Eosinophilic Esophagitis-Catching Up with the Hype Train: A Systematic Overview and Review of the Literature of the Emerging Disease

Abstract

Background: Eosinophilic esophagitis (EoE) is a chronic, immune-mediated esophageal disorder characterized by Th2-driven inflammation. Clinically, it manifests as esophageal dysfunction, including dysphagia and food impaction, and is frequently associated with atopic comorbidities. Methods: Diagnosis is established via histologic confirmation of ≥15 eosinophils per high-power field (hpf) on esophageal biopsy. Clinical presentation varies, ranging from subtle dysphagia to severe complications necessitating urgent endoscopic intervention. Results: Disease progression is characterized by esophageal remodeling, encompassing fibrosis, angiogenesis, and muscular hypertrophy. Management strategies require individualized, long-term approaches aimed at symptom control and prevention of structural complications. Discussion: Advances in the last decade have refined diagnostic criteria, standardized endoscopic scoring systems, and introduced novel therapeutic agents, including biologics. This review synthesizes current evidence regarding epidemiology, clinical manifestations, diagnostics, and therapeutic strategies.

Keywords: eosinophils; esophagus; inflammation; mucosa.

Figure 1

Endoscopic findings in patients with EoE: (a) Partial and soft mucosal edema. (b) Concentric rings and strictures of moderate severity. (c) Severe strictures with scattered whitish exudates localized within or adjacent to the narrowed areas and (d) Diffuse whitish exudates broadly covering most of the esophageal surface.

Figure 2

Histology from the esophagus of a patient with EoE stained with H&E. Figure 2 demonstrates the tissue before treatment with PPI, showing infiltration of numerous eosinophils in the mucosa (white arrows) with the formation of eosinophilis micro-abscess (black arrow) at 40x magnification.

Figure 3

Histology from the esophagus of a patient with EoE stained with H&E. Figure 3 demonstrates the same tissue after 12 weeks of PPI treatment, where there is no presence of eosinophils or any other histologic characteristic of an active disease.