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RICHARD A. MACDONALD, M.D.

Arch Intern Med. 1962;110(4):424-434.

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

There are at present a number of concepts of the pathogenesis of cirrhosis, the most widely held of which is that cirrhosis develops as degeneration, nodular regeneration, and fibrosis occur in sequence.^1-4 According to this view, a variety of etiologic factors damage liver cells, many of which die while others regenerate. Foci of nodular regeneration are thought to occur in this way, compressing the stroma that formerly surrounded necrotic cells, giving rise to fibrous bands.

In studies of rat and human liver in various stages of cirrhosis I have found a different sequence of events in the development of the cirrhotic process. Using tritiated thymidine (H³-thymidine) and autoradiography to detect proliferating cells, the earliest change giving rise to fibrosis was proliferation of cells of blood vessels and lymphatics. From these studies, the pathogenesis of nutritional cirrhosis is suggested to be as follows. Swelling of liver and Kupffer . . . [Full Text PDF of this Article]

Author Affiliations
BOSTON

From the Mallory Institute of Pathology, Boston City Hospital, and the Department of Pathology, Harvard Medical School.

Footnotes
Submitted for publication April 23, 1962; accepted June 5.

Aided by Grants H-3647 and A-1519 from the U.S. Public Health Service and by a Contract with the Office of the Surgeon General, U.S. Army.

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