USE OF CHOLECYSTOKININ TO PREVENT THE DEVELOPMENT OF PARENTERAL NUTRITION-ASSOCIATED CHOLESTASIS

Background: Neonates are at high risk for the development of parentera l nutrition-associated cholestasis when receiving a prolonged course o f total parenteral nutrition (TPN). Although this cholestasis is of un known etiology, it may result from a lack of gastrointestinal hormone formation, including cholecystokinin, which normally occurs after ente ral feedings. Methods: Two groups of neonates were studied. The treatm ent group consisted of 21 consecutive, prospectively enlisted neonates receiving TPN for >14 days. The nontreatment group consisted of 21 in fants from the 2 years preceding the study who were matched to the tre atment group by gestational age, diagnosis, and duration of TPN. The m ajor outcome determinant was direct bilirubin. Cholestasis was defined as a direct bilirubin >2.0 mg/dL and was considered severe if the dir ect bilirubin was >5.0 mg/dL after other causes were ruled out. Result s: The mean direct bilirubin levels in the nontreated group progressiv ely rose over time, whereas the mean direct bilirubin in the treated g roup remained level. The incidence of infants with a direct bilirubin >2.0 mg/dL was 24% and 43% in the CCK+ and CCK- groups, respectively, and was not significant (p = .14). The percentage of infants with a di rect bilirubin >5.0 mg/dL was 9.5% and 38% in the treatment and nontre atment groups, respectively, and was significant, p = .015. Conclusion s: Levels of direct bilirubin were lower in the treated compared with the nontreated group. These findings suggest that cholecystokinin prop hylaxis in high-risk neonates may help prevent the development of pare nteral nutrition-associated cholestasis.