What is heparin-induced thrombocytopenia (HIT)?
The pro-thrombotic effects of heparin were first recognized in 1957 but the full syndrome of HIT was not described until 1973 when it was recognized that heparin could cause the formation of antibodies that resulted in a syndrome of low platelets (thrombocytopenia) and–paradoxically–more clots. The platelet count would return to normal if heparin was stopped and would recur if heparin were given again. HIT is felt to be caused by an immune reaction to the drug and can be recognized clinically and confirmed by appropriate blood tests. HIT is a very serious clinical problem; however, not all people who have HIT antibodies actually develop clinical HIT. Treatment of HIT consists first of stopping heparin. In place of heparin, other drugs have been tried, including warfarin, ancrod and aspirin. More recently, drugs that inhibit thrombin directly such as lepirudin, danaparoid and argatroban have been used. It has been determined that warfarin should not be used in the acute phase of HIT s
