Abnormalities of the Physiology of Copper in Wilson's Disease
- 1 May 1971
- journal article
- research article
- Published by American Medical Association (AMA) in Archives of Neurology
- Vol. 24 (5) , 385-390
- https://doi.org/10.1001/archneur.1971.00480350019001
Abstract
The whole-body turnover of cupric chloride (67Cu) was determined in 22 normal and other control subjects, 12 patients with cirrhosis of the liver, 21 known homozygotes of Wilson's disease, 9 presumptive heterozygotes (parents), and 15 family members (14 of whom were siblings), in a Chinese population (Taiwan) and an American population (San Francisco). The results obtained showed that whole-body retention of copper was prolonged in both homozygotes and heterozygotes of Wilson's disease, and in cirrhotic patients with ascites and/or hepatocellular failure. In the absence of clinical and laboratory evidence of hepatocellular insufficiency with or without ascites, prolonged whole-body turnover of copper may be used to identify the genetic defect of Wilson's disease.Keywords
This publication has 2 references indexed in Scilit:
- The Question of Copper Deficiency in ManThe American Journal of Clinical Nutrition, 1964
- Metabolism of copper in manActa Medica Scandinavica, 1944