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To the Editor.

I. Herbert Scheinberg, MD
Bronx, NY

Arch Neurol. 1973;29(6):449.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor..—

Although the patient described by Schraeder et al¹ seems to have suffered from polymyositis, perhaps a reaction to penicillamine, it is very probable that she does not have Wilson disease. On the basis of the evidence presented, she is more likely to be a heterozygous carrier of one "Wilson disease gene."

Deficiency, or absence, of ceruloplasmin in the serum is seen in about 95% of individuals with Wilson disease—abnormal homozygotes — but is also noted in at least 10% of heterozygous carriers of this gene. About one in 200 individuals in the general population is such a carrier² so that one would expect to find about one in 2,000 individuals whose deficiency of ceruloplasmin is a consequence of this heterozygosity. Since the prevalence of Wilson disease itself is of the order of one in 200,000,² only one of every 100 patients with hyperceruloplasminemia will be a . . . [Full Text PDF of this Article]

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