A Controlled Study of Potential Therapeutic Effect of Oral Zinc in Manifesting Carriers of Wilson Disease

A Controlled Study of Potential Therapeutic Effect of Oral Zinc in Manifesting Carriers of Wilson Disease

The assumption is that in some of the carriers, the increase in enzymes reflects tissue damage due to excess copper. The reduction of the amount of copper absorbed will decrease excess copper in the liver, which will result in a decrease in the level of liver enzymes. Zinc causes the induction of metalothionines in the intestine, which in turn prevents absorption of copper from the digestive system. Zinc administration in Wilson's patients causes the depletion of copper deposits and constitutes one of the cornerstones in the treatment of this disease.

The research group is composed of patients over the age of 18 referred for unexplained elevation of liver enzymes and carry a single mutation in the ATP7B gene. After a washout period of 3 months these patients will be re-checked for liver enzymes and if high will receive zinc therapy at a dose of 300 mg / day for 6 months, after which the liver enzymes will be checked again.

Inclusion Criteria:

patients over the age of 18 unexplained elevation of liver enzymes patients that carry a single mutation in the ATP7B gene.

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Exclusion Criteria:

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