Shifted TFPI/tissue factor balance drives paradoxically delayed thrombin initiation in active pediatric IBD

Introduction Inflammation–coagulation crosstalk in pediatric inflammatory bowel disease (IBD) promotes endothelial activation, tissue factor (TF) expression, and enhanced thrombin generation [ 1 ] [ 2 ]. Paradoxically, active disease shows prolonged thrombin generation lag time despite global hypercoagulability [ 3 ] [ 4 ]. We hypothesized that elevated tissue factor pathway inhibitor (TFPI), reflecting endothelial perturbation, modulates initiation-phase kinetics. We conducted a longitudinal study relating disease activity to plasma TFPI, TF activity (TFA), thrombin generation under TFPI-sensitive conditions, and endothelial/inflammatory biomarkers. Method Newly diagnosed pediatric IBD patients (ages 7–18 years; ulcerative colitis [UC] n=8, Crohn's disease [CD] n=8 per ECCO/ESPGHAN criteria) were recruited prospectively. Blood was sampled at disease onset and remission (PUCAI/PCDAI