Eosinophilic Oesophagitis (EoE)

📋 Key Information Summary

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Definition: Eosinophilic oesophagitis (EoE) is a chronic, immune-mediated oesophageal disease characterised by symptoms of oesophageal dysfunction and ≥15 eosinophils per high-power field (eos/HPF) on oesophageal biopsy, after exclusion of secondary causes.
Epidemiology: Rising incidence in Australia (estimated 1 in 100–500 adults; peak prevalence in Caucasian males aged 30–50 years). Increasingly recognised in children and adolescents.
Diagnosis requires: Upper GI endoscopy with ≥6 biopsies from both proximal and distal oesophagus showing ≥15 eos/HPF, plus exclusion of PPI-responsive oesophageal eosinophilia (PPI-REE) and other secondary causes of oesophageal eosinophilia.
PPI therapy is now part of EoE treatment: PPIs are no longer solely a diagnostic exclusion criterion — they are considered first-line therapy for EoE in their own right, with up to 50% histological response rates.
Topical swallowed corticosteroids (TSC): Budesonide orodispersible tablet (Jorveza®) or swallowed fluticasone propionate from an MDI are the cornerstone pharmacological treatments, with histological remission rates of 50–70%.
Elimination diets: Empiric elimination diets (6-food, 4-food, or 2-food) are effective alternatives, with step-up or step-down approaches guided by endoscopic and histological response.
Dupilumab: Now PBS-listed (Authority Required) for moderate-to-severe EoE in adults and adolescents ≥12 years refractory to at least one standard therapy.
Treatment targets: The goal is histological remission (<15 eos/HPF, ideally <6 eos/HPF), symptomatic improvement, and endoscopic remission (normalised EREFS score).
Monitoring: Repeat endoscopy with biopsies 8–12 weeks after initiating or changing therapy; then periodic surveillance for long-term maintenance patients.
Complications: Progressive fibrostenosis leads to oesophageal strictures and food impaction. Endoscopic oesophageal dilation is required for symptomatic strictures unresponsive to medical therapy.
Maintenance therapy: Most patients require long-term maintenance treatment to prevent relapse; abrupt cessation of therapy typically results in recurrence of eosinophilia and symptoms within weeks.
ATSI considerations: EoE data in Aboriginal and Torres Strait Islander populations are limited; access to endoscopy and specialist gastroenterology services in remote and regional Australia remains a significant barrier.

Diagnosis

The diagnosis of EoE is based on the presence of oesophageal symptoms accompanied by oesophageal mucosal eosinophilia, after exclusion of other causes. Updated 2024 guidelines from the International Gastrointestinal Eosinophil Research (TIGERS) consortium and AGREE consensus provide the current framework.

Histological Criteria

The hallmark of EoE is the presence of ≥15 eosinophils per high-power field (eos/HPF) in at least one oesophageal biopsy specimen, in the absence of secondary causes of oesophageal eosinophilia. This threshold has been validated in both adult and paediatric populations across multiple international studies.

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Biopsy protocol is critical: A minimum of 6 biopsies should be obtained from at least two oesophageal locations (proximal and distal oesophagus). This increases diagnostic sensitivity from ~70% to >95%. Fewer than 6 biopsies risks false-negative results due to the patchy nature of eosinophilic infiltration.

Additional histological features that support the diagnosis include eosinophil microabscesses, surface layering of eosinophils, eosinophil degranulation, basal zone hyperplasia, and dilated intercellular spaces. These features should be reported by the pathologist even if the 15 eos/HPF threshold is not met in all specimens.

Endoscopic Features — EREFS Classification

The Endoscopic Reference Score (EREFS) system standardises the reporting of endoscopic findings in EoE. The following five features are each graded from 0 (absent) to 3 (severe):

EREFS Feature	Description	Grade 0	Grade 1	Grade 2	Grade 3
R — Rings	Concentric mucosal rings	None	Mild (visible with insufflation)	Moderate (persistent)	Severe (non-traversable)
E — Exudates	White plaques or spots	None	Mild (<10% surface)	Moderate (10–30%)	Severe (>30%)
E — Furrows	Linear longitudinal grooves	None	Mild	Moderate	Severe
F — Oedema (Fr)	Mucosal oedema / loss of vascularity	None	Mild	Moderate	Severe
S — Strictures	Fixed luminal narrowing	None	Mild (≥14 mm)	Moderate (10–13 mm)	Severe (<10 mm)

The EREFS score correlates with histological disease severity and can be used to track response to therapy. A total EREFS score ≤2 is considered endoscopic remission. Note that a normal-appearing oesophagus at endoscopy does not exclude EoE — up to 25% of patients with confirmed EoE have a macroscopically normal mucosa, underscoring the importance of systematic biopsies.

