Abstract OBJECTIVE: To observe changes in plasma motilin (MOT) level among preterm infants after birth, to investigate the relationship between plasma motilin level and feeding intolerance (FI), and to clarify the possible risk factors. METHODS: A total of 112 preterm infants were divided into feeding tolerance (FT) group (n=59) and FI group (n=53). Their plasma MOT levels were measured by radioimmunoassay on days 1, 4, 7 and 14 of life. The clinical data of FI group were collected and subjected to multivariate logistic regression analysis. RESULTS: Compared with the FT group, the FI group showed significantly lower plasma MOT levels on days 1, 4, 7 and 14 of life (P<0.05), and there was a positive correlation between plasma MOT level and gestational age, age in days, and volume of enteral feeding in the FI group. The lower the gestational age, the longer the FI duration. There was a negative correlation between the plasma MOT level on day 1 of life and the FI duration (r=-0.913, P<0.001). Gestational age and prenatal use of glucocorticoid were protective factors for FI, while fetal distress, placental abnormality and perinatal infection were risk factors for FI. CONCLUSIONS: Change in plasma MOT level may be closely related to the development of FI in preterm infants. Early monitoring of plasma MOT level may be useful for predicting the occurrence of FI.
［1］Guglielmi FW, Regano N, Mazzuoli S, Fregnan S, Leogrande G, Gulielmi A, et al. Cholestasis induced by total parenteral nutrition［J］. Clin Liver Dis, 2008, 12(1):97-110.
［3］A.S.P.E.N. Board of Directors and the clinical guidelines task force. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients［J］. JPEN J Parenter Enteral Nutr, 2002, 26(Suppl): 38SA-41SA.
［4］Chen CY, Chen HL. The risk factors of parenteral nutrition-associated cholestasis in preterm infants［J］. Pediatr Neonatal, 2009, 50(5):181-183.
［5］Willis TC, Carter BA, Rogers SP, Hawthorne KM, Hicks PD, Abrams SA. High rates of mortality and morbidity occur in infants with parenteral nutrition-associated cholestasis ［J］. JPEN J Parenter Enteral Nutr, 2010, 34(1): 32-37.
［8］Hsieh MH, Pai W, Tseng HI, Yang SN, Lu CC, Chen HL. Parenteral nutrition-associated cholestasis in premature babies: risk factors and predictors［J］. Pediatr Neonatol, 2009, 50(5):202-207.
［9］Robinson DT, Ehrenkranz RA. Parenteral nutrition-associated cholestasis in small for gestational age infants［J］. J Pediatr, 2008, 152(1):59-62.
［10］Costa S, Maggio L, Sindico P, Cota F, De Carolis MP, Romagnoli C. Preterm small for gestational age infants are not at high risk for parenteral nutrition-associated cholestasis［J］. J Pediatr, 2010, 156(4): 575-579.
［11］Fuchs M, Sanyal AJ. Sepsis and cholestasis［J］. Clin Liver Dis, 2008, 12(1):151-172.
［12］Shin JI, Namgung R, Park MS, Lee C. Could lipid infusion be a risk for parenteral nutrition-associated cholestasis in low birth weight neonates?［J］. Eur J Pediatr, 2008, 167(2):197-202.
［13］Fallon EM, Le HD, Puder M. Prevention of parenteral nutrition-associated liver disease: role of omega-3 fish oil ［J］. Curr opin organ transplant, 2010, 15(3):334-340.
［14］Klein CJ, Ravenis M, Kusenda C, Scavo L. Parenteral nutrition-associated conjugated hyperbilirubinemia in hospitalized infants［J］. J Am Diet Assoc, 2010, 110(11):1684-1695.
［15］Kumpf VJ. Parenteral nutritionassociated liver disease in adult and pediatric patients［J］. Nutr Clin Pract, 2006, 21(3):279-290.
