Several papers have reported severe liver disease in association with
massive hepatic copper accumulation, which do not seem to be either of
the recognised copper associated liver diseases, namely Wilson's dise
ase and Indian childhood cirrhosis. A further case is reported in whic
h novel copper kinetic studies were carried out using the stable isoto
pe Cu-65, showing that this patient did not suffer from Wilson's disea
se. It is suggested that these cases can be divided into two groups on
the basis of age, clinical course, and history of excessive copper in
gestion. The benefits of using Cu-65 for in vivo studies of copper met
abolism is discussed.