Hemophilia B (PTC Deficiency, or Christmas Disease)

AMA Arch Intern Med. 1959;103(5):762-775. doi:10.1001/archinte.1959.00270050084014.
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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


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