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Hamostaseologie 1999; 19(01): 30-41
DOI: 10.1055/s-0038-1660375
Übersichtsarbeiten/Review Articles
Schattauer GmbH

Differentialdiagnose der akuten Thrombozytopenie

V. Kiefel
1   Institut für Klinische Immunologie und Transfusionsmedizin, Universität Leipzig
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Publication Date:
27 June 2018 (online)

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Zusammmenfassung

Akut eintretende Thrombozytopenien werden häufig durch pathophysiologische Vorgänge ausgelöst, die einen beschleunigten Abbau oder Verbrauch von Plättchen bedingen. Thrombozytäre Autoantikörper lassen sich bei unterschiedlichen Verlaufsformen von Autoimmunthrombozytopenie nachweisen: der akuten postinfektiösen Autoimmunthrombozytopenie, der chronischen AITP und der zyklisch verlaufenden Thrombozytopenie. Medikament-induzierte Immunthrombozytope-nien werden entweder durch Medikament-abhängige Antikörper verursacht oder durch thrombozytäre Autoantikörper. Beide Typen von Antikörpern reagieren mit Determinanten auf den thrombozytären Glykoproteinen llb/llla, Ib/IX oder V. Die seltene, als Komplikation von Transfusionen auftretende posttransfusionelle Purpura entsteht im Rahmen einer »überschießenden« Alloimmunreaktion gegen Plättchenantigene. Charakteristisch für thrombotisch-thrombozytopenische Purpura und hämolytisch-urämisches Syndrom sind ein durch Aktivierung von Plättchen ausgelöster, beschleunigter Abbau und eine Hämolyse, klinisch kommt es zu Symptomen im Bereich des ZNS und der Nieren. Durch einen erhöhten Verbrauch bedingt kommt es auch bei Patienten mit einer Verbrauchs-koagulopathie zu einer Thrombozytopenie.

Schlüsselwörter

Thrombozytopenie - Purpura - hämolytisch-urämisches Syndrom - disseminierte intravasale Gerinnung - thrombozytäre Antikörper
 

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