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V. GILSANZ, M.D.; J. M. SEGOVIA, M.D.; H. CASTRO MENDOZA, M.D.

AMA Arch Intern Med. 1955;95(5):727-734.

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

We regard it of interest to report our study of three brothers affected with Wilson's disease, in two of whom the process appeared with its most characteristic clinical picture and in one of whom the only finding in relation to this disease was the presence of amino-aciduria.

The nature of the hepatolenticular degeneration that appears in Wilson's disease is yet unknown, but in the last few years, by evaluation of the disturbances of the metabolism of copper and the amino acids eliminated in the urine, new concepts have been brought forth which are worthy of further research.

Baker,¹ in 1948, summarized the theories which up to that time had tried to explain the nature of Wilson's disease as follows: 1. It is a degenerative process affecting the liver and brain. 2. It is an acquired disease, and both organs are damaged simultaneously by an endogenous toxin. 3. The primary . . . [Full Text PDF of this Article]

Author Affiliations
Madrid, Spain

From the Department of Internal Medicine, University of Madrid (Professor, Dr. Gilsanz).

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