Urinary copper losses in infants receiving free amino acid solutions
Open Access
- 1 March 1982
- journal article
- research article
- Published by Elsevier in The American Journal of Clinical Nutrition
- Vol. 35 (3) , 542-545
- https://doi.org/10.1093/ajcn/35.3.542
Abstract
Plasma amino acids and the 24-h urinary excretion of copper and amino acids were measured in 18 infants receiving 0.4 g N/kg/day as free amino acids as part of a total parenteral nutrition regimen. Urinary copper excretion correlated positively with total excretion of α-amino nitrogen, in general, and the excretion of glycine, methionine, histidine, and lysine, in particular. Infants who received FreAmine II as compared to FreAmine III generally had increased plasma concentrations of glycine and methionine and increased urinary excretion of total α-amino nitrogen, glycine, methionine, and of copper. Chronic losses of copper in the urine of infants receiving free amino acid solutions may contribute to copper depletion and the development of a copper deficiency syndrome.This publication has 11 references indexed in Scilit:
- 650 SERUM COPPER AND CERULOPLASMIN IN THE PREMATURE INFANTPediatric Research, 1981
- Serum copper concentrations in sick and well preterm infantsThe Journal of Pediatrics, 1980
- A controlled trial of glucose versus glucose and amino acids in premature infantsThe Journal of Pediatrics, 1979
- Effect of diet on plasma aminograms of low birth weight infantsThe American Journal of Clinical Nutrition, 1977
- Changes in total, nondiffusible, and diffusibleplasma zinc and copper during infancyThe Journal of Pediatrics, 1973
- Copper deficiency in long-term parenteral nutritionThe Journal of Pediatrics, 1972
- The State of Copper in Human Serum: Evidence for an Amino Acid-bound Fraction *Journal of Clinical Investigation, 1967
- COPPER DEFICIENCY IN INFANCYPediatrics, 1964
- A modified procedure for the automatic analysis of amino acidsAnalytical Biochemistry, 1960
- Localization of Cu64 in Serum Fractions Following Oral Administration: An Alteration in Wilson's DiseaseExperimental Biology and Medicine, 1954