Acute promyelocytic leukaemia and acquired α-2-plasmin inhibitor deficiency: a retrospective look at the use of epsilon-aminocaproic acid (Amicar) in 30 patients

Authors

  • T. Wassenaar,

    Corresponding author
    1. University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
    2. University of Wisconsin Paul P. Carbone Comprehensive Cancer Center, Madison, WI, USA
    • 600 Highland Avenue, H4/534 Madison, WI 53792, USA.
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  • J. Black,

    1. University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
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  • B. Kahl,

    1. University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
    2. University of Wisconsin Paul P. Carbone Comprehensive Cancer Center, Madison, WI, USA
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  • B. Schwartz,

    1. University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
    2. University of Wisconsin Paul P. Carbone Comprehensive Cancer Center, Madison, WI, USA
    Current affiliation:
    1. University of Illinois, Urbana, IL, USA.
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  • W. Longo,

    1. University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
    2. University of Wisconsin Paul P. Carbone Comprehensive Cancer Center, Madison, WI, USA
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  • D. Mosher,

    1. University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
    2. University of Wisconsin Paul P. Carbone Comprehensive Cancer Center, Madison, WI, USA
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  • E. Williams

    1. University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
    2. University of Wisconsin Paul P. Carbone Comprehensive Cancer Center, Madison, WI, USA
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Abstract

Bleeding diathesis and a hyper-fibrinolytic state often accompany a diagnosis of Acute Promyelocytic Leukaemia (APML). This complication can have grave effects if not successfully treated, with a 10–20% incidence of haemorrhagic death. We hypothesized that α-2-antiplasmin levels would correlate with the risk for bleeding, and that administration of epsilon-aminocaproic acid (EACA) would attenuate that risk. To assess this, we conducted a retrospective chart review analyzing 30 APML patients, 17 of whom were treated with EACA. Thirty patients were treated, 21 with primary induction therapy. Patients with low α-2-antiplasmin levels were treated with a coagulopathy protocol consisting of low-dose heparin, EACA and blood product support. Seventeen patients (57%) developed haemorrhagic complications during their treatment. The presence and grade of haemorrhage appeared to be associated with the α-2-antiplasmin level. There were no grade IV haemorrhages or episodes of haemorrhagic death. One episode of central venous catheter associated thromboembolism and three deaths from infection during chemotherapy were observed. α-2-Antiplasmin levels are a reliable surrogate for fibrinolysis and haemorrhagic risk in patients with APML. Treatment with EACA is a rational way to pharmacologically inhibit fibrinolysis, is associated with a low incidence of severe haemorrhagic events, and appears to be safe with a low risk of thrombosis. Randomized clinical trials further assessing the efficacy and potential toxicity of EACA in inhibiting fibrinolysis in patients with APML are needed. Copyright © 2008 John Wiley & Sons, Ltd.

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