When heparins promote thrombosis: review of heparin-induced thrombocytopenia.
نویسندگان
چکیده
Heparin-induced thrombocytopenia (HIT; sometimes known as HIT type II) is a serious, immune system– mediated complication of heparin therapy often resulting in devastating thromboembolic outcomes. Although nomenclature distinctions have been made historically between this condition and the non–immune system–mediated, asymptomatic transient drop in platelet count in some patients receiving heparin (sometimes known as HIT type I), the term “HIT” is now preferably reserved for the immune system–mediated condition.1 An estimated 1 in 100 patients who receive unfractionated heparin for at least 5 days will develop HIT-associated thrombosis.2 The pervasive use of heparins makes HIT one of the most important adverse drug reactions confronting physicians. Heparin is routinely used for thromboprophylaxis or treatment in many clinical settings, including cardiovascular surgery and interventional procedures, acute coronary syndromes, venous thromboembolism, atrial fibrillation, peripheral occlusive disease, dialysis, and extracorporeal circulation. It is among the most frequently prescribed medications in the United States, with 1 trillion units used3 and 12 million patients treated4 annually. Because thrombocytopenia is common in hospitalized patients, occurring in up to 58% of critically ill patients, and can be caused by a variety of factors,5 HIT unfortunately often remains unrecognized. However, consistent with standard clinical practice for life-threatening conditions, HIT should be suspected in a heparin-treated patient who has thrombocytopenia with or without thrombosis. Increased awareness and a high degree of suspicion for HIT are critical to ensure its prompt recognition, diagnosis, and treatment. Advances in understanding the pathophysiology of HIT and its natural history have led to current treatment recommendations—specifically, that heparin must be discontinued immediately and alternative anticoagulation must be initiated.6 Herein we review the pathogenesis, frequency, natural history, diagnosis, and treatment of HIT.
منابع مشابه
Ik-Kyung Jang and Marcie J. Hursting When Heparins Promote Thrombosis: Review of Heparin-Induced Thrombocytopenia
When Heparins Promote Thrombosis: Review of Heparin-Induced Thrombocytopenia Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 2005 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Circulation doi: 10.1161/CIRCULATIONAHA.104.518563 2005;111:2671-2683 Circulation. http://circ.ahajournals.org/con...
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1 Suh JS, Aster RH, Visentin GP. Antibodies from patients with heparin-induced thrombocytopenia/thrombosis recognize different epitopes on heparin: platelet factor 4. Blood 1998; 91:916–922 2 Jang IK, Hursting MJ. When heparins promote thrombosis: review of heparin-induced thrombocytopenia. Circulation 2005; 11:2671–2683 3 Amiral J, Peynaud-Debayle E, Wolf M, et al. Generation of antibodies to ...
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For the last two decades, heparins have been widely used as anticoagulants. Besides numerous advantages, up to 5% patients with heparin administration suffer from a major adverse drug effect known as heparin-induced thrombocytopenia (HIT). This typical HIT can result in deep vein thrombosis, pulmonary embolism, occlusion of a limb artery, acute myocardial infarct, stroke, and a systemic reactio...
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ورودعنوان ژورنال:
- Circulation
دوره 111 20 شماره
صفحات -
تاریخ انتشار 2005