Clinical manifestations of nutritional copper deficiency in infants and children.
A series of reports in the 1960s highlighted nutritional copper deficiencies in infants and children recovering from malnutrition in Peru; since that time, a cascade of additional cases in premature infants, in patients receiving total parenteral nutrition, and in those receiving special diets or unmodified cow milk have been reported. The identification by Danks that Menkes syndrome, a genetically determined defect in copper absorption and utilization, is responsible for the observed clinical manifestations provided further insight into the physiopathologic effects of copper deficiency. New information on the metabolism and physiologic role of copper, plus the identification of additional copper metalloenzymes and improvement in how to determine copper status, has fueled interpretation and speculation on how and why the classic signs of copper deficiency occur, as well as on the possible effects of mild deficiencies. Also under scrutiny are potential interactions between other elements and the effects of other elements, even when given in acceptable amounts, on copper status. There should be no constraints in thinking on other possible effects of impaired copper status in humans. I review some of the history of nutritional copper deficiency in infants and children and attempt to interpret some of the clinical manifestations in light of newly acquired information.
Cordano
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Scientific Advisory Board of the Nutritional Research Institute, Lima, Peru.
D000818:Animals; D015362:Child Nutrition Disorders / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D003300:Copper / Q000172:deficiency* / Q000502:physiology / Q000627:therapeutic use; D003677:Deficiency Diseases / Q000209:etiology / Q000503:physiopathology; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D007235:Infant, Premature, Diseases / Q000209:etiology / Q000503:physiopathology
D003300:Copper