The Overlooked Burden of Atopic Comorbidities in Eosinophilic Esophagitis: Insights from a Real-Life Comprehensive...

Background/Objectives: Eosinophilic esophagitis (EoE) is a T2-mediated disease characterized by dysphagia and food impaction. It is often associated with other atopic disorders and is considered a late manifestation of the "atopic march". In clinical practice, allergic comorbidities are frequently underdiagnosed and primarily based on self-reporting, potentially underestimating the true burden of T2-related pathology. To address this, a multidisciplinary task force was established at our tertiary center to systematically evaluate newly diagnosed patients with EoE. Methods: This cross-sectional observational study included patients referred for EoE evaluation from January 2022. Clinical history was collected prospectively, with systematic assessment for T2 comorbidities. All patients underwent an esophagogastroduodenoscopy with esophageal biopsies. Following EoE diagnosis, patients were referred to dermatology, ENT, immunology, and respiratory specialists. Results: A total of 43 patients were enrolled. Anamnestic T2 comorbidities were reported by 88% of patients. Rhinitis was the most common, while at baseline, no patients reported chronic rhinosinusitis with nasal polyps (CRSwNP). After specialist evaluation, diagnoses of asthma, food allergy, and atopic dermatitis remained stable, while eight patients previously reporting rhinitis were newly diagnosed with CRSwNP. Overall, 65% of patients had ≥2 T2 comorbidities in addition to EoE, and 25% had ≥3. Conclusions: Our findings support a multidisciplinary approach to assess T2 comorbidities in patients with EoE, with a high overall prevalence (95.3%) and frequent coexistence of multiple atopic conditions. CRSwNP was frequently underdiagnosed and only identified after rhinofibroscopy. Although our data needs to be confirmed in larger multicenter studies, our results suggest that relying solely on patient-reported history or single-specialty evaluation risks underestimating the systemic nature of the T2 inflammatory pathway in EoE.