Serum Copper is Decreased in Premature Newborns and Increased in Newborns with Hemolytic Jaundice (Technical Briefs‪)‬

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 (6-8). 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).