OA07.2. Baseline Mucosal Impedance on High-Resolution Impedance Manometry Distinguishes Active From Inactive Eosinophilic Esophagitis

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Abstract Topic Benign Disease: Eosinophilic Esophagitis Background Active inflammation in eosinophilic esophagitis (EoE) disrupts the mucosal barrier, leading to dilated intercellular spaces and decreased transepithelial electrical resistance. Mucosal impedance (MI) has been used to assess mucosal integrity in EoE. We evaluated whether baseline MI measured by high-resolution impedance manometry (HRIM) distinguishes active and inactive EoE. Methods We retrospectively reviewed data from patients with EoE who underwent endoscopic esophageal biopsies within three months of HRIM from 2018-2026 at our tertiary referral center and had no treatment changes between studies. We excluded patients with a history of foregut surgery, erosive esophagitis, or Barrett’s esophagus. Demographics, endoscopy and pathology results were collected by chart review. Active EoE was histologically defined as ≥15 eosinophils per high-power field. Esophageal baseline MI was measured in the 30-second landmark period for the whole esophagus (from 2 cm above LES to 2 cm below UES), distal esophagus (from 2–7 cm above LES), and mid/proximal esophagus (from 10 cm above LES to 2 cm below UES). Mann–Whitney U or T tests were used for comparisons . Optimal MI thresholds were identified by Youden index with 10,000 bootstrap validations, and interrater reliability was assessed using two-way mixed effects intraclass correlation coefficients. Results Seventy-three patients were included: 37 (51%) female, median age 52 years, median BMI 27.2 kg/m2. Fifty-seven patients (78%) had atopic history, including seasonal allergies (38, 52%), asthma (31, 42%), eczema (21, 29%), and food allergies (19, 26%). Thirty-nine patients (53%) were receiving proton pump inhibitors, 25 (34%) were not on EoE therapy, 5 (6.8%) were on swallowed topical steroids, 3 (4.1%) were on dupilumab, and 1 (1.4%) was on an elimination diet. Esophageal strictures were present in 23 patients (32%), and 45 (62%) had active EoE. Baseline MI measurement showed high interrater reliability (n=50, 2 raters; intraclass correlation coefficient 0.937–0.963, p<0.001). Basal mean and minimal impedance were significantly lower in active EoE across all segments, greatest in the distal esophagus (all p<0.05; Figure 1). ROC analysis showed high discrimination of distal mean MI, with a cutoff ≤1.91 kΩ (AUC=0.837, sensitivity 67.9%, specificity 86.7%, Youden 0.545; Figure 2). Conclusion Baseline mucosal impedance during HRIM distinguishes active from inactive EoE, with strongest discrimination in the distal esophagus, supporting MI as a potential, minimally-invasive physiologic marker of mucosal inflammation and disease activity. Clinically, MI may serve as an adjunct tool in dysphagia evaluation, prompting EoE-directed biopsy when abnormal, aiding management in biopsy–symptom discordance, and potentially supporting disease monitoring in selected patients. Larger prospective studies are warranted.

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