Heparin-induced thrombocytopenia: laboratory studies

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Heparin-induced thrombocytopenia: laboratory studies.

This report describes studies into the pathophysiology of heparin-induced thrombocytopenia. The IgG fraction from each of nine patients with heparin-induced thrombocytopenia caused heparin-dependent platelet release of radiolabeled serotonin. Both the Fc and the Fab portions of the IgG molecule were required for the platelet reactivity. The platelet release reaction could be inhibited by the Fc...

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Heparin induced thrombocytopenia

Abstract Background and Objectives Heparin is still a commonly used anticoagulant in prophylaxis and treatment of thromboembolic events. Heparin-induced thrombocytopenia (HIT) is a life-threating adverse drug reaction of heparin. The diagnosis of HIT is made based on two important criteria, firstly clinical evaluation and secondly laboratory testing. In this comprehensive review, the authors w...

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Laboratory tests for the diagnosis of heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is associated with high morbidity and mortality. Because the pathophysiology of this complex disorder has remained unclear, so has the development of supportive diagnostic laboratory assays. The currently available laboratory methods for HIT diagnosis include several platelet function assays: the platelet aggregation assay, platelet aggregation with simult...

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Platelet count monitoring and laboratory testing for heparin-induced thrombocytopenia.

OBJECTIVE Heparin-induced thrombocytopenia (HIT) is an antibody-mediated adverse drug reaction that paradoxically is associated with a brief but dramatically increased risk for thrombosis (transient acquired thrombophilia). The objective of this article is to provide practical recommendations for platelet count monitoring in patients receiving heparin, as well as for selection of laboratory ass...

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Heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused by antibodies to complexes of platelet factor 4 (PF4) and heparin. Pathogenic antibodies to PF4/heparin bind and activate cellular FcγRIIA on platelets and monocytes to propagate a hypercoagulable state culminating in life-threatening thrombosis. It is now recognized that anti-PF4/heparin antibodies devel...

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ژورنال

عنوان ژورنال: Blood

سال: 1988

ISSN: 0006-4971,1528-0020

DOI: 10.1182/blood.v72.3.925.bloodjournal723925