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Clinical and Laboratory Observations

DAVID CAYER, M.D.

Arch Intern Med. 1947;80(5):644-654.

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

THE CONCEPTS of the origin and therapy of hepatic disease have changed radically in recent years. The belief that cirrhosis is caused by toxic substances, most notably alcohol, is being replaced by the concept that the primary etiologic factor is probably a dietary deficiency or that multiple etiologic agents, acting through a mechanism which produces fatty infiltration of the liver, may be responsible. This concept is supported by the experimental production of cirrhosis in animals deprived of proteins, amino acids and vitamins.

THE EXPERIMENTAL PRODUCTION AND PREVENTION OF HEPATIC DAMAGE AND CIRRHOSIS

The relationship of diet to hepatic damage in laboratory animals has been known for some time. Curtis and Newburgh produced necrosis of the liver in rats by adding as little as 0.75 per cent cystine to a diet low in casein.¹ The severity of the lesions was related to the amount of cystine used. Lillie in 1932 . . . [Full Text PDF of this Article]

Author Affiliations
WINSTON-SALEM, N. C.

From the Department of Internal Medicine, Bowman Gray School of Medicine of Wake Forest College, and the North Carolina Baptist Hospital.

Footnotes
Studies on vitamin levels were done under a grant from the John and Mary R. Markle Foundation.

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