[Management of heparin-induced thrombocytopenia]

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P Aouizerate1, M Guizard

  • 1Service Pharmacie, Centre Hospitalier Général, Meaux, France. p-aouizerate@ch-meaux.fr

Therapie
|April 2, 2003
PubMed

Immune-mediated (type II) heparin-induced thrombocytopenia (HIT) is a common and potentially serious averse effect of heparin therapy. Early diagnosis is needed in order to prevent complications such as venous and arterial thromboembolic events. Clinical management of patients with type II HIT is difficult. In most cases, immediate cessation of heparin therapy is required, and continuation with alternative antithrombotic treatment is recommended. Currently, there is no consensus about the optimal anticoagulation therapy for type II HIT. A literature review regarding new antithrombotics and their role in HIT was carried out, using Medline. The pharmacologic characteristics as well as the clinical evaluation of direct inhibitors of thrombin (argatroban, inogatran, melagatran, ximelagatran, efegatran and napsagatran) and fondaparinux, a synthetic pentasaccharide were reported. There new anticoagulants are not available yet in France, so sodium danaparoid and lepirudin are the only effective antithrombotics officially induced in HIT, and constitute an important therapeutic advance. A procedure for HIT prophylaxis or thrombosis treatment with HIT was assessed. No comparative test concerning sodium danaparoid and lepirudin is available. The selection could not be based on clinical arguments, but the cost of treatment could constitute a selection criterion. The comparison of the treatment cost for a patient weighing 70 kg, and presenting with symptomatic HIT, was in favour of sodium danaparoid. Because of the increased risk of haemorrhage with lepirudin, and the less convenient administration methods for this drug, the prescription of sodium danaparoid as first-line therapy, following a test of platelet aggregation can be justified. The monitoring of a treatment by sodium danaparoid or by lepirudin could be carried out within our establishment. For all these reasons, we chose the systematic use of lepirudin in the event for symptomatic HIT thus in emergency. In patients presenting asymptomatic HIT, or with a history of HIT and for which a surgical operation requiring an active anticoagulant was programmed, sodium danaparoid must preferentially be used, only if the test of crossed reactivity with sodium danaparoid is negative. The absence of crossed reactivity of the heparin-dependent antibodies against sodium danaparoid should be systematically tested, imperatively during the acute phase of HIT. The conversion to vitamin K antagonists must be considered as soon as possible, after HIT correction. HIT should be largely prevented by limiting the duration of heparin administration and by monitoring platelet numeration, twice-weekly during the first three weeks of treatment, and in the event of its prolongation, to be carried out once a week. This approach should decrease the number of cases of thrombocytopenia due to heparin.

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