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January 1969

Coagulation Defects in Acute Promyelocytic Leukemia

Author Affiliations


From the Hematology Laboratory and the Circulation Laboratory, Tufts University School of Medicine and Boston City Hospital, Boston. Doctor Rand is currently a Public Health Service trainee in endocrinology and metabolism, Department of Medicine, Flower and Fifth Ave-; nue Hospital, New York. Doctor Moloney is currently with the Department of Medicine, Harvard Medical School, and the Division of Hematology, Peter Bent Brigham Hospital, Boston.

Arch Intern Med. 1969;123(1):39-47. doi:10.1001/archinte.1969.00300110041007

Four patients with acute promyelocytic leukemia manifested multiple coagulation abnormalities including hypofibrinogenemia, prolongation of prothrombin and thrombin times, and varying deficiencies of coagulation factors. One of the patients (patient 2) showed rising levels of fibrinogen without changes in other coagulation factors on heparin therapy and demonstrated widespread intravascular coagulation on postmortem examination. Another patient (patient 1) had positive tests for active fibrinolysis and an absolute lack of the usual postmortem thrombi. The current hypotheses of the pathogenesis of the coagulation abnormalities are presented as well as guide to therapeutic management.