Exclusion of Secondary Oesophageal Eosinophilia

Before a diagnosis of EoE can be confirmed, secondary causes of oesophageal eosinophilia must be excluded. The following differential diagnoses should be considered and addressed:

Secondary Cause	Key Differentiating Features
Gastro-oesophageal reflux disease (GORD)	Usually <15 eos/HPF; responds to PPI therapy; distal oesophagus predominant
PPI-responsive oesophageal eosinophilia (PPI-REE)	Now considered part of the EoE spectrum; PPIs are therapeutic, not just diagnostic
Hypereosinophilic syndrome	Peripheral eosinophilia >1500/μL; multi-organ involvement; cardiac risk
Achalasia	Oesophageal manometry shows failed peristalsis and incomplete LES relaxation
Crohn's disease	Usually colonic or ileal involvement; granulomas on biopsy
Connective tissue disorders	Scleroderma — oesophageal hypomotility; systemic features present
Drug hypersensitivity	Temporal relationship to drug exposure (e.g., azathioprine, tacrolimus)
Parasitic infection	Stool ova, cysts, and parasites; Strongyloides serology in at-risk patients

Diagnostic Investigations

Essential

Upper GI endoscopy with oesophageal biopsies

≥6 biopsies from proximal and distal oesophagus. MBS Item 30475 (diagnostic upper GI endoscopy). EREFS scoring should be performed and documented at every procedure.

Essential

Full blood examination (FBE) with differential

MBS Item 65070. Assess for peripheral eosinophilia (may be elevated in up to 40% of EoE patients) and exclude hypereosinophilic syndrome.

Available

Serum total IgE and specific IgE (allergen panel)

MBS Item 71118 (specific IgE). Identify potential food triggers and concurrent atopic disease (asthma, eczema, allergic rhinitis) present in 50–70% of EoE patients.

Available

Oesophageal high-resolution manometry (HRM)

MBS Item 11820. Consider if motility disorder suspected or prior to dilation. Not routinely required for EoE diagnosis.

Specialist

Allergen-specific patch testing / skin prick testing

Performed by allergist/immunologist. May guide targeted elimination diet. Sensitivity and specificity are suboptimal for EoE-specific food triggers; empiric approaches often preferred.

Specialist

Stool ova, cysts, parasites + Strongyloides serology

MBS Item 69316. To exclude parasitic causes of eosinophilia, particularly in patients with eosinophilia on FBE, tropical exposure, or immunosuppression.

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Diagnostic tip: In patients with food bolus impaction, always perform a follow-up endoscopy with biopsies after the acute episode resolves. Up to 50% of adults presenting with food bolus impaction are ultimately diagnosed with EoE.

Treatment

The goals of EoE treatment are to achieve histological remission (<15 eos/HPF, ideally <6 eos/HPF), resolve symptoms, and prevent fibrostenotic complications. Treatment options include PPI therapy, topical swallowed corticosteroids, elimination diets, and biologic therapy. Choice of initial therapy depends on disease severity, patient preference, comorbidities, and access.

PPI Therapy — First-Line

PPIs are now considered a first-line treatment for EoE, not merely a diagnostic exclusion tool. Approximately 30–50% of patients with oesophageal eosinophilia achieve histological remission with PPI monotherapy. The mechanism involves both acid suppression and direct anti-eosinophilic effects (reduction of eotaxin-3, inhibition of IL-4/IL-13 signalling).

