Heparin-induced thrombocytopenia pathophysiology: Difference between revisions
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Revision as of 18:59, 10 December 2011
Heparin-induced thrombocytopenia |
Differentiating Heparin-induced thrombocytopenia from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]
Overview
Heparin-induced thrombocytopenia is diagnosed when the platelet count falls by > 50% typically after 5-10 days of heparin therapy. It is caused by antibodies to complexes between heparin and platelet factor 4 (PF4). These antibody complexes stimulates the procoagulant pathways due to activation of platelet and endothelium.
Pathophysiology
- It is caused by antibodies to complexes between heparin and platelet factor 4 (PF4).
- More than 90% patients have these anti–PF4-heparin antibodies in their plasma.
- These antibodies bind to the platelet's surface and induce their activation by cross-linking Fc IIA receptors and bind to the surface of the endothelium, inducing procoagulant activity.
- Platelets activated with these antibodies, increase their release of platelet factor 4 (PF4). Thus, a viscous cycle continues.