Abstract
The effects of the oral administration of copper were studied in 1. infants with nutritionally induced cooper deficiency; 2. children receiving copper sulfate as an emetic after toxic ingestions. 1. Seven marasmic infants were rehabilitated with a high calorie-adequate protein-low copper diet. In 2 of them where initial determinations were performed, serum ceruloplasmin concentration was normal. With recovery and rapid growth, copper deficiency developed, and all 7 exhibited hypoceruloplasminemia. The intact metalloprotein was deficient both by oxidase and immunochemical assays. Apoceruloplasmin could not be detected immunochemically. Thus both the copper prosthetic group and the apoprotein were deficient. In each of the 7, ceruloplasmin levels rose after the administration of copper, 0.10–0.30 mg/kg/day. 2. Copper sulfate, 250 mg, was administered orally as an emetic to 4 children after toxic ingestions. Although vomiting occurred within 5 minutes, a rise of serum copper of 14, 22, 30 and 71 μg% was observed. Serum ceruloplaxmin concentration increased significantly in 3 of the children within 12 hours. Thus it appears that copper either stimulates de novo synthesis of ceruloplasmin or combines with apoceruloplasmin in the liver to form the metalloprotein which is then released into the peripheral blood. It is possible that in Wilson's disease this mechanism may be impaired. Because copper is corrosive and absorbed, even after prompt emesis, it does not appear to be a safe emetic, as recently advocated, particularly when the agent ingested has the same effects as toxic doses of copper. (APS)
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Holtzman, N., Graham, G., Charache, P. et al. 75 Effect of Copper on Serum. Ceruloplasmin Concentration. Pediatr Res 1, 219 (1967). https://doi.org/10.1203/00006450-196705000-00082
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DOI: https://doi.org/10.1203/00006450-196705000-00082