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Esomeprazole

Nexium® · Proton pump inhibitor

Adult dose 20–40 mg PO BD (higher end preferred for EoE)

Paediatric dose 1 mg/kg/dose PO BD (max 20 mg/dose in children <20 kg; 40 mg/dose ≥20 kg)

Route / Frequency Oral, 30 minutes before meals, BD

Duration Initial trial: 8–12 weeks; long-term maintenance if responding

Renal adjustment No dose adjustment required (eGFR >15). Avoid long-term use in severe CKD without monitoring.

PBS status ✔ PBS General Benefit

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Pantoprazole

Somac® · Proton pump inhibitor

Adult dose 40 mg PO BD

Paediatric dose ≥5 years: 20 mg PO BD (weight <40 kg); 40 mg PO BD (≥40 kg)

Route / Frequency Oral, before meals, BD

Duration 8–12 weeks initial; ongoing if responding

Renal adjustment No adjustment required

PBS status ✔ PBS General Benefit

Topical Swallowed Corticosteroids (TSC)

If PPI therapy is insufficient, or as first-line in moderate-to-severe disease, topical swallowed corticosteroids are the mainstay of pharmacological treatment. These agents deliver corticosteroid directly to the oesophageal mucosa with minimal systemic absorption. Histological remission rates range from 50–70%.

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Budesonide orodispersible tablet

Jorveza® · Topical corticosteroid · PBS Authority

Adult dose 1 mg PO BD (dissolve on tongue, do not chew or swallow whole). May increase to 2 mg BD if partial response.

Paediatric dose Off-label: budesonide viscous slurry 1 mg PO BD (0.5 mg/5 mL in children <10 kg). Jorveza® not PBS-subsidised for <18 years.

Route / Frequency Oral (orodispersible tablet), BD, 30 minutes before meals

Duration Induction: 6–12 weeks. Maintenance: continue at lowest effective dose if responding.

Renal adjustment Not required (minimal systemic absorption)

PBS status ⚠ PBS Authority Required — Moderate-to-severe EoE, ≥18 years, refractory to PPI or as first-line with significant stricture risk

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Fluticasone propionate (swallowed MDI)

Flixotide® · Topical corticosteroid

Adult dose 250–500 μg actuated into mouth and swallowed (NOT inhaled) BD. Rinse mouth but do not eat/drink for 30 minutes.

Paediatric dose <10 years: 125 μg swallowed BD; ≥10 years: 250 μg swallowed BD

Route / Frequency Oral (actuated into mouth, then swallowed), BD

Duration Induction: 6–12 weeks. Maintenance: continue if responding.

Renal adjustment Not required

PBS status ✔ PBS General Benefit (for asthma indication; EoE use is off-label but widely used in Australia)

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Candidiasis risk: Oropharyngeal candidiasis occurs in 5–15% of patients on topical swallowed corticosteroids. Counsel patients to rinse the mouth and spit after each dose. If symptomatic candidiasis develops, treat with oral nystatin suspension or a single dose of fluconazole 150 mg PO, and consider dose reduction.

Elimination Diets

Empiric elimination diets are an effective, drug-free alternative for EoE management, particularly in motivated patients and those wishing to avoid long-term corticosteroids. Histological remission rates vary by approach: 6-food elimination ~70%, 4-food ~60%, 2-food ~45%.

6-Food

Six-Food Elimination Diet (SFED)

Eliminates dairy, wheat, egg, soy, fish/seafood, and nuts (peanut + tree nuts). Most comprehensive approach.

Efficacy: ~70% histological remission

4-Food

Four-Food Elimination Diet

Eliminates dairy, wheat, egg, and legumes/soy. A pragmatic step-down from SFED.

Efficacy: ~60% histological remission

2-Food

Two-Food Elimination Diet

Eliminates dairy and wheat only. Simplest empiric approach; increasingly used as first-line dietary strategy.

Efficacy: ~45% histological remission

Protocol: Foods are eliminated for 6 weeks, followed by repeat endoscopy with biopsies. If histological remission is confirmed, foods are reintroduced sequentially (one food group every 6–8 weeks) with repeat endoscopy after each reintroduction to identify triggers. Dietitian involvement is essential to ensure nutritional adequacy, particularly in children.

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Referral to a dietitian with EoE experience is recommended for all patients undertaking elimination diets. This is critical for paediatric patients to prevent growth faltering and micronutrient deficiencies (calcium, iron, B12).

