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Research Article: Urinary fatty acid binding protein 2 as a biomarker of intestinal injury in pediatric celiac disease

Date Published: 2026-06-10

Abstract:
Celiac disease (CeD) is an autoimmune enteropathy triggered by gluten in genetically predisposed individuals, causing intestinal damage and impaired gut barrier integrity. Current diagnostic methods, such as serology and intestinal biopsy, are costly and invasive. Intestinal fatty acid binding protein (FABP2), exclusively expressed in the cytosol of mature enterocytes and released during injury, offers a potential non-invasive alternative biomarker. This study aimed to evaluate urinary FABP2 levels in pediatric patients undergoing gastrointestinal assessment or CeD follow-up to determine its potential as a non-invasive biomarker of intestinal integrity. In this retrospective cross-sectional study, urinary FABP2 was measured in 103 pediatric patients evaluated for intestinal permeability using the lactulose/mannitol test. Based on serology and symptomatology, patients were categorized as controls ( n =?65), CeD on gluten-free diet (GFD)?>?6 months ( n =?26), or active CeD ( n =?12). Associations between FABP2 levels, serology, symptoms, and diagnosis were analyzed. FABP2 levels were significantly elevated in active CeD patients (47.7?pg/mL) compared with controls (9.65?pg/mL) ( p <?0.05), but not in CeD patients on GFD (15.0?pg/mL). A receiver operating characteristic curve analysis confirmed the diagnostic potential of FABP2 as a biomarker for celiac disease (area under the curve?=?0.7269; cutoff?=?23.7?pg/mL; sensitivity?=?66.7%, specificity?=?76.9%). Our findings indicate that urinary FABP2 reflects intestinal epithelial injury and may serve as a non-invasive biomarker for assessing gut integrity and disease activity in CeD. However, larger prospective studies with histological correlation are needed to validate its diagnostic utility.

Introduction:
Celiac disease (CeD) is an immune-mediated enteropathy triggered by the ingestion of gluten in genetically susceptible individuals, with a prevalence of ?1% of the global population ( 1 , 2 ). Key, well-defined contributors to CeD pathogenesis include genetic factors HLA DQ 2 and HLA DQ8, an environmental trigger (gluten prolamines), and the involvement of autoantigens, in particular tissue transglutaminase 2 IgA (tTG-IgA 2) ( 3 ). The intestinal epithelium comprises several different cell types, such as…

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