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    Subjects/Medicine/Eosinophilic Esophagitis — Trachealization and Furrows
    Eosinophilic Esophagitis — Trachealization and Furrows
    medium
    stethoscope Medicine

    A 24-year-old man with a 10-year history of asthma and atopic dermatitis presents with a 1-year history of intermittent solid-food dysphagia and two episodes of food bolus impaction requiring endoscopic disimpaction. He reports heartburn unresponsive to high-dose PPI therapy. Upper endoscopy reveals concentric esophageal rings ("trachealization"), longitudinal linear furrows, scattered white plaques, pale mucosa, and decreased caliber. Esophageal biopsies from proximal and distal esophagus show ≥15 eosinophils per high-power field with eosinophil microabscesses, basal zone hyperplasia, and lamina propria fibrosis. The endoscopic findings marked **C** in the diagram are consistent with which diagnosis?

    A. Eosinophilic esophagitis with Th2-mediated immune response to food antigens
    B. Pill esophagitis with stricture formation from caustic injury
    C. Reflux esophagitis with secondary eosinophilic infiltration from GERD
    D. Candida esophagitis with ring formation from chronic fungal infection

    Explanation

    Why "Eosinophilic esophagitis with Th2-mediated immune response to food antigens" is right

    The clinical presentation—young adult male with atopy (asthma, atopic dermatitis), solid-food dysphagia, food bolus impaction, and PPI-refractory heartburn—combined with the pathognomonic endoscopic findings of concentric rings ("trachealization" or "feline esophagus"), longitudinal furrows, white plaques (eosinophilic microabscesses), pale mucosa, and decreased caliber, and the diagnostic histology of ≥15 eosinophils per high-power field with eosinophil microabscesses and basal zone hyperplasia, definitively establishes eosinophilic esophagitis (EoE). EoE is a chronic, immune/antigen-mediated esophageal disease driven by a Th2 immune response to food antigens (commonly milk, wheat, egg, soy, nuts, seafood), with strong association with atopy. The diagnosis requires both clinical symptoms of esophageal dysfunction and eosinophil-predominant inflammation on histology (≥15 eosinophils/hpf from ≥2 levels). [AGA/ACG EoE Guidelines 2024; UEG Joint EoE Guidelines 2024]

    Why each distractor is wrong

    • Reflux esophagitis with secondary eosinophilic infiltration from GERD: While PPI-refractory reflux can occur in EoE, reflux esophagitis alone does not produce the characteristic concentric rings, longitudinal furrows, and white plaques seen in EoE. Reflux esophagitis typically shows erythema, erosions, and ulceration, not the "trachealization" pattern. The ≥15 eosinophils/hpf is diagnostic of EoE, not secondary to GERD.
    • Candida esophagitis with ring formation from chronic fungal infection: Candida esophagitis presents with white plaques (pseudomembranes) and erythema, but does not produce concentric rings or longitudinal furrows. The histology would show fungal hyphae and pseudohyphae, not eosinophil microabscesses and basal zone hyperplasia. Candida is not associated with atopy or Th2-mediated immunity.
    • Pill esophagitis with stricture formation from caustic injury: Pill esophagitis (e.g., from doxycycline) causes focal ulceration and strictures at the site of contact, not diffuse concentric rings or longitudinal furrows. It is not associated with atopy, and histology would show acute inflammation and ulceration, not eosinophil-predominant infiltration with microabscesses.
    High-YieldNEET PG
    EoE is the diagnosis when you see concentric rings ("trachealization"), longitudinal furrows, white plaques, and ≥15 eosinophils/hpf in a young atopic patient with solid-food dysphagia and food bolus impaction—even if PPI-refractory heartburn is present.

    [AGA/ACG EoE Guidelines 2024; UEG Joint EoE Guidelines 2024]

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