P275 New non-invasive biomarkers of intestinal inflammation in pediatric inflammatory bowel diseases and their correlation with fecal calprotectin – pilot study.
Szymanska, E.(1);Bierla, J.(2);Wierzbicka, A.(3);Dadalski, M.(4);Konopka, E.(5);Cukrowska, B.(5);Kierkus, J.(6);
(1)Children's Memorial Health Institute, Department of Gastroenterology- Hepatology- Feeding Disorders and Pediatrics, Warsaw, Poland;(2)Children's Memorial Health Institute- Warsaw- Poland., 2. Department of Patomorphology-, Warsaw, Poland;(3)The Children’s Memorial Health Institute- Warsaw- Poland, Department of Biochemistry and Experimental Medicine, Warsaw, Poland;(4)The Children's Memorial Health Institute- Warsaw- Poland., Department of Gastroenterology- Hepatology- Feeding Disorders and Pediatrics, Warsaw, Poland;(5)The Children’s Memorial Health Institute- Warsaw- Poland, Department of Patomorphology, Warsaw, Poland;(6)The Children’s Memorial Health Institute- Warsaw- Poland, Department of Gastroenterology- Hepatology- Feeding Disorders and Pediatrics, Warsaw, Poland;
Current data indicates that increased intestinal permeability leading to intestinal damage plays a key role in the pathogenesis of inflammatory bowel diseases (IBD) and correlates with disease flare. Therefore, recently, the role of non-invasive biomarkers in both diagnosis and monitoring IBD is emphasized.
Zonulin is the protein that increases permeability in the epithelial layer of the small intestine by reversibly modulating the intercellular tight junctions.
Fatty acid binding proteins (FABPs) are intracellular proteins expressed in several tissues including intestine. Intestinal FABP (I-FABP) is a plasma and urine marker of intestinal damage.
The aim of this study was to investigate fecal and serum zonulin and I-FABP in pediatric IBD patients and theircorrelation with fecal calprotectin (FCP).
Seventy-one individuals: 32 Crohn’s disease (CD) patients, 33 ulcerative colitis (UC) patients and 6 controls were examined for fecal and serum zonulin and plasma I-FABP. Values were correlated to FCP and to each other for all children included in the study. A stool specimen and blood samples were collected during check-up visit at hospital. Then fecal and serum zonulin, I-FABP and FCP were tested by ELISA test. Non-parametric statistical tests were used for data analysis.
The level of fecal zonulin and FCP were higher in IBD patients compared to control group (CG): median for CD – 113.6(53.6-150) ng/mL, 46 (7-551) ug/g; UC – 115.3 (50.7-150.4) ng/mL, 40 (16.0-251.2) ug/g; CG – 60.8 (31.8-81.2) ng/mL, 41.5 (31.0-97.7) ug/g, respectively, (P<0.05). No statistically significant difference in concentrations of serum zonulin and I-FABP was reported between patients and CG (P=0.55). The only correlation that has been reported was between fecal zonulin and FCP and the strongest one was in CD: CD – R = 0.73, UC – R = 0.67, All – R=0.67, CG – R=0.65.
Accordnig to our results it seems that only fecal zonulin may serve as another, next to FCP, biomarker of intestinal damage in IBD. However, both fecal and serum zonulin as well as I-FABP need further studies to assess their usefulness in diagnostics and monitoring in IBD.