Title of article :
Heparin-Induced Thrombocytopeni
Author/Authors :
David B. Brieger، نويسنده , , Koon-Hou Mak، نويسنده , , Kandice Kottke-Marchant، نويسنده , , Eric J. Topol، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1998
Pages :
11
From page :
1449
To page :
1459
Abstract :
Heparin-induced thrombocytopeni (HIT) is potentially serious complication of heparin therapy and is being encountered more frequently in patients with cardiovascular disease as use of anticoagulant therapy becomes more widespread. Our understanding of the pathophysiology of this immune-mediated condition has improved in recent years, with heparin–platelet factor 4 complex as the culprit antigen in most patients. New sensitive laboratory assays for the pathogenic antibody are now available and should permit an earlier, more reliable diagnosis, but their optimal application remains to be defined. For patients in whom HIT is diagnosed, immediate discontinuation of heparin infusions and elimination of heparin from all flushes and ports are mandatory. Further management of patients with HIT is problematic at present, as there are no readily available alternative anticoagulant agents in the United States with proven efficacy in acute coronary disease. The direct thrombin inhibitors appear to be the most promising alternatives to heparin, when continued use of heparin is contraindicated, and the results of several multicenter trials evaluating their application in patients with HIT are awaited.
Keywords :
ELISA , immunoglobulin , Enzyme-linked immunosorbent assay , Ig , LMW , low molecular weight , PF4 , platelet factor 4 , HIPA , heparin-induced platelet aggregation , HIT , heparin-induced thrombocytopenia
Journal title :
JACC (Journal of the American College of Cardiology)
Serial Year :
1998
Journal title :
JACC (Journal of the American College of Cardiology)
Record number :
480689
Link To Document :
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