Dupilumab — Biologic Therapy for Refractory EoE

Dupilumab (Dupixent®) is a fully human monoclonal antibody targeting IL-4Rα, thereby blocking both IL-4 and IL-13 signalling — key drivers of type 2 inflammation in EoE. It is approved by the TGA and listed on the PBS (Authority Required) for moderate-to-severe EoE in adults and adolescents ≥12 years who are refractory to, intolerant of, or have contraindications to at least one standard treatment (PPI, TSC, or elimination diet).

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Dupilumab

Dupixent® · Anti-IL-4Rα monoclonal antibody

Adult/adolescent dose 300 mg SC once weekly (after loading dose of 600 mg SC = 2 × 300 mg injections at two separate sites)

Paediatric dose <12 years or <40 kg: not PBS-subsidised; limited data. Specialist use only.

Route / Frequency Subcutaneous injection, weekly (adults ≥60 kg); may use 200 mg SC weekly for adults 30–<60 kg

Duration Ongoing — cessation typically leads to disease recurrence

Renal adjustment Not required

Hepatic adjustment Not required

PBS status ⚠ PBS Authority Required — Adult and adolescent ≥12 years with moderate-to-severe EoE refractory to ≥1 standard therapy

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Important: Dupilumab can induce conjunctivitis in up to 10–15% of EoE patients (higher than in atopic dermatitis trials). Educate patients to report eye symptoms promptly. Ophthalmology referral should be considered for persistent cases. Do not use in patients with active helminth infections — treat parasitic infections before initiating dupilumab.

Treatment Algorithm — Step-Up Approach

Step 1

PPI monotherapy

Esomeprazole 40 mg PO BD or pantoprazole 40 mg PO BD for 8–12 weeks. Reassess with endoscopy + biopsies.

Step 2

Add topical swallowed corticosteroid

Budesonide orodispersible 1 mg PO BD (or fluticasone 500 μg swallowed BD) + continue PPI. Reassess at 8–12 weeks.

Step 3

Elimination diet ± PPI

Consider 2-food or 4-food empiric elimination with dietitian support. 6-week elimination trial with repeat endoscopy.

Step 4

Biologic therapy

Dupilumab 300 mg SC weekly for refractory moderate-to-severe EoE. May continue PPI or TSC concurrently.

Monitoring & Complications

Response Assessment — Repeat Endoscopy

All patients should undergo repeat upper GI endoscopy with oesophageal biopsies 8–12 weeks after initiating or changing therapy. This is the gold standard for assessing treatment response. Symptom assessment alone is unreliable — many patients have discordance between symptoms and histological activity, particularly adults who may have adapted to chronic dysphagia.

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Symptoms do not reliably predict histological activity. Up to 50% of adults with persistent oesophageal eosinophilia report subjective symptom improvement. Endoscopy with biopsies remains the only reliable method to confirm histological remission. Do not rely on symptom questionnaires alone.

Treatment Targets

Updated consensus guidelines define three domains of remission, all of which should be assessed:

Histological remission

<15 eos/HPF (ideally <6 eos/HPF = complete response)

Primary endpoint in clinical trials; most reliable marker of disease control

Endoscopic remission

EREFS total score ≤2

Document EREFS at every endoscopy; correlates with fibrosis risk

Symptomatic remission

Clinically meaningful improvement in dysphagia/food impaction

Use validated instruments: EoE-PRO, DSQ, or PedsQL-EoE (paediatric)

Long-Term Maintenance

EoE is a chronic, relapsing condition. Histological relapse occurs in the majority of patients within weeks to months of discontinuing therapy. Long-term maintenance therapy is therefore recommended for most patients, using the lowest effective dose of the treatment that induced remission.

Week 0

Initiate therapy (PPI, TSC, or elimination diet)

Week 8–12

First follow-up endoscopy with biopsies. Assess histological, endoscopic, and symptomatic response.

If remission achieved

Transition to maintenance therapy (step-down dose of PPI/TSC, or ongoing elimination diet with periodic reassessment)

Every 1–2 years

Surveillance endoscopy in stable maintenance patients to assess for subclinical fibrosis progression and confirm ongoing histological remission

If non-response

Step up therapy (see treatment algorithm). Consider alternative TSC, elimination diet, or dupilumab.

