Kinetics of 64copper in primary biliary cirrhosis

✍ Scribed by A. Roelof Janssens; Cornelis J. A. Van Den Hamer

• Publisher: John Wiley and Sons
• Year: 1982
• Tongue: English
• Weight: 673 KB
• Volume: 2
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840020614

✦ Synopsis

To assess the pathogenetic mechanisms involved in the accumulation of copper in primary biliary cirrhosis (PBC), the kinetics of 64Copper ("Cu) were studied in 6 healthy volunteers, 3 patients with PBC (Stages I to 111) and a normal liver copper, and 7 patients with PBC (Stages I1 to IV) and a high liver copper. The kinetics of oral and i.v. administered "Cu in patients with a normal liver copper were similar to those in controls. In patients with a high liver copper, the initial disappearance rate from the plasma of i.v. administered "Tu was more rapid, the disap earance rate from the liver of "Cu taken up by this organ was slower, and the fecal excretion of Cu less as compared with the two other groups of subjects. In addition, the fecal excretion of orally administered g4Cu was less in these patients. Computation of the rate of absorption of orally administered s4Cu revealed no differences between the three groups. Two of the patients with a high liver copper were decopperized by treatment with D-penicillamine. In these patients, the disappearance rate of i.v. administered %u from the liver and the secondary reappearance rate of 'Wu into plasma became normal; however, the fecal excretion of "Cu remained low. It is concluded that there is no pathognomonic alteration of copper metabolism in PBC, but that in some patients, copper accumulates in the liver due to decreased biliary excretion and increased clearance from the plasma, and that dilution of the tracer dose a large amount of stable copper is responsible for all abnormalities of g4Cu kinetics encountered in PBC, except low fecal excretion, which is caused by impairment of biliary excretion.