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Blood, 1 January 2005, Vol. 105, No. 1, pp. 139-144.
Prepublished online as a Blood First Edition Paper on September 23, 2004; DOI 10.1182/blood-2004-05-2010.
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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Effect of fondaparinux on platelet activation in the presence of heparin-dependent antibodies: a blinded comparative multicenter study with unfractionated heparin
Pierre Savi,
Beng H. Chong,
Andreas Greinacher,
Yves Gruel,
John G. Kelton,
Theodore E. Warkentin,
Petra Eichler,
Dick Meuleman,
Maurice Petitou,
Jean-Pascal Herault,
Roger Cariou, and
Jean-Marc Herbert
From the Sanofi-Synthélabo Recherche, Toulouse, France; Department of Medicine, St George Hospital, Kogarah, Australia; Department of Immunology and Transfusion Medicine, Ernst-Moritz-Arndt-University, Greifswald, Germany; Service d'Hématologie-Hémostase, Hôpital Trousseau, Tours, France; Platelet Immunology Laboratory, McMaster University, Hamilton, ON, Canada; and NV Organon, Oss, The Netherlands.
Heparin-induced thrombocytopenia (HIT) is a complication of heparin therapy caused by antibodies against a complex of platelet factor 4 and heparin. Fondaparinux (Arixtra) is a new synthetic selective factor Xa inhibitor. We performed a serologic study to determine the cross-reactivity of HIT sera with fondaparinux. Using a prospective, blinded study design, 39 clinically and serologically confirmed sera from patients with HIT and 15 control sera were sent to 3 different laboratories, each of which specialized in a particular HIT assay. These include the serotonin release assay, heparin-induced platelet agglutination assay, and platelet aggregation assay. Two of 82 assays (2.4%) performed in the presence of control sera were positive, both with unfractionated heparin. In the presence of HIT sera, 75 of 94 (79.8%) evaluable assays were positive with unfractionated heparin; fondaparinux was significantly (P < .001) less reactive than unfractionated heparin, only 3 of 91 evaluable assays (3.3%) being positive. Using flow cytometry, unlike unfractionated heparin, fondaparinux did not induce the binding of PAC1 and anti-CD62 monoclonal antibodies or of annexin V to platelets with HIT sera. Together, these results suggest that fondaparinux is nonreactive to HIT sera and raise the possibility that the drug may be used for prophylaxis and treatment of thrombosis in patients with a history of HIT.
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