Complications

Untreated or poorly controlled EoE can lead to progressive oesophageal remodelling and fibrosis, resulting in significant morbidity:

Complication	Management
Food bolus impaction	Urgent endoscopic retrieval (MBS Item 30475). Emergent flexible endoscopy preferred over rigid oesophagoscopy in most centres. Consider general anaesthesia if prolonged impaction >24 hours. After resolution, schedule follow-up endoscopy + biopsies to confirm EoE diagnosis and initiate therapy.
Fibrostenotic strictures	Endoscopic oesophageal dilation (bougie or balloon). Serial dilations in increments of 1–2 mm to minimise perforation risk (perforation rate <1% when performed by experienced endoscopists). Always combine with medical therapy — dilation alone does not address the underlying inflammatory process.
Oesophageal perforation	Rare (<0.5% of dilations in experienced hands). Suspect if chest pain, crepitus, or haemodynamic instability post-dilation. Urgent CT thorax with oral contrast. Surgical consultation for contained perforation; emergency surgery for free perforation.
Subepithelial fibrosis	Often clinically silent in early stages. Detected by EREFS scoring (rings, strictures) and functional luminal imaging probe (EndoFLIP, specialist centres). Emphasises the importance of early, effective anti-inflammatory therapy to prevent irreversible remodelling.

Oesophageal Dilation

Endoscopic oesophageal dilation is indicated for patients with symptomatic fibrostenotic strictures that fail to resolve with medical therapy alone. Key principles:

Always combine with ongoing anti-inflammatory therapy (PPI, TSC, or dupilumab)
Use bougie (Savary-Gilliard) or balloon dilation based on operator expertise and stricture characteristics
Serial sessions preferred — dilate by 1–2 mm per session to minimise mucosal tears and perforation risk
Target diameter of 15–17 mm is generally sufficient for symptom resolution
Post-procedure: observe for 2–4 hours; soft diet for 24 hours; paracetamol for discomfort

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When to refer for dilation: Dysphagia to solid foods, endoscopic stricture (diameter <13 mm), history of food impaction, or failure of medical therapy to improve EREFS stricture score after 12 weeks of treatment.

Special Populations

👶 Paediatric EoE

Diagnostic criteria: Same as adults (≥15 eos/HPF). Presenting symptoms vary by age — feeding difficulties and failure to thrive in infants/toddlers; vomiting, abdominal pain, and food refusal in children; dysphagia in adolescents.

PPIs: First-line. Esomeprazole 1 mg/kg/dose PO BD or pantoprazole (≥5 years) 20–40 mg PO BD.

TSC: Swallowed fluticasone MDI (125–250 μg BD) is the most commonly used agent in paediatric practice in Australia. Budesonide viscous slurry is an alternative (off-label preparation).

Elimination diets: Frequently used as first-line in children. Dietitian involvement is essential. Monitor growth (weight and height centiles) and micronutrient status (iron, calcium, vitamin D, B12).

Dupilumab: Not PBS-subsidised for paediatric EoE in Australia. Limited data in <12 years.

🤰 Pregnancy & Breastfeeding

PPIs: Pantoprazole is the preferred PPI in pregnancy (Category B1, most safety data). Esomeprazole is Category B3.

TSC: Budesonide — Category B3. Low systemic bioavailability when used as orodispersible tablet or slurry; generally considered acceptable if clinically necessary. Fluticasone MDI — Category B3, minimal systemic absorption.

Dupilumab: Category B1 but limited pregnancy data. Avoid unless benefits clearly outweigh risks. Discontinue ≥10 weeks before planned conception where possible.

Elimination diets: Safe in pregnancy but ensure adequate nutritional supplementation. Dietitian review essential.

🫘 Renal Impairment

PPIs: Generally safe in CKD. Monitor magnesium levels with long-term use (hypomagnesaemia risk). No dose adjustment for eGFR >15.

TSC: Minimal systemic absorption — no renal dose adjustment required.

Dupilumab: Not renally cleared — no dose adjustment required.

