Abstract
THERE is some doubt1 about the relevance of abnormal copper metabolism to the pathogenesis of hepato-lenticular degeneration (Wilson's disease), but the most important aspect of therapy at present is the mobilization and excretion of tissue copper and the reduction of absorption of copper from the gastro-intestinal tract. The majority viewpoint was well expressed by Scheinberg when he wrote “… it is difficult to believe, from the evidence already at hand, that chronic copper toxicity is not the basis of this disease”2. At the present time, the cupruretic drug of choice is penicillamine (ββ-dimethylcysteine) first introduced in 1956 (ref. 3).
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References
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O'REILLY, S., BANK, W. New Oral Chelating Agent for Treatment of Wilson's Disease. Nature 212, 1597–1598 (1966). https://doi.org/10.1038/2121597a0
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DOI: https://doi.org/10.1038/2121597a0
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