Dysphagia Knowledge Hub — 吞嚥困難知識庫
Eosinophilic Oesophagitis (EoE) and Swallowing Difficulties
Eosinophilic oesophagitis (EoE) is a chronic, immune-mediated oesophageal disease characterised by eosinophil-predominant inflammation of the oesophageal epithelium. Once considered rare, EoE has emerged as a leading cause of dysphagia in children and young adults in high-income countries over the past two decades, with prevalence estimated at 1–5 per 10,000 in Western populations and rising (Dellon & Hirano, 2018). In Hong Kong and other East Asian cities, awareness is growing alongside increasing diagnosis rates, though population-specific epidemiological data remain limited.
Immune-Mediated Mechanism
EoE results from dysregulated type 2 immune responses to food and environmental allergens. The key immunological pathway involves activation of Th2 lymphocytes and mast cells, release of interleukin-4 (IL-4), IL-5, and IL-13, and subsequent recruitment of eosinophils from the peripheral blood into the oesophageal epithelium. IL-5 is the key cytokine driving eosinophil production and survival; this is clinically exploited in biologic therapies.
Normal oesophageal epithelium contains no eosinophils. In EoE, the eosinophil infiltrate (defined diagnostically as ≥15 eosinophils per high-power field on biopsy) triggers epithelial barrier dysfunction, sub-epithelial fibrosis, oesophageal remodelling, and ultimately reduced oesophageal compliance and motility. These structural changes — rather than acute inflammation alone — account for the progressive dysphagia and food impaction characteristic of the condition.
Allergen sensitisation in EoE is predominantly food-driven, with the six major culprit foods being milk, wheat, eggs, soy, nuts, and seafood/shellfish. Environmental aeroallergens (pollen, dust mite) also play a role in some patients, explaining seasonal symptom exacerbations reported by a subset.
Presentations: Food Impaction and Dysphagia
The cardinal symptom of EoE is dysphagia for solid foods. Patients classically report food “getting stuck” at the mid-chest or lower throat level, often requiring liquid to wash food down, prolonged meal times, avoidance of certain textures (steak, bread, raw vegetables), and habitually cutting food into very small pieces. Many patients have compensated for years before seeking medical attention, making symptom duration history essential.
Food impaction — a solid bolus becoming completely lodged in the oesophagus — occurs in up to 33–54% of EoE patients and is the presentation that most commonly prompts acute emergency evaluation. Patients present with total dysphagia (inability to swallow even saliva), excessive salivation, and chest or throat discomfort. Emergency endoscopy with bolus removal is required; the underlying oesophageal mucosa will typically reveal the characteristic EoE mucosal changes (furrows, rings, exudates, crêpe-paper fragility).
In children, presentations are more varied: feeding refusal, vomiting, failure to thrive, and abdominal pain are common, while the classical adult dysphagia presentation may be absent.
Endoscopy with Oesophageal Biopsy
Diagnosis requires both endoscopic evaluation and histological confirmation. Upper endoscopy (oesophago-gastro-duodenoscopy, OGD) characteristically shows a range of mucosal findings in EoE:
- Oesophageal rings (trachealization, concentric rings): most specific finding
- Linear furrows: longitudinal grooves in the mucosa
- White exudates or plaques: eosinophilic microabscesses
- Mucosal pallor and oedema
- Crêpe-paper/fragile mucosa: tears easily on passage of endoscope
- Fixed oesophageal rings (strictures): indicating fibrotic remodelling in advanced or long-standing disease
However, endoscopic findings alone are insufficient; up to 10–30% of EoE cases have grossly normal-appearing mucosa on endoscopy. Oesophageal biopsies are mandatory. Current guidelines (Dellon et al., 2022) recommend at least six biopsies from two or more oesophageal levels (proximal and distal) to achieve adequate sensitivity, given the patchy distribution of eosinophilic infiltrate.
The diagnostic eosinophil threshold is ≥15 eosinophils per high-power field (eos/hpf) in at least one biopsy specimen, in the absence of other causes of oesophageal eosinophilia (gastro-oesophageal reflux disease, parasitic infection, hypereosinophilic syndrome, Crohn’s disease).
Treatment: Elemental Diet, PPI, and Steroids
Treatment of EoE follows a “3Ds” framework: dietary therapy, drugs, and dilation.
