 4–6 weeks, one of the two is reintroduced alone to identify the trigger, escalating further only if remission isn’t achieved. Identifies triggers earlier and avoids unnecessary restriction, but is less effective (40–55% histological remission).

Swallowed topical corticosteroids

The mainstay of pharmacological treatment, generally continued lifelong in the absence of dietary intervention. Budesonide slurry (1mg/2mL nebuliser solution mixed with 3–5g sucralose powder, e.g. Splenda) swallowed, twice daily was historically used, prepared by the patient — a reasonable efficacy (64% symptom/histological response) but limited uptake because of the preparation burden.

This has now largely been superseded by an orodispersible budesonide tablet, which is mucoadhesive and provides prolonged local release with reduced systemic absorption. Clinical/histological remission is around 85% at 12 weeks (75% with longer-term follow-up), making it the most effective currently available therapy for adults. To access induction therapy on the PBS, patients need histological confirmation and must be treated by a gastroenterologist, or a surgeon or physician experienced in eosinophilic oesophagitis; maintenance therapy can then be prescribed, in consultation with that specialist, once an 8-week follow-up endoscopy confirms histological remission (under 5 eosinophils/hpf).

Patient instructions to maximise efficacy: take after a meal, let the tablet dissolve on the tip of the tongue over 2–5 minutes, then wait 30 minutes before eating, drinking, oral hygiene or other oral medications. The main adverse effect is oral/pharyngeal/oesophageal candidiasis (usually mild-to-moderate, not dose-related) — treat with topical or systemic antifungal therapy while continuing the budesonide.

Proton pump inhibitors

An appropriate and widely used option even though eosinophilic oesophagitis is not itself an acid reflux disorder — PPIs reduce acid-mediated exacerbation of inflammation, may improve mucosal barrier integrity to food triggers, and have direct anti-inflammatory (cytokine-modulating) effects. The histological response is typically modest, around 40–50% of patients; continue if response is confirmed on repeat biopsy.

Acute food bolus impaction

Assess for perforation and cervical surgical emphysema, then arrange urgent endoscopy with anaesthetic support for airway protection. Biopsies should ideally be taken above and below the impaction site; suction cap-assisted extraction improves safety and efficacy. Antispasmodics, muscle relaxants, glucagon and soft drinks have no role in management.

Fibrostenotic strictures

Endoscopic dilatation (e.g. Savary-Gilliard or through-the-scope dilators) is effective for narrow-calibre oesophagus or dominant strictures in advanced disease. Ongoing medical therapy to control inflammation reduces how often repeat dilatation is needed. For refractory cases, oral prednisolone may be required — seek expert advice.

Emerging therapies

Monoclonal antibodies targeting the atopic/inflammatory cascade — dupilumab, benralizumab, etrasimod — are under investigation for eosinophilic oesophagitis specifically. Early data are promising but not yet established for this indication.