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RUDI SCHMID, M.D.

AMA Arch Intern Med. 1958;101(3):669-674.

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

Bilirubin, the principal breakdown product of the prosthetic group of hemoglobin and of other hemeproteins, is normally excreted with the bile. In health, the liver is very efficient in disposing of the amount of pigment, which is continuously produced by the physiological turnover of hemeproteins, so that the plasma is nearly free of bilirubin. In liver disease, however, or in instances of obstruction in the biliary duct system, bilirubin excretion usually becomes impaired, causing a rise in the plasma bilirubin concentration eventually leading to clinical jaundice.

A different type of jaundice is present in hemolytic disease where the accelerated red cell destruction leads to overproduction of bilirubin in amounts which may exceed the capacity of the liver to excrete the pigment. The term "retention jaundice" has been applied to the latter, whereas the former is spoken of as "regurgitation jaundice." ^1-3 While both types of icterus result from a quantitative . . . [Full Text PDF of this Article]

Author Affiliations
Boston

From the Thorndike Memorial Laboratory and the Second and Fourth (Harvard) Medical Services, Boston City Hospital, and the Department of Medicine, Harvard Medical School.

Footnotes
Accepted for publication Dec. 13, 1957.

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