Use of Cholecystokinin to Prevent the Development of Parenteral Nutrition-Associated Cholestasis

Abstract

Background: Neonates are at high risk for the development of parenteral nutrition-associated cholestasis when receiving a prolonged course of total parenteral nutrition (TPN). Although this cholestasis is of unknown etiology, it may result from a lack of gastrointestinal hormone formation, including cholecystokinin, which normally occurs after enteral feedings. Methods: Two groups of neonates were studied. The treatment group consisted of 21 consecutive, prospectively enlisted neonates receiving TPN for > 14 days. The nontreatment group consisted of 21 infants from the 2 years preceding the study who were matched to the treatment group by gestational age, diagnosis, and duration of TPN. The major outcome determinant was direct bilirubin. Cholestasis was defined as a direct bilirubin >2.0 mg/dL and was considered severe if the direct bilirubin was >5.0 mg/dL after other causes were ruled out. Results: The mean direct bilirubin levels in the nontreated group progressively rose over time, whereas the mean direct bilirubin in the treated group 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 direct bilirubin >5.0 mg/dL was 9.5% and 38% in the treatment and nontreatment groups, respectively, and was significant, p = .015. Conclusions: Levels of direct bilirubin were lower in the treated compared with the nontreated group. These findings suggest that cholecystokinin prophylaxis in high-risk neonates may help prevent the development of parenteral nutrition-associated cholestasis. (journal of Parenteral and Enteral Nutrition 21:100-103, 1997)