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Heparin-induced decrease in circulating antithrombin-III

E Marciniak, J P Gockerman

    Lancet (London, England)
    |September 17, 1977
    PubMed
    Summary
    This summary is machine-generated.

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    Continuous heparin therapy significantly depletes plasma antithrombin-III (AT-III), a key proteinase inhibitor. This reduction may explain thromboembolic complications observed during long-term heparin treatment.

    Area of Science:

    • Pharmacology
    • Hematology
    • Biochemistry

    Background:

    • Antithrombin-III (AT-III) is a crucial proteinase inhibitor responsible for heparin's anticoagulant effect.
    • Understanding AT-III levels is vital for interpreting clinical data during heparin therapy.

    Purpose of the Study:

    • To investigate the impact of continuous intravenous heparin infusion on plasma antithrombin-III (AT-III) concentrations.
    • To determine if prolonged heparin exposure affects AT-III levels and its binding capacity.

    Main Methods:

    • Plasma AT-III concentrations were measured in 26 patients undergoing heparin therapy (24 continuous infusion, 2 repeated injections).
    • AT-III binding capacity and antigenic protein levels were assessed throughout treatment.
    • AT-III levels were monitored after heparin cessation.

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    Main Results:

    • Heparin therapy, particularly continuous infusion, caused a progressive reduction in plasma AT-III levels.
    • The decrease in AT-III was observed even in a patient with congenital AT-III deficiency.
    • Plasma AT-III levels returned to normal within 2-3 days after discontinuing heparin.
    • Single doses of heparin did not result in a significant decrease in AT-III.

    Conclusions:

    • Prolonged heparin administration significantly depletes AT-III, impacting its proteinase inhibitor function.
    • AT-III depletion during heparin therapy may contribute to the occurrence of thromboembolic complications.
    • These findings are clinically relevant for managing patients on heparin therapy.