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ARMAND J. QUICK, Ph.D., M.D.; CLARA V. HUSSEY, M.S.

AMA Arch Intern Med. 1959;103(5):762-775.

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

In 1947, it was shown by means of a new procedure, the prothrombin consumption test, that blood did not contain thromboplastin either free or in a precursor state but that it was formed as the result of an interaction between a platelet factor and what was assumed to be at that time a single plasma constituent which was lacking in hemophilia.¹ Five years later Schulman and Smith² reported a patient whose clinical condition was indistinguishable from hemophilia but whose defective prothrombin-consumption time was corrected by plasma from a known hemophiliac. They concluded that their patient lacked a plasma factor different from thromboplastinogen, the agent deficient in hemophilia, but which was equally as essential for the formation of plasma thromboplastin. No specific name other than X was given to this new factor. Interestingly, a week after Schulman and Smith sent their manuscript for publication, Aggeler and his associates ³ . . . [Full Text PDF of this Article]

Author Affiliations
Milwaukee

From the Department of Biochemistry, Marquette University School of Medicine.

Footnotes
Submitted for publication July 30, 1958.

This work was supported by a grant (H1612-C12) from the National Heart Institute, National Institutes of Health, United States Public Health Service.

The name hemophilia B has been used because the disease is clinically and genetically very similar to classical hemophilia. PTC (plasma thromboplastin component) deficiency is the term used to denote the activity in normal serum, and thromboplastinogen, to indicate the factor lacking in classical hemophilia.

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