Heparin induced thrombocytopenia.
Research article published in The Journal of the Association of Physicians of India (2008)
Abstract
Heparin induced thrombocytopenia (HIT) is a serious and life endangering complication of heparin therapy. It usually occurs after 5-14 days of continuous heparin therapy. It is immune mediated. Heparin, in the affected individual binds with platelet factor 4 (PF-4) and forms a highly antigenic Heparin PF-4 complex which leads to the generation of specific IgG Heparin PF4 antibodies (also called HIT antibodies). HIT antibodies may activate the platelets via Fcy receptor causing the release of highly coagulable micro particles which promote thrombosis--both venous and arterial. However, all patients with HIT antibodies do not progress to HIT with thrombosis (HITT). HIT can present as asymptomatic thrombocytopenia. It can also present with alarming features of venous and/or arterial thromboembolism, for example, pulmonary embolism from deep vein thrombosis (DVT), limb gangrene warranting amputation, cerebrovascular attack (CVA) or myocardial infarction (MI). Rare manifestation of HIT includes necrotizing skin lesion, acute anaphylactoid reaction following IV heparin bolus and acute adrenal apoplexy due to massive adrenal vein thrombosis. The diagnosis is based upon the combination of unexplained thrombocytopenia, demonstration of HIT antibodies, clinical profile and outcome of the case following withdrawal of heparin and administration of non-heparin anticoagulant like Lepirudin, Argatroban or Danaparoid. The choice of alternative anticoagulant depends upon the availability, cost, monitoring facilities and administrative guidelines.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Resumen
Heparin induced thrombocytopenia.
Por qué esto importa para la hirudoterapia
Este artículo revisa la fisiopatología, la presentación clínica y el manejo de la trombocitopenia inducida por heparina (TIH), una complicación potencialmente mortal de la terapia con heparina. Destaca la retirada de la heparina y la administración de anticoagulantes alternativos, nombrando explícitamente la lepirudina como una opción. La lepirudina es una forma recombinante del anticoagulante derivado de la sanguijuela hirudina, lo que conecta este artículo con la aplicación farmacéutica de componentes salivales de la sanguijuela. Sin embargo, el estudio se enfoca ampliamente en el manejo de la TIH y no investiga sanguijuelas vivas ni el potencial terapéutico más amplio del secretoma natural de la sanguijuela, lo que hace que su relevancia para la ASH sea puramente indirecta.
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Añadido a la biblioteca ASH: May 28, 2026 · Última actualización del sitio: June 18, 2026