“…7,8 It is widely thought that HIT antibodies bind to heparin/ PF4 complexes formed on or near the platelet membrane when heparin is infused, and that the resulting immune complexes induce platelet activation, release of platelet granule contents, and formation of procoagulant microparticles when immunoglobulin G (IgG) Fc domains engage platelet FcgRIIa (CD32) receptors. 3,9 The half-life of unfractionated heparin administered intravenously is only about 2 hours, 10 yet thrombotic risk persists for at least several weeks after an episode of HIT, 7,11,12 and occasional patients with "delayed HIT" develop acute thrombocytopenia and thrombosis a week or more after their last exposure to heparin. [13][14][15][16] These manifestations of heparin sensitivity, occurring long after heparin has been cleared from the circulation, are not well understood.…”