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CONGENITAL HYPOPROTHROMBINEMIC STATES
ARMAND J. QUICK, M.D.;
ANTHONY V. PISCIOTTA, M.D.;
CLARA V. HUSSEY, M.S.
AMA Arch Intern Med. 1955;95(1):2-14.
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THE DISCOVERY of a case of congenital hypoprothrombinemia in 1941 by Rhoads and Fitz-Hugh 1 marked the beginning of an important advance in the study of hemorrhagic diseases. This case had been diagnosed and regarded as hemophilia for nine years. Only after the prothrombin-time test became available was it possible to differentiate such a condition readily from hemophilia. From the early studies * it became evident that cases of this type were congenital and likely familial. All were tacitly accepted as true hypoprothrombinemia. The discovery of the labile factor (proaccelerin, Factor V, or ac-globulin) in 1943 clearly demonstrated that the prothrombin time could be prolonged by a deficiency of this new factor, and the prediction that such a lack might cause a hemorrhagic disease 9 was borne out when, less than two years later, Owren 10 reported a patient with a bleeding tendency who lacked this agent. Shortly thereafter, members of
. . . [Full Text PDF of this Article]
Author Affiliations
Milwaukee
From the Department of Biochemistry, Marquette University School of Medicine.
Footnotes
This work was supported by a grant (H-1612 C7) from the National Heart Institute, National Institutes of Health, United States Public Health Service.
Drs. Mila Pierce and Albert T. Kwedar gave us opportunity to study their patients and permission to include our findings in this paper, and Dr. Benjamin Alexander studied the plasma of one of the patients.
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