🫁 Hepatic Impairment

PPIs: Esomeprazole — reduce maximum dose to 20 mg/day in severe hepatic impairment (Child-Pugh C). Pantoprazole — no dose adjustment required.

TSC: No hepatic dose adjustment needed.

Dupilumab: Not hepatically metabolised — no dose adjustment required.

Aboriginal and Torres Strait Islander Health Considerations

Epidemiology & data gaps

EoE prevalence data in Aboriginal and Torres Strait Islander populations are extremely limited. Available registry data from Australian tertiary centres suggest EoE is diagnosed less frequently in Indigenous Australians, but this likely reflects diagnostic access disparities rather than true lower incidence. The rising national EoE incidence may disproportionately affect Indigenous Australians given the higher burden of atopic disease, food insecurity, and environmental risk factors.

Endoscopy access

Upper GI endoscopy — the cornerstone of EoE diagnosis — requires access to procedural gastroenterology services. Aboriginal and Torres Strait Islander peoples in remote and very remote Australia often have limited or no local access to endoscopy, requiring transfer to regional or metropolitan centres. Wait times for diagnostic endoscopy in the public system can exceed 6–12 months in some jurisdictions. The Australian Commission on Safety and Quality in Health Care (ACSQHC) identifies procedural access as a key driver of diagnostic delay.

Medication access & PBS

Budesonide orodispersible tablet (Jorveza®) requires PBS Authority approval, which necessitates specialist gastroenterologist involvement. In remote communities, specialist follow-up may be infrequent. Dupilumab (Dupixent®) also requires PBS Authority and ongoing specialist monitoring. PPIs and swallowed fluticasone are PBS General Benefit and more accessible but still require adequate pharmacy services. The Section 100 Remote Area Aboriginal Health Services programme can assist with medication supply in eligible areas.

Elimination diet feasibility

Empiric elimination diets require access to diverse, affordable food options. In remote communities with limited fresh food availability and high food costs, multi-food elimination diets may be impractical or nutritionally hazardous. The 2-food elimination approach (dairy and wheat) may be the most feasible option, but even this can be challenging. Dietitian support via telehealth (MBS Items 81300–81360) can assist, but community-specific dietary counselling is preferred.

Recommended strategies

Support mobile endoscopy programmes and GP-led diagnostic pathways where feasible. Use telehealth for specialist gastroenterology review (MBS Items 91822–91827). Prioritise PBS-accessible treatments (PPIs, swallowed fluticasone) as first-line in settings where specialist services are limited. Engage Aboriginal Health Workers and Practitioners in patient education and treatment adherence support. Advocate for inclusion of Indigenous Australians in EoE research registries to build an evidence base for this population.

📚 References

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3. Dellon ES, Liacouras CA, Molina-Infante J, et al. Updated International Consensus Diagnostic Criteria for Eosinophilic Esophagitis: Proceedings of the AGREE Conference. Gastroenterology. 2018;155(4):1022–1033.e10.
4. Molina-Infante J, Bredenoord AJ, Cheng E, et al. Proton pump inhibitor-responsive oesophageal eosinophilia: an entity challenging current diagnostic criteria for eosinophilic oesophagitis. Gut. 2016;65(3):524–531.
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6. Miehlke S, Lucendo AJ, Straumann A, et al. Budesonide orodispersible tablets for induction and maintenance of remission in adult patients with eosinophilic esophagitis. Lancet Gastroenterol Hepatol. 2022;7(9):838–849.
7. Hirano I, Collins MH, Assouline-Dayan Y, et al. Dupilumab efficacy and safety in adults and adolescents with eosinophilic oesophagitis: a randomised, double-blind, placebo-controlled, phase 3 trial (Part A). Lancet. 2022;400(10363):1553–1565.
8. Molina-Infante J, Arias Á, Alcedo J, et al. Step-up approach for eosinophilic oesophagitis based on a randomised controlled trial. Gut. 2018;67(12):2130–2137.
9. Warners MJ, Vlieg-Boerstra BJ, Verheij J, et al. Elemental and elimination diet in adult eosinophilic oesophagitis. Aliment Pharmacol Ther. 2017;45(4):544–554.
10. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander health performance framework: Gastrointestinal diseases. Canberra: AIHW; 2023.
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