Background and Objectives: Conventional practice is to reduce or eliminate copper (Cu) supplementation in the parenteral nutrition of infants with cholestasis because of the increased risk of hepatotoxicity. However, there are reports of Cu deficiency in cholestatic infants because of Cu reduction in their parenteral nutrition. The objectives of the present study are to determine the proportion of cholestatic infants who develop elevated serum Cu while receiving a nonreduced dose of parenteral Cu, to evaluate potential clinical factors that affect serum Cu in cholestatic infants, and to evaluate the impact of serum Cu on liver disease.
Patients and Methods: This is a retrospective review of 28 cholestatic infants receiving 20 μg · kg−1 · day−1 of Cu via parenteral nutrition. Age-adjusted references were used to determine normality of serum Cu levels. Multiple linear regression analyses were performed to determine predictors of serum Cu and alanine aminotransferase (ALT).
Results: Serum Cu levels were elevated in 2 infants (7%). On average, infants received 80% of their energy intake from parenteral nutrition for 3 months. Intestinal failure was present in 50% of the patients. Birth weight, gestational age, and ALT were identified as predictors of serum Cu (R2 = 0.53; P = 0.0001). Serum Cu, gestational age, and total bilirubin were associated with serum ALT (R2 = 0.43; P = 0.001).
Conclusions: Supplementation of parenteral Cu at 20 μg · kg−1 · day−1 does not lead to a significant increase in Cu toxicity or worsening of liver disease in cholestatic infants.
*Department of Pediatrics, Emory University School of Medicine, Atlanta, USA
†Department of Pharmacy and Clinical Nutrition, Children's Healthcare of Atlanta, GA, USA
‡Department of Pediatrics, University of Arkansas for Medical Sciences and Arkansas Children's Hospital, Little Rock, AR, USA.
Received 18 August, 2008
Accepted 31 August, 2009
Address correspondence and reprint requests to Juliana Frem, MD, Assistant Professor, University of Arkansas for Medical Sciences, Department of Pediatrics, Gastroenterology, Hepatology, and Nutrition, Arkansas Children's Hospital, 800 Marshall St, #512-7, Little Rock, AR 72202 (e-mail: firstname.lastname@example.org).
This work was sponsored by the Gerber Foundation (J.F. and C.R.C.) and the National Institutes of Health grant 5K12RR017643 and 1KL2RR025009 (C.R.C.).
The authors report no conflicts of interest.