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Discovered in 1916, heparin has been the anticoagulant drug of choice for nearly 100 years. At this time, more than one trillion units of heparin are used annually in the United States.4 Heparin is highly effective in the prevention and treatment of numerous thromboembolic disorders, offers rapid anticoagulation, enables healthcare professionals to monitor its therapeutic activity through laboratory testing, and is relatively inexpensive.
In up to 35% of patients, however, heparin can also cause heparin-induced thrombocytopenia (HIT). (HIT type 2 will be referred to as HIT throughout this Web site.) HIT type 2, the most serious form of HIT, occurs in up to 5% of heparin patients and has potentially catastrophic sequelae.1 It is most common in patients receiving intravenous unfractionated heparin, but also occurs in patients receiving low-molecular weight heparin, heparin flushes, hemodialysis, and heparin-coated catheters.1, 2
Although the anticoagulant effects of heparin may be reversed with the use of protamine sulfate, reversal of these effects is not an effective treatment for HIT.5



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