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NORMAN ROSENTHAL, M.D.; SIDNEY P. ZIMMERMAN, M.D.; SHEPARD SHAPIRO, M.D.

Arch Intern Med. 1946;77(4):420-427.

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

Despite the tremendous strides made in recent years in the understanding of the properties of prothrombin, its metabolic cycle remains a matter of conjecture. As far as is known, the liver is the site of production of prothrombin, and the precursor of thrombin is liberated into the circulating blood continuously and in excess. Of the fate and possible additional functions of prothrombin practically nothing is known. The manner in which vitamin K and dicoumarin (3,3'-methylene-bis-[4-hydroxycoumarin] ) exert their respective influences on the prothrombin-elaborating system likewise remains obscure. The evidence to prove that the liver is the major, if not the sole, locus for the synthesis of prothrombin is as yet neither complete nor conclusive. The conception is based on the demonstration that hepatocellular damage, artificially induced or occurring clinically, is accompanied with prothrombinopenia. Which of the components of the liver, the hepatic parenchymatous cells or the elements of the reticuloendothelial system . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

From the Third (New York University) Division, Goldwater Memorial Hospital, and the Department of Medicine, New York University College of Medicine.

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