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May 1971

Abnormalities of the Physiology of Copper in Wilson's Disease: I. The Whole-Body Turnover of Copper

Author Affiliations

San Francisco and Taipei, Taiwan
From the Clinical Study Center, San Francisco General Hospital, San Francisco, and the Clinical Investigation Unit, NAMRU-2, Taipei, Taiwan.

Arch Neurol. 1971;24(5):385-390. doi:10.1001/archneur.1971.00480350019001

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.

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