Role of intestinal fatty acid binding protein in the non-invasive diagnosis of celiac disease in children
Role of intestinal fatty acid binding protein in the non-invasive diagnosis of celiac disease in children

Role of intestinal fatty acid binding protein in the non-invasive diagnosis of celiac disease in children

Indian J Gastroenterol. 2025 Jul 9. doi: 10.1007/s12664-025-01796-2. Online ahead of print.

ABSTRACT

OBJECTIVES: Intestinal fatty acid binding protein (IFABP) is a marker of intestinal epithelial injury and has been studied as a surrogate for predicting villous atrophy. The aim of this study was to evaluate the utility of IFABP in the non-invasive diagnosis of celiac disease (CeD) in children.

METHODS: Symptomatic children with positive anti-tissue transglutaminase antibody underwent a duodenal biopsy and IFABP measurement. Controls were included who had both tissue transglutaminase antibody (tTG) and IFABP measured. We evaluated the performance of IFABP in the diagnosis of CeD by generating the receiver operating characteristic (ROC) curve.

RESULTS: Total 123 children were screened; 98 had a positive anti-tTG, 74 patients aged 8.5 ± 4.0 years were diagnosed to have CeD and 24 patients had a normal biopsy. Seventy-six children aged 8.4 ± 4.0 years were enrolled as controls. Serum IFABP was significantly higher in children with CeD; median 918 pg/mL (interquartile range [IQR] = 630-1316) as compared to controls; median 386 pg/mL (IQR = 125-581) (p < 0.001). We observed increasing serum IFABP levels with a higher Marsh grade of mucosal injury (p < 0.001). Sensitivity and specificity for diagnosis of CD were 51% and 88% at serum IFABP level > 920 pg/mL and area under the curve (AUC) of 0.79 (0.67-0.90). In children with CD and a tTG 1-10 of normal, this cut-off could make a diagnosis without biopsy in 28/34 cases.

CONCLUSION: Serum IFABP can improve the non-invasive diagnosis of CeD in children with elevated tTG-IgA titers in a subset of patients and also has good correlation with the degree of villous atrophy.

PMID:40632482 | DOI:10.1007/s12664-025-01796-2