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Technical Briefs |
1 Institute of Child Health and2 Department of Clinical Biochemistry, "Aghia Sophia" Childrens Hospital, Athens, Greece;3 Neonatology Department, "Alexandra" Maternity Hospital, Athens, Greece;4 First Department of Pediatrics, Athens University, Athens, Greece
aaddress correspondence to this author at: Department of Clinical Biochemistry, "Aghia Sophia" Childrens Hospital, 115 27 Athens, Greece; fax 30-210-7467171, e-mail biochem@paidon-agiasofia.gr or jpapasotiriou@ath.forthnet.gr
| The first 300 words of the full text of this article appear below. |
Copper is an active component of several enzyme systems, including cytochrome c oxidase and superoxide dismutase (1), and is essential for the prevention of anemia and leucopenia. It is important for the maturation of collagen and the maintenance of skeletal and vascular integrity because of its involvement in the lysyl oxidase enzyme system (2). Deficiency of copper is associated with an increased incidence of infection, as seen in patients with Menke kinky-hair disease, an inherited disease with low copper concentrations (3). The mechanism by which high copper concentrations interact with genetic control systems, leading to liver damage, is still unknown (4). The normal term infant is born with a generous liver copper store, and copper deficiency in neonates is a rare event (5). Copper deficiency has been associated with anemia, neutropenia, and bone demineralization in both preterm and full-term infants (6)(7)(8).
Ceruloplasmin, the major serum copper-transporting protein, is synthesized in the liver, but its precise role in copper metabolism is unclear. Neonatal hepatic ceruloplasmin synthesis occurs after birth and is associated with a gradual increase in plasma concentrations (9).
We report the concentrations of copper in healthy and jaundiced full-term and premature infants and their correlations with hemoglobin, bilirubin, and liver enzymes.
The study was approved by the Greek Ethical Committee, and parental consent was obtained. The study comprised 303 neonates (full-term and premature). Newborns with obstructive jaundice or with infections or inflammatory process were excluded. All patients underwent routine laboratory tests to determine the etiology of their jaundice (see Table 1 in the Data Supplement that accompanies the online version of this Technical Brief at http://www.clinchem.org/content/vol50/issue7/) (10)(11). Patients were divided into the following groups (Table 1
Newborns with hemolytic jaundice (n = 179).
Newborns with nonhemolytic jaundice (n = 124).
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