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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Question 1GastrointestinalMedium
A 27-year-old man presents with a 2-year history of solid-food dysphagia and one episode of food impaction requiring endoscopic disimpaction. He eats slowly, chews excessively, and washes meals down with water. He has asthma and eczema. Upper endoscopy shows linear furrows, concentric rings, and scattered white exudates; biopsies from the distal and proximal esophagus show 35 eosinophils per high-power field. He has had no prior therapy. Which of the following is the most appropriate initial management?
ASystemic corticosteroid taper
BOral montelukast daily therapy
COral proton pump inhibitor
DEmpiric esophageal dilation
EOral H2 receptor antagonist
Reveal answer & full explanation
Correct answer: C — Oral proton pump inhibitor
ASystemic corticosteroid taper
BOral montelukast daily therapy
COral proton pump inhibitor✓
DEmpiric esophageal dilation
EOral H2 receptor antagonist
Why Oral proton pump inhibitor is correct
This is biopsy-confirmed eosinophilic esophagitis (EoE): esophageal dysfunction plus >=15 eosinophils/HPF with classic EREFS findings (furrows, rings, exudates) in a young atopic man with no competing cause.
First-line therapy is one of the 3 Ds (Drugs, Diet, Dilation), chosen by phenotype and patient preference. A high-dose PPI taken twice daily for 8 weeks is a guideline-endorsed first-line drug option that is inexpensive and well tolerated; a swallowed topical corticosteroid is an equally acceptable first-line drug alternative but is not offered here.
A PPI is now classified as a treatment for EoE rather than a way to exclude it, so PPI-responsive eosinophilia falls within the EoE spectrum.
Why the others are wrong
Oral montelukast daily therapy — leukotriene receptor antagonists have been trialed in EoE and do not produce histologic remission or durable symptom control, so montelukast is not a guideline-endorsed EoE therapy despite being attractive in a patient with asthma and eczema.
Systemic corticosteroid taper is not used for EoE; the effective steroid strategy is a swallowed topical agent (budesonide or fluticasone) to limit systemic exposure, not a systemic course.
Empiric esophageal dilation is reserved for symptomatic strictures or a narrow-caliber esophagus; it relieves obstructive symptoms but does not treat the underlying inflammation and is not appropriate as sole initial therapy.
Oral H2 receptor antagonist — tempting because a PPI is first-line and both drugs suppress acid, but the PPI response in EoE is thought to reflect anti-inflammatory effects beyond acid suppression; H2 receptor antagonists are not a guideline-endorsed EoE therapy and do not reliably induce histologic remission.
Question 2GastrointestinalMedium
A 26-year-old man presents to the emergency department after a piece of steak became lodged in his throat during dinner, requiring endoscopic disimpaction. He reports a 3-year history of intermittent solid-food dysphagia for which he eats slowly and washes meals down with water. His heartburn has not improved on a high-dose proton pump inhibitor. He has smoked half a pack of cigarettes daily for 8 years and drinks five or six beers most evenings. Endoscopy shows concentric rings and linear furrows, and biopsies reveal 28 eosinophils per high-power field. Which of the following is the strongest risk factor for this patient's condition?
ALong-term cigarette smoking
BChronic heavy alcohol intake
CCoexisting atopic disorders
DHelicobacter pylori infection
EChronic gastroesophageal reflux
Reveal answer & full explanation
Correct answer: C — Coexisting atopic disorders
ALong-term cigarette smoking
BChronic heavy alcohol intake
CCoexisting atopic disorders✓
DHelicobacter pylori infection
EChronic gastroesophageal reflux
Why Coexisting atopic disorders is correct
This patient has eosinophilic esophagitis (EoE): solid-food dysphagia, food impaction, PPI-unresponsive symptoms, endoscopic rings and furrows, and >=15 eosinophils/HPF on biopsy (here 28/HPF).
EoE is a Th2-driven, antigen-mediated disease; a personal history of atopy (asthma, eczema, allergic rhinitis, IgE-mediated food allergy) is present in 50-80% of patients and is the single strongest and most consistent risk factor.
IL-5 and IL-13 from the atopic Th2 response recruit eosinophils to the esophageal epithelium, driving the inflammation and remodeling.
Why the others are wrong
Helicobacter pylori infection: a risk factor for peptic ulcer disease and gastric cancer; if anything, H. pylori is inversely associated with atopy and EoE rather than a risk factor.
Chronic heavy alcohol intake: a risk factor for esophageal squamous cell carcinoma and reflux, not for eosinophil-predominant inflammation.
Long-term cigarette smoking: a risk factor for esophageal squamous cell carcinoma, reflux, and peptic disease; it is not linked to the Th2-mediated pathophysiology of EoE.
Chronic gastroesophageal reflux — his PPI-refractory heartburn makes reflux tempting, and acid injury can draw a few eosinophils into the distal esophagus, but EoE is an antigen-driven Th2 disease rather than a consequence of acid exposure; dense eosinophilia with rings and furrows reflects allergic inflammation, and atopy, not reflux, is its consistent risk factor.
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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
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; at least 6 biopsies from at least 2 levels (proximal/mid and distal esophagus) (eosinophils are patchy)
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 — start with the least restrictive empiric diet, 1-food (milk) or 2-food (milk, wheat), with a dietitian, stepping up to 4-food (adds egg, soy) or 6-food (adds nuts, seafood) if there is no histologic response; 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
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 at least 6 biopsies from at least 2 esophageal levels (proximal/mid and distal) — 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 2025 — Dellon ES, Muir AB, Katzka DA, et al. ACG Clinical Guideline: Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol 2025;120:31-59
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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