![]() ![]() The released microparticles increase the production of thrombin, which is responsible for the thrombotic events. 11,12 Platelet activation also leads to the release of PF4 from the granules, thereby perpetuating the cycle of complex formation and platelet activation. These anti-heparinPF4 complex antibodies activate platelets via FcγIIa receptors and cause the release of prothrombotic microparticles, platelet consumption, and thrombocytopenia. HIT occurs as a result of the binding of antibodies, typically immunoglobulin (Ig) G, to the heparin-PF4 complex. When heparin binds to PF4 a complex is formed that undergoes a conformational change and exposes new epitopes that act as immunogens. Heparin has a high affinity for platelet factor 4 (PF4), a positively charged tetrameric protein found in the alpha granules of platelets and on the surface of cells such as endothelial cells and platelets. Given the importance of this complication and the widespread use of heparins, HIT should be suspected in all patients treated with heparin who develop thrombocytopenia with or without thrombosis. 9 Consequently, the diagnosis of HIT is not straightforward and requires that other processes be ruled out this has meant that despite its seriousness, HIT is underdiagnosed. ![]() ![]() It has been calculated that 1 in every 100 patients who receive unfractionated heparin for at least 5 days develop HIT associated with thrombosis 8 however, up to 58% of critical patients admitted to hospital present thrombocytopenia not induced by heparin. Patients with HIT classically present absolute thrombocytopenia or a relative reduction in the number of platelets that is associated with an increase in the relative (odds ratio, 20-40) 1-5 and absolute frequency (risk of thrombosis, 30%-75%) of thrombosis. HIT is an autoimmune complication of treatment with heparins. Although bleeding is the most commonly diagnosed complication associated with the use of any type of heparin, another potentially more serious complication is heparin-induced thrombocytopenia (HIT). Heparin is currently the most widely used anticoagulant. En esta revisión se discute los aspectos diagnósticos y el manejo de este síndrome. Una vez que se confirma serológicamente el diagnóstico de TIH o la sospecha es alta, se debe suspender el tratamiento con heparina y valorar el tratamiento con anticoagulantes alternativos. La demostración de la activación plaquetaria dependiente de heparina con métodos antigénicos o funcionales confirma el diagnóstico. La monitorización del recuento plaquetario en pacientes que reciben heparina permite el diagnóstico precoz de la TIH. El síntoma principal es una trombocitopenia brusca, con una caída del 50% en el recuento plaquetario con respecto a los valores basales, y/o complicaciones trombóticas que aparecen 5 a 14 días tras el comienzo del tratamiento con heparina. Se debe a la formación de anticuerpos contra el complejo heparina-factor plaquetario 4, que secundariamente activa las plaquetas y la coagulación y finalmente produce un aumento en la formación de trombina. Todos los pacientes expuestos a heparina de cualquier tipo y a cualquier dosis están en riesgo de TIH. La complicación más común y reconocida del tratamiento con heparina es la hemorragia, pero una complicación potencialmente más peligrosa es el desarrollo de la trombocitopenia inducida por heparina (TIH). This review contains a discussion of the diagnosis and treatment of this syndrome. Once the diagnosis of HIT has been confirmed serologically or there is a high level of suspicion of HIT, heparin must be suspended and treatment with an alternative anticoagulant should be considered. Demonstration of heparin-dependent platelet activation using an antigen or functional assay confirms the clinical diagnosis. ![]() Heparin-induced thrombocytopenia can be detected early in patients receiving heparin by monitoring the platelet count. The main symptom is the sudden onset of thrombocytopenia involving a drop in the platelet count to less than 50% of the basal level, with or without the appearance of thrombotic complications some 5 to 14 days after the start of heparin therapy. It is due to the formation of antibodies against the heparinplatelet factor 4 complex, which cause secondary activation of platelets, coagulation and, finally, increased thrombin production. All patients exposed to heparin, irrespective of the dose and route of administration, are at risk of developing HIT. However, a potentially more dangerous complication is the development of heparin-induced thrombocytopenia (HIT). Hemorrhage is the most common and best-recognized complication of heparin treatment. ![]()
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