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Haemostatic problems in acute leukaemia.

J T Wilde1, J M Davies

  • 1University Department of Haematology, Royal Liverpool Hospital, UK.

Blood Reviews
|December 1, 1990
PubMed
Summary
This summary is machine-generated.

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Disseminated intravascular coagulation (DIC) in acute leukaemia often results from leukaemic blast cells directly activating fibrinogen. Treatment involves chemotherapy and blood products, with heparin

Area of Science:

  • Hematology
  • Oncology
  • Pathophysiology

Background:

  • Disseminated intravascular coagulation (DIC) is a common complication in acute leukaemia, particularly acute promyelocytic leukaemia.
  • Leukaemic blast cells can trigger DIC through conventional coagulation pathways or direct fibrinogen activation via released proteases.
  • Primary fibrinolysis is a less common cause of bleeding in acute leukaemia, often secondary to DIC.

Purpose of the Study:

  • To review the mechanisms of DIC in acute leukaemia.
  • To discuss treatment strategies for leukaemia-associated DIC.
  • To evaluate the role of heparin in managing DIC during leukaemia treatment.

Main Methods:

  • Literature review of studies on DIC in acute leukaemia.
  • Analysis of proposed mechanisms for DIC initiation.

Related Experiment Videos

  • Examination of treatment protocols and clinical trial data.

    • Main Results:

    • Direct fibrinogen activation by blast cell proteases is a likely predominant mechanism for DIC initiation.
    • Primary fibrinolysis is rare, with bleeding more often secondary to DIC.
    • Chemotherapy and blood product support are primary treatments; heparin's role is debated but may reduce hemorrhagic death at low doses.

    Conclusions:

    • Leukaemic blast cells play a central role in initiating DIC through various mechanisms.
    • Effective management of leukaemia-associated DIC relies on prompt chemotherapy and supportive care.
    • Low-dose heparin may be beneficial in reducing hemorrhagic complications in certain cases.