The administration of<unk>  can cause the development of<unk>  antibodies, suggesting<unk>  may act as a hapten, thus may be targeted by the immune system. In<unk> , the immune system forms antibodies against<unk>  when it is bound to a protein called platelet factor 4 (PF4). These antibodies are usually of the IgG class and their development usually takes about 5 days. However, those who have been exposed to<unk>  in the last few months may still have circulating IgG, as IgG-type antibodies generally continue to be produced even when their precipitant has been removed. This is similar to immunity against certain microorganisms, with the difference that the<unk>  antibody does not persist more than three months.<unk>  antibodies have been found in individuals with<unk>  and thrombosis who had no prior exposure to<unk> , but the majority are found in people who are receiving<unk> . The IgG antibodies form a complex with<unk>  and PF4 in the bloodstream. The tail of the antibody then binds to the FcγIIa receptor, a protein on the surface of the platelet. This results in platelet activation and the formation of platelet microparticles, which initiate the formation of blood clots; the platelet count falls as a result, leading to<unk> . In addition, the reticuloendothelial system (mostly the spleen) removes the antibody-coated platelets, further contributing to the<unk> . Formation of PF4-heparin antibodies is common in people receiving<unk> , but only a proportion of these develop<unk>  or thrombosis. This has been referred to as an "iceberg phenomenon".
Heparin-induced thrombocytopenia
Sticky platelet syndrome
Venom-induced consumption coagulopathy
Pseudo gray platelet syndrome
Drug-induced thrombocytopenic purpura
Gray platelet syndrome
Disseminated intravascular coagulation
Immune thrombocytopenic purpura