302 - Fecal Eosinophil-Derived Neurotoxin (EDN) as a Diagnostic and Disease Progression Marker in Eosinophilic Gastrointestinal Diseases

Publication Number: 2292.302

Yuichi Taniyama, Department of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Suzu, Ishikawa, Japan; Masaaki Usami, Department of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa city, Ishikawa, Japan; Hanae Miyazawa, Department of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan., Kanazawa, Ishikawa, Japan; Yusuke Matsuda, Kanazawa University, Kanazawa, Ishikawa, Japan; Tetsujiro Shirahashi, Department of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan., Kanazawa, Ishikawa, Japan; Tomoko Toma, Department of Pediatrics, Kanazawa University, Kanazawa, Ishikawa, Japan; Taizo Wada, Kanazawa University, Kanazawa, Ishikawa, Japan

Background: Eosinophilic gastrointestinal disease (EGID) is caused by eosinophilic inflammation of the gastrointestinal tract, leading to chronic digestive symptoms, protein leakage, and growth disorders. It occurs across a wide age range, including infants. While gastrointestinal endoscopy is necessary for diagnosis and disease assessment, it can be highly invasive and challenging in pediatric patients. Eosinophil-derived neurotoxin (EDN), an eosinophil degranulation protein, is known as an indicator reflecting eosinophilic inflammation.

Objective: We investigated whether fecal EDN is helpful for diagnosing EGID and assessing disease activity.

Design/Methods: We analyzed 6 pediatric cases of EGID diagnosed at our hospital between 2012 and 2024 (age at diagnosis: 12 months to 8 years, median age 3.5 years) . All 6 cases primarily involved gastroenteritis, while 3 cases also had lesions in the esophagus. We compared pre-treatment fecal EDN levels in EGID patients with those in 12 healthy controls, 5 cases of ulcerative colitis in the active phase, and 7 cases of Crohn's disease in the active phases. In addition, a total of 703 fecal EDN samples obtained during the clinical course of EGID were analyzed to assess whether EDN levels significantly correlated with the EGID activity score described in the Japanese clinical practice guidelines for EGID.

Results: Fecal EDN levels prior to EGID treatment initiation (median 579,500 [IQR 172,563-1,290,000] ng/mL) were markedly elevated compared to healthy controls (median 880 [IQR 557.5-1,650] ng/mL). Compared to ulcerative colitis (median 5,500 [IQR 2,425-82,500] ng/mL) and Crohn's disease (median 8,630 [IQR 5,128-25,900] ng/mL), EDN levels were also significantly higher in EGID (Figure 1). Correlation analysis between fecal EDN levels obtained during the course of EGID treatment and disease activity scores revealed a significant positive correlation with a Spearman rank correlation coefficient ρ = 0.411 (p < 0.0001) .

Conclusion(s): Fecal EDN levels were significantly elevated in EGID patients compared with healthy controls and other gastrointestinal diseases, and showed progression consistent with disease activity. Fecal EDN may serve as a useful noninvasive biomarker for diagnosis and disease monitoring in pediatric EGID, in which frequent endoscopic examinations are difficult.

Figure 1
Comparison of Fecal EDN Levels Between pre-treatment EGID Patients, Healthy Controls, and Other Gastrointestinal Diseases