Gastrointestinal · PANCE / PANRE

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

EREFS endoscopic classification of EoE — scored for severity at diagnosis and follow-up.

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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