Elemental Diet
An amino acid-based elemental formula provides complete nutrition while eliminating all intact food proteins — the antigenic triggers for EoE. Studies in children and adults demonstrate histological remission rates of 90–98% with strict elemental diet (Liacouras et al., 2005). However, palatability is poor (the formula tastes unpleasant), oral intake compliance is difficult for adults, and nasogastric tube feeding is sometimes required. Elemental diet is rarely used as a first-line strategy in adult EoE except in refractory cases or as a diagnostic challenge.
Empirical Six-Food Elimination Diet (SFED)
The most widely used dietary approach is the empirical elimination of the six most common trigger foods (milk, wheat, egg, soy, nuts, seafood), with reintroduction as a food trigger identification protocol. Meta-analysis by Arias et al. (2014) found histological remission rates of approximately 72% with SFED. A stepwise approach — beginning with two-food (milk and wheat) elimination and escalating — reduces unnecessary dietary restriction.
Proton Pump Inhibitors (PPI)
PPIs are now established as a first-line therapy for EoE. The mechanism extends beyond acid suppression: PPIs have direct anti-eosinophilic effects, reducing eotaxin-3 expression in oesophageal epithelium. Dellon et al. (2020) demonstrated histological remission rates of approximately 50% with PPI therapy (omeprazole 20–40 mg twice daily for 8–12 weeks) — comparable to topical steroids. PPIs are often continued long-term given the chronic relapsing nature of EoE.
Topical (Swallowed) Corticosteroids
Swallowed fluticasone (250–880 mcg/day from an MDI inhaler, swallowed not inhaled) or swallowed budesonide (orodispersible tablet or viscous slurry) are the primary steroid formulations. Histological remission rates are 60–75% (Dellon et al., 2012). Oesophageal Candida colonisation occurs in approximately 10% of patients on topical steroids; oral hygiene and monitoring are important. Systemic side effects are uncommon at standard doses.
Dupilumab (anti-IL-4/IL-13 biologic) received FDA approval for EoE in 2022, with Phase 3 trial data showing histological and symptomatic remission in approximately 60% of patients (Dellon et al., 2022). It is available in HK as an imported drug via compassionate use or private prescription for refractory cases.
Food Reintroduction Protocol
After achieving histological remission (repeat OGD with biopsy at 8–12 weeks of treatment), single food groups are reintroduced sequentially. Each food group is introduced for six weeks, followed by repeat OGD and biopsy to identify trigger foods. The process is lengthy but defines individual trigger foods, allowing the least restrictive long-term diet compatible with remission. Typical reintroduction sequence: seafood, nuts, eggs, soy, wheat, dairy — reintroducing dairy last as it is the most common trigger.
HK Allergy Clinic Referral
In Hong Kong, EoE management typically involves gastroenterology (for endoscopy and medical management) and allergy/immunology (for allergen identification and dietary management). The Chinese University of Hong Kong (CUHK) and University of Hong Kong (HKU) both have clinical units with EoE experience. Paediatric EoE is managed through paediatric gastroenterology services at PWH and QMH. Dietitians with experience in elimination diets and food reintroduction protocols are essential team members. SLTs contribute to management when significant dysphagia affects oral intake, particularly when food impaction events have led to anxiety-related feeding avoidance.
References
- Arias A, Gonzalez-Cervera J, Tenias JM, et al. (2014). Efficacy of dietary interventions for inducing histologic remission in patients with eosinophilic esophagitis: a systematic review and meta-analysis. Gastroenterology, 146(7), 1639–1648.
- Dellon ES, Gonsalves N, Hirano I, et al. (2013). ACG clinical guideline: evidence based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis. American Journal of Gastroenterology, 108(5), 679–692.
- Dellon ES, Hirano I. (2018). Epidemiology and natural history of eosinophilic esophagitis. Gastroenterology, 154(2), 319–332.
- Dellon ES, Katzka DA, Collins MH, et al. (2012). Budesonide oral suspension improves symptomatic, endoscopic, and histologic parameters compared to placebo in patients with eosinophilic esophagitis. Gastroenterology, 152(4), 776–786.
- Liacouras CA, Spergel JM, Ruchelli E, et al. (2005). Eosinophilic esophagitis: a 10-year experience in 381 children. Clinical Gastroenterology and Hepatology, 3(12), 1198–1206.