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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