Abstract
Acute promyelocytic leukemia (APL) is characterized by frequent complications due to a distinct coagulopathy. While advances in treatments have improved long-term survival, hemorrhagic and thrombotic complications remain the most common causes of death and morbidity. Improved understanding of the mechanisms of the coagulopathy associated with APL may lead to therapeutic interventions to mitigate the risk of hemorrhage and thrombosis.
Highlights
Acute promyelocytic leukemia (APL) is caused by a translocation of the retinoic acid receptor alpha (RARα) on chromosome 17, most commonly with the promyelocytic leukemia gene (PML) on chromosome 15, which leads to clonal proliferation of promyeloblasts [1]
APL promyeloblasts express high levels of Annexin II, a receptor and activator of tissue plasminogen activator (tPA)/urokinase plasminogen activator (uPA) resulting in uncontrolled generation of plasmin and hyperfibrinolysis. (C) Mechanistic impact of therapeutic interventions routinely used in APL
Hemorrhagic syndromes vary from easy bruising or purpura to hematomas and even intracranial hemorrhage, the most serious complication and the main cause of early death
Summary
Acute promyelocytic leukemia (APL) is caused by a translocation of the retinoic acid receptor alpha (RARα) on chromosome 17, most commonly with the promyelocytic leukemia gene (PML) on chromosome 15, which leads to clonal proliferation of promyeloblasts [1]. This review will present the current interventions used to mitigate the hemorrhagic risks and emphasize potential treatment strategies and novel agents that merit clinical investigation to decrease coagulopathy-related death in these patients. A number of investigators have reported increased levels of tissue factor pathway inhibitor (TFPI) in patients with APL.
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