P083 Intestinal fatty acid binding protein as a biomarker of intestinal damage in children with coeliac and Crohn’s disease
C. M. Clark*1, A. Kountouri1, M. MacKinder1, R. Hansen2, R. K. Russell2, K. Gerasimidis1
1University of Glasgow, Human Nutrition, School of Medicine, Glasgow, United Kingdom, 2Royal Hospital for Children, Department of Paediatric Gastroenterology, Glasgow, United Kingdom
There is need to develop new markers of gut inflammation and mucosal damage. Intestinal fatty acid–binding protein 2 (i-FABP) is an abundant cytosolic protein found in epithelial cells of the small intestine and proximal colon. Evidence suggests it as a potential biomarker of intestinal damage.
In this prospective study, we aimed to determine whether serum and urine i-FABP levels are a useful marker for intestinal damage in children with Crohn’s disease and coeliac disease.
i-FABP was measured in urine and plasma using the Human FABP2/i-FABP Quantikine ELISA Kit from 23 children with Crohn’s and 12 children with Coeliac disease. Samples were analysed before and after treatment with exclusive enteral nutrition (EEN) (n = 5) and gluten-free diet (n = 12), respectively, and compared with healthy controls (urine n = 9 and plasma n = 24). Urine samples from all patients were corrected for creatinine. Results were compared with redundant blood samples of children with acute benign conditions.
A significantly higher median concentration of plasma i-FABP was found in children with Coeliac disease at diagnosis (2014 ± 1992, IQR: 963.5 pg/ml) compared with healthy controls (1014.0 ± 450.4, IQR: 540.3 pg/ml) (p = 0.001). Compared with diagnosis, plasma i-FABP significantly decreased after 6 months (1 238 ± 542, IQR: 665.3 pg/ml) (p = 0.009) but not at 12 months treatment on gluten-free diet (1 733 ± 750, IQR: 1 288.0 pg/ml). There was no significant difference with healthy controls in plasma i-FABP after 6 months on gluten-free diet, but there was a significant difference with healthy controls after 12 months of gluten-free diet.
In children with Crohn’s disease, plasma and urinary i-FABP did not differ from healthy controls before or after treatment with EEN.
For Crohn’s and Coeliac disease, no significant differences in i-FABP were found between groups or during treatment in urine samples.
Plasma but not urinary i-FABP might have potential use as a biomarker of improvement of small bowel damage, and adherence on gluten-free diet in children with coeliac disease. This does not seem to be the case in the small sample of Crohn’s disease children we studied. This finding can be explained by the nature of the diseases and the distribution of i-FABP in the intestine. i-FABP is found in decreasing amounts in the jejunum, duodenum, ileum, and colon (4.8, 2.2, 1.0, and 0.3 μg/g-ww, respectively); and i-FABP is expressed in the top cells of the villi, the site of atrophy in coeliac disease. This may make it a reliable marker of coeliac disease activity, especially in the initial stages of the disease, as the villi are the first to be affected.