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Heparin-induced thrombocytopenia (HIT) is the development of thrombocytopenia (a low platelet count), due to the administration of various forms of heparin, an anticoagulant. HIT predisposes to thrombosis (the abnormal formation of blood clots inside a blood vessel ).
Discontinuation of heparin is critical in a case of heparin-induced thrombocytopenia (HIT). Beyond that, however, clinicians generally treat to avoid thrombosis. [32] Treatment may include a direct thrombin inhibitor, such as lepirudin or argatroban. Other "blood thinners" sometimes used in this setting include bivalirudin and fondaparinux.
Not all patients with heparin antibodies will develop thrombocytopenia. Also, a benign form of thrombocytopenia is associated with early heparin use, which resolves without stopping heparin. Approximately one-third of patients with diagnosed heparin-induced thrombocytopenia will ultimately develop thrombotic complications. [31]
Heparin-induced thrombocytopenia (HIT) is due to an immune system reaction against the anticoagulant drug heparin (or its derivatives). [1] Though it is named for associated low platelet counts, HIT is strongly associated with risk of venous and arterial thrombosis. [19]
More rarely, this phenomenon had previously been described as an autoimmune phenomenon in people who had not been exposed to heparin. [29] One striking feature of thrombocytopenia in the presence of anti-PF4 antibodies is the propensity of some to develop thrombosis, a phenomenon called heparin-induced thrombocytopenia if heparin is involved. [30]
Once the Heparin therapy is initiated, the patient's PTT (partial thromboplastin time) levels will be monitored closely per hospital protocol to prevent excessive anti-coagulation. If a patient is allergic to Heparin or has a condition known as Heparin-induced Thrombocytopenia (HIT), an alternative intravenous anti-coagulate may be used.
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