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HYPOFIBRINOGENEMIA DUE TO INCREASED FIBRINOLYSIS IN TWO PATIENTS WITH ACUTE PROMYELOCYTIC LEUKEMIA
Author(s) -
CHAN T. K.,
CHAN G. T. C.,
CHAN VIVIAN
Publication year - 1984
Publication title -
australian and new zealand journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0004-8291
DOI - 10.1111/j.1445-5994.1984.tb03760.x
Subject(s) - hypofibrinogenemia , medicine , acute promyelocytic leukemia , fibrinolysis , leukemia , afibrinogenemia , cardiology , fibrinogen , gastroenterology , genetics , retinoic acid , biology , gene
Two patients with acute promyelocytic leukemia and severe bleeding associated with hypofibrinogenemia were studied. The markedly shortened whole blood clot lysis time and dilute clot lysis time suggested that the defect was an increase in fibrinolysis. Although disseminated intravascular coagulation could not be totally excluded as an alternative mechanism, excessive fibrinolysis was confirmed as the pathogenic cause by the prompt response to the administration of tranexamic acid. The low circulating plasminogen, α 2 plasmin inhibitor level and the presence of α 2 plasmin inhibitor‐protease complex in both patients suggested that the increased fibrinolysis probably resulted from the liberation of plasminogen activator from the promyelocyte.