DRUG-INDUCED IMMUNE THROMBOCYTOPENIA
Abstract
Drug-induced immune thrombocytopenia (DIIT) is a consequence of destruction or inadequate activation of platelets by immune system provoked by current or previous presence of a drug in human organism. Annual incidence of DIIT is around 10 cases on 1,000,000 inhabitants. There are four proposed mechanisms behind the DIIT: (1) binding of drug-dependent antibodies for platelets; (2) blocking of fibrinogen binding for glycoprotein receptors IIb-IIIa; (3) drug-independent antibodies against platelets; and (4) creation of drug-antibody immune complexes which further activate platelets and lead to thromboses. Regardless of the DIIT mechanism, it is of paramount importance that physicians think of drugs as possible causes when they encounter low platelet count in a patient. Key therapeutic measure is discontinuation of the offending drug, while platelet transfusion is used only after extreme drop of platelet count. Heparin-induced thrombocytopenia is an exception, because it also requires treatment of thromboses with direct thrombin inhibitors.
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