What Is New
GI dysmotility, critically ill, dysmotility
CRITICAL ILLNESS, CRITICALLY ILL, DYSMOTILITY
Cholecystokinin (CCK, dysmotility) and intestinal fatty acid-binding protein 2 (I-FABP2, damage to enterocytes) concentrations decreased during pediatric intensive care unit stay, whereas glucagon (dysmotility) concentrations increased, and leptin (dysmotility) and citrulline (enterocyte function) concentrations remained stable.The course of CCK, leptin, glucagon, I-FABP2, and citrulline concentrations were not associated with the enteral nutrition intake as a percentage of predicted resting energy expenditure as a proxy of FI.Predicting the patients’ tolerance to enteral nutrition (EN) would help clinicians optimize individual nutritional intake and potentially clinical outcomes (So far, results of studies examining the usefulness of biomarkers in the prediction of FI in critically ill patients have been conflicting (Cholecystokinin (CCK) and peptide-YY (PYY) are both gut hormones and markers for GI dysmotility, as they both inhibit GI motility and delay gastric emptying (We hypothesized that CCK, PYY, leptin, glucagon, I-FABP2 and citrulline might be useful in predicting EN advancement (ENA) and FI symptoms (FIS) in critically ill children. This study aimed to investigate the course of these GI biomarkers and their association with ENA longitudinally in the first 5 days of pediatric critical illness.