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.
O'Reilly S, Strickland GT, Weber PM, Beckner WM, Shipley L. Abnormalities of the Physiology of Copper in Wilson's Disease: I. The Whole-Body Turnover of Copper. Arch Neurol. 1971;24(5):385–390. doi:10.1001/archneur.1971.00480350019001
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