Hamostaseologie 1999; 19(01): 1-12
DOI: 10.1055/s-0038-1660372
Übersichtsarbeiten/Review Articles
Schattauer GmbH

Heparin-induzierte Thrombozytopenie – Pathogenese und Behandlung

A. Greinacher
1   Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald
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Publikationsverlauf

Publikationsdatum:
27. Juni 2018 (online)

Zusammenfassung

Heparin bindet aufgrund seiner negativen Ladung an Thrombozytenproteine. Hierdurch werden Thrombozyten leicht aktiviert. Dies kann bei Krankheiten, bei denen per se die Thrombozyten aktiviert sind, z.B. periphere arterielle Verschlußkrankheiten, zum Abfall der Thrombozyten führen. Diese nicht-immunologischen Wechselwirkungen von Heparin und Thrombozyten sind klinisch von untergeordneter Bedeutung. Viel wichtiger, da in einigen Fällen mit lebensbedrohlichen neuen thromboembolischen Komplikationen verbunden, ist die immunologische Heparin-induzierte Thrombozytopenie (HIT). Betroffene Patienten bilden Antikörper, die an Komplexe aus Thrombozytenproteinen und Heparin binden. Diese Immunkomplexe aktivieren Thrombozyten und Endothelzellen. Dies führt zu einer massiven Verstärkung der Thrombinbildung mit der Konsequenz der Gerinnungsaktivierung. Daher müssen betroffene Patienten weiter antikoaguliert werden. Hierfür stehen vor allem zwei Medikamente zur Verfügung: Rekombinantes Hirudin (Lepirudin, Refludan®) und Danaparoid-Natrium (Orgaran®). Hirudin ist ein direkter Thrombininhibitor, Danaparoid-Natrium zeigt vor allem Anti-Faktor-Xa-Aktivität. Die wichtigsten Therapieoptionen bei ङ IT-Patienten werden in dem Artikel diskutiert.

 
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