The unique hemostatic dysfunction in acute promyelocytic leukemia

Hau C. Kwaan*

*Corresponding author for this work

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

The hemostatic abnormalities seen in acute promyelocytic leukemia (APL) are unique and account for much of the morbidity and mortality of this disorder. Almost all patients present at diagnosis with laboratory findings of intravascular coagulation along with increased fibrinolysis. This unusual combination is correlated to the clinical manifestations with high risk of both bleeding and thrombosis. Recent studies have revealed that the leukemic promyelocytes in APL express increased amounts of tissue factor as well as elements of the fibrinolytic system, including tissue plasminogen activator, annexin A2, and plasminogen activator inhibitor type 1. These changes are responsive to differentiation therapy with all-trans-retinoic acid (ATRA) or with arsenic trioxide (ATO). Despite a dramatic reduction in mortality seen since the introduction of differentiation therapy with ATRA or with ATO, a large number of deaths still occur before complete remission is achieved. The early deaths are mostly attributable to the presenting coagulopathy. The prevention and management of this hemostatic abnormality have thus far been unsuccessful and remain a challenge to bring about a higher cure rate for this disease.

Original languageEnglish (US)
Pages (from-to)332-336
Number of pages5
JournalSeminars in thrombosis and hemostasis
Volume40
Issue number3
DOIs
StatePublished - Apr 2014

Keywords

  • acute promyelocytic leukemia
  • annexin A2
  • fibrinolysis
  • tPA
  • tissue factor

ASJC Scopus subject areas

  • Hematology
  • Cardiology and Cardiovascular Medicine

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