Amerikanische Gesellschaft für Hirudotherapie

Heparin-induced thrombocytopenia.

Research article published in Journal of thrombosis and haemostasis : JTH (2003)

Zuletzt aktualisiert: June 18, 2026Geprüft von: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Narrative reviewKlinische StudienChong · Journal of thrombosis and haemostasis : JTH, 2003

Abstract

Heparin-induced thrombocytopenia (HIT) is not only a common but also a potentially serious drug adverse effect. Unlike other drug-induced thrombocytopenias, HIT does not usually cause bleeding, but instead causes thrombosis. Thrombosis in HIT can lead to limb gangrene (requiring leg amputation) or even death. HIT is mediated by an antibody that recognizes an epitope on the platelet factor 4 (PF4)-heparin complex. The antibody-PF4-heparin complex binds to FcgammaRII receptors on the platelet surface and cross-links the receptors. This induces intense platelet activation and platelet aggregation, and simultaneously activates blood-coagulation pathways. These changes are probably the basis of the thrombotic events in HIT. Diagnosis of HIT should be made mainly on clinical criteria but should be confirmed whenever possible by laboratory tests, particularly in patients with comorbid conditions, in whom the diagnosis of HIT cannot be made with certainty without testing. The tests for HIT antibodies are either immunoassays (e.g. ELISA), or functional tests, (e.g. 14C-serotonin release assay). Once a clinical diagnosis of HIT is made, heparin should be ceased immediately and treatment with an alternative anticoagulant (such as danaparoid, r-hirudin or argatroban) commenced. This should continue for at least 5 days unless the diagnosis of HIT is subsequently proven to be incorrect. Warfarin should also be commenced when the patient is clinically stable and thrombosis is under control. There should be an overlap of a few days between warfarin and the alternative anticoagulant therapy.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal ArticleReview
Indexed MeSH termsAnimalsAnticoagulantsEndothelium, VascularEpitopesHeparinHumansImmunoassayMiceMice, TransgenicModels, BiologicalThrombocytopeniaThrombosis

Zusammenfassung

Heparin-induced thrombocytopenia.

Warum dies für die Hirudotherapie relevant ist

This review article covers the pathophysiology, diagnosis, and management of heparin-induced thrombocytopenia (HIT), describing it as an antibody-mediated prothrombotic disorder involving PF4-heparin immune complexes, platelet FcγRII receptor cross-linking, and platelet activation, and recommending cessation of heparin with initiation of alternative anticoagulants including r-hirudin. Relevant to ASH because it identifies recombinant hirudin as a recognized alternative anticoagulant for HIT management. Caveat: This is a general review that mentions r-hirudin only as one of several options (alongside danaparoid and argatroban) without providing detailed evidence specific to hirudin, and it does not address live leech therapy.

Zitation

Heparin-induced thrombocytopenia.

Chong · Journal of thrombosis and haemostasis : JTH, 2003

Verwandter klinischer Kontext

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