Abstract
Heparin, a negatively charged glycosaminoglycan (3000–30,000 Da), is an anticoagulant released by mast cells and basophils during the normal clotting process [1]. Heparin is widely used for the treatment and prophylaxis of thromboembolic diseases in medical and surgical patients [1]. Heparin-induced thrombocytopenia (HIT) is one of the most serious adverse events associated with this drug. HIT is an immune-mediated, prothrombotic complication that occurs with unfractionated heparin (UFH) and to a lesser extent with low-molecular-weight heparin (LMWH) [2]. The fundamental paradox of HIT results from a platelet-activating immune response triggered by the interaction of heparin with a specific platelet protein, platelet factor 4 (PF4) [3].
Highlights
Heparin, a negatively charged glycosaminoglycan (3,000– 30,000 Da), is an anticoagulant released by mast cells and basophils during the normal clotting process [1]
Summary and conclusion Heparin-induced thrombocytopenia (HIT) is an immune-mediated, prothrombotic complication that occurs with unfractionated heparin (UFH) and to a lesser extent with low-molecular-weight heparin (LMWH)
The diagnosis of HIT can be established by laboratory testing for the presence of HIT antibodies
Summary
A negatively charged glycosaminoglycan (3,000– 30,000 Da), is an anticoagulant released by mast cells and basophils during the normal clotting process [1]. In HIT type II, heparin infusion displaces PF4 and produces structural changes on it, leading to the formation of a PF4/heparin complex This complex is recognized as aforeign’ antigen and triggers an immune response, which is characterized by the release of IgG antibodies that bind to the PF4/heparin complexes with subsequent clustering of the platelet Fc-receptors (FcχRIIa, FcχRIIIa) resulting in platelet activation. Not all patients who have heparin antibodies develop platelet activation and clinically relevant HIT. Thisdelayed onset’ HIT is associated with large numbers of anti-PF4/heparin antibodies, which lead to platelet activation in the absence of heparin [3] This entity may be clinically relevant in patients who are discharged early from the hospital after surgical interventions.
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