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:

 na