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Introduction Considerable attention has been given to alterations in copper, especially in diseases which affect primarily the liver and corpus striatum. As early as 1929 Vogt 1 was able to demonstrate an increase in the amount of copper in the liver and brain in hepatolenticular degeneration (Wilson's disease). Haurowitz 2 confirmed this (1930), and by 1936, Policard et al. 3 observed the presence of copper in the iris. Elimination in the urine of elevated amounts of copper was later noted by Porter 4 (1951). A survey of the literature dealing with the relationship of copper to hepatolenticular degeneration has recently been made by Cumings 5 (1959), who has made noteworthy contributions on the neurochemistry of this disease. Similar studies of other disorders of the liver and the corpus striatum followed those of hepatolenticular degeneration, especially when there was any suggested functional relationship between the two. Cumings 6 (1954) investigated other
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Courville et al. (1963) studied this question.
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