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Updated: Jan 12, 2026

Author Spotlight: Investigating the Pathophysiology of Eosinophilic Esophagitis
Published on: May 10, 2024
The Role of Eosinophilic Cationic Protein in Inflammatory Bowel Disease
Paul Grama1,2,3, Tamás Ilyés4, Naomi A Ciurea1,2
11st Internal Medicine Department, George Emil Palade University of Medicine, Pharmacy, Science and Technology of Târgu Mureș, Târgu Mureș, ROU.
Abstract:
Introduction Eosinophils contribute to inflammatory bowel disease (IBD) pathogenesis by infiltrating the intestinal mucosa and releasing pro-inflammatory mediators, including eosinophilic cationic protein (ECP). Although biomarkers like C-reactive protein and fecal calprotectin commonly assess IBD activity, the clinical utility of eosinophil-derived markers like ECP is unclear. Our aims were to compare serum ECP across ulcerative colitis (UC), Crohn's disease, and healthy controls, with the prespecified primary contrast UC vs. controls. Our secondary objectives were to examine associations between ECP and disease activity (CDAI, MAYO scores) and quality of life, and explanatory objectives were to assess correlations with white blood cells and neutrophil and eosinophil counts and explore UC-control discrimination. Methods We conducted an observational study including 50 IBD patients (20 Crohn's disease patients, 30 UC patients) and 32 healthy controls. Clinical data recorded included disease duration, Crohn's Disease Activity Index (CDAI), Mayo score for UC, and quality of life (IBDQ questionnaire). Serum ECP (enzyme immunoassay), eosinophil counts, and routine blood tests were measured. Statistical analysis employed Kruskal-Wallis with Dunn's post-hoc tests, Mann-Whitney U tests, and Spearman's correlation. Ethical approval and informed consent were obtained. Results Median serum ECP differed significantly among controls, Crohn's, and UC patients (16,807 (13,007-24,314) pg/mL vs 18,496 (12,261-28,231) vs 24,224 (17,335-32,997); p=0.03). UC patients had significantly higher ECP than controls (p=0.008), while the increase in Crohn's disease was not significant (p=0.418). ECP was higher in UC compared to Crohn's disease, though this difference did not reach statistical significance (p=0.128). No significant differences emerged between Crohn's disease and UC in total leukocyte count, eosinophil count, disease duration, or Inflammatory Bowel Disease Questionnaire (IBDQ) scores (all p>0.1). Serum ECP positively correlated with total leukocyte (r=0.279, p=0.049) and neutrophil counts (r=0.298, p=0.036) across IBD patients. No significant correlations existed between ECP and patient age, disease duration, CDAI, Mayo score, IBDQ, or eosinophil count (all p>0.1). Conclusion In this cross-sectional cohort, serum ECP was higher in UC vs controls and showed only modest associations with leukocytosis, while not tracking CDAI, partial Mayo, or IBDQ. These findings are hypothesis-generating and consistent with eosinophil involvement; they do not demonstrate mechanism or clinical utility and require prospective validation.
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