Eosinophilic Esophagitis (EoE)
Chronic Th2-mediated esophageal inflammation with ≥15 eosinophils/HPF, causing dysphagia and food impaction.
Also known as: EoE, eosinophilic esophagitis, allergic esophagitis
Overview
Chronic, immune/antigen-mediated esophageal disease characterized clinically by symptoms of esophageal dysfunction and histologically by eosinophil-predominant inflammation (≥15 eosinophils/HPF) on biopsy, after excluding other causes of esophageal eosinophilia.
Epidemiology
Prevalence ~50-100 per 100,000; rising sharply since the 1990s (true increase plus recognition). Male predominance (3:1). Most common cause of food impaction in young adults. Strong association with atopy (asthma, eczema, allergic rhinitis, food allergies) in 50-80%.
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Risk factors
- Atopic disease (asthma, eczema, allergic rhinitis, IgE-mediated food allergies)
- Family history of EoE or atopy
- Male sex
- White race
- Early-life antibiotic exposure, C-section, formula feeding (proposed)
- Living in cold or arid climates
Pathophysiology
Genetically susceptible individuals develop Th2-driven response to food or aeroallergens. IL-5 and IL-13 recruit eosinophils to the esophageal epithelium. Chronic eosinophilic inflammation causes basal cell hyperplasia, lamina propria fibrosis, and remodeling, producing rings, strictures, and a narrow-caliber esophagus.
Clinical presentation
Symptoms
- Adults: solid-food dysphagia (hallmark), food impaction, chest pain, heartburn unresponsive to PPI
- Children: feeding difficulties, vomiting, abdominal pain, failure to thrive
- Coping behaviors: slow eating, excessive chewing, drinking water with meals, avoiding meats/bread
Signs / physical exam
- Often normal exam
- Signs of atopy: eczema, allergic shiners, nasal crease
- Acute food impaction → drooling, inability to handle secretions
Classic findings
Young atopic male presenting with steakhouse syndrome (food impaction) — EoE until proven otherwise.
Differential diagnosis
- GERD — Heartburn predominant; responds to PPI; distal-predominant; eosinophilia (if present) usually <15/HPF and resolves with PPI — note: PPI-responsive eosinophilia is now considered part of EoE spectrum
- Achalasia — Dysphagia to solids AND liquids, regurgitation; manometry with absent peristalsis and failure of LES relaxation
- Esophageal stricture (peptic, caustic, radiation) — Focal narrowing on imaging/EGD; identifiable cause
- Schatzki ring / esophageal web — Episodic solid-food dysphagia, no inflammation; thin diaphragm at GEJ on barium
- Pill esophagitis — Acute onset after offending medication
- Infectious esophagitis (Candida, HSV, CMV) — Immunocompromised; odynophagia; characteristic EGD findings
- Hypereosinophilic syndrome / eosinophilic gastroenteritis — Systemic eosinophilia; involvement beyond esophagus
Diagnostic workup
Diagnostic criteria
Symptoms of esophageal dysfunction + ≥15 eosinophils/HPF on esophageal biopsy + exclusion of other causes. PPI-responsive esophageal eosinophilia is no longer a separate entity — it is considered part of the EoE spectrum (PPI is now a treatment, not a diagnostic exclusion).
Labs
- No specific blood test; peripheral eosinophilia in some patients but not required
- Allergy testing (skin prick, specific IgE) of limited diagnostic value but helps identify aeroallergens
Imaging
- Upper endoscopy with biopsy — REQUIRED for diagnosis; minimum 2-4 biopsies from distal AND proximal esophagus (eosinophils are patchy)
- EGD findings (EREFS score): Edema (loss of vascular pattern), Rings (trachealization/feline esophagus), Exudates (white plaques), Furrows (linear), Strictures
- Esophagram if stricture or narrow-caliber esophagus suspected
Diagnostic algorithm
| EREFS Feature | Endoscopic Finding | Significance |
|---|---|---|
| E — Edema | Loss of vascular markings, pallor | Active inflammation |
| R — Rings | Concentric rings (trachealization, feline esophagus) | Chronic remodeling |
| E — Exudates | White plaques/papules | Eosinophil microabscesses |
| F — Furrows | Longitudinal linear furrows | Active inflammation |
| S — Strictures | Focal or diffuse narrowing | Fibrotic remodeling |
Treatment
First-line
- The 3 D's: Drugs, Diet, Dilation — selected based on patient preference and disease phenotype
- PPI — omeprazole, pantoprazole, esomeprazole — high-dose BID × 8 weeks; histologic response 30-50%; continue if responsive
- Topical (swallowed) corticosteroid — budesonide oral suspension (FDA-approved) or fluticasone (off-label MDI puffed and swallowed without spacer) × 8-12 weeks; histologic response 60-80%; rinse mouth to prevent candidiasis
- Elimination diet — empiric 6-food (milk, wheat, egg, soy, nuts, seafood) or 4-food (milk, wheat, egg, soy) elimination; sequential reintroduction with repeat biopsy to identify trigger
- Esophageal dilation — for symptomatic strictures or narrow-caliber esophagus; does not treat inflammation
Second-line / adjunct
- Dupilumab (anti-IL-4Rα biologic) — FDA-approved for ≥1 yr old; weekly SC injection; for refractory disease or where steroids/diet fail
- Step-up combination of PPI + topical steroid
- Maintenance therapy is required — symptoms and inflammation recur with discontinuation
- Targeted elimination based on allergy testing has lower yield than empiric elimination
Complications
- Esophageal stricture and narrow-caliber esophagus
- Food impaction requiring emergent endoscopic disimpaction
- Esophageal perforation (rare; spontaneous or during impaction/dilation)
- Impaired quality of life from dietary restriction and eating-related anxiety
- Malnutrition and growth failure in children
PANCE pearls
- Biopsy the esophagus in ANY adult with food impaction — incidence of EoE in this population approaches 50%.
- Take 2-4 biopsies from BOTH distal and proximal esophagus — eosinophils are patchy and isolated distal sampling misses 15-20% of cases.
- Repeat EGD with biopsy 8-12 weeks after starting therapy — histologic remission, not symptoms, guides ongoing management.
- Symptomatic improvement does not equal histologic remission; persistent inflammation drives fibrosis even when patients feel better.
- Avoid dilation as initial therapy — controls symptoms but not inflammation; risk of mucosal tears.
- PPI-responsive esophageal eosinophilia and EoE share genetics and Th2 biology — the 2018 AGREE consensus removed PPI trial from diagnostic criteria.
- Counsel patients that EoE is chronic and relapsing — therapy is maintenance, not curative.
References
- ACG 2013 — Dellon ES et al. ACG Clinical Guideline: Evidenced Based Approach to the Diagnosis and Management of Esophageal Eosinophilia and EoE. Am J Gastroenterol 2013;108:679-692
- AGREE 2018 — Dellon ES et al. Updated International Consensus Diagnostic Criteria for Eosinophilic Esophagitis: Proceedings of the AGREE Conference. Gastroenterology 2018;155:1022-1033
- AGA/JTF 2020 — Hirano I et al. AGA Institute and the Joint Task Force on Allergy-Immunology Practice Parameters Clinical Guidelines for the Management of EoE. Gastroenterology 2020;158:1776-1786
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