Use of cholecystokinin to prevent the development of parenteral nutrition-associated cholestasis

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.

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.

The mean direct bilirubin levels in the nontreated group progressively rose over time, whereas the mean direct bilirubin 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.

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.