Abstract
Zinc sulfate as treatment for Wilson disease (WD) was developed in Europe in the 1960–70s and later; zinc acetate was developed and investigated in the United States from the 1970 to 1980s onward. Zinc has a different mechanism of action compared to oral chelators and thus may serve as replacement for these drugs in WD when intolerance develops or as maintenance therapy after adequate decoppering has taken place. Neurological deterioration, as frequently complicating institution of d-penicillamine in neurological WD, is comparatively uncommon with zinc, and thus zinc may be the preferred primary therapy in this situation. It may have a role in treating clinically silent WD. Recent findings as to how copper is handled in hepatocytes suggest new mechanisms of action for zinc, possibly advantageous for treating WD.
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