Hamostaseologie 1988; 08(01): 8-17
DOI: 10.1055/s-0038-1659943
Originalarbeiten
Schattauer GmbH

Vitamin K und medikamenteninduzierte Hypoprothrombinämie

H. Bechtold
*   Caritaskrankenhaus, Bad Mergentheim
,
K. Andrassy
**   Medizinische Universitäts-Klinik, Heidelberg
› Author Affiliations
Further Information

Publication History

Publication Date:
25 June 2018 (online)

Zusammenfassung

Aus den vorliegenden Untersuchungen und aus den Mitteilungen der Literatur läßt sich auf die Bedeutung folgender zwei Faktoren für die Genese der Cephalosporin-induzierten HP schlieβen:

1. Latenter Vitamin-K-Mangelzustand des Organismus durch fehlende oder reduzierte exogene Vitamin-K-Zufuhr (z.B. bei ausschlieβlich parenteraler Ernährung) und möglicherweise durch Unterdrückung der Vitamin-K2-produzie-renden (Dünn-)Darmflora.

2. Kumarinartige Hemmung des Vit-amin-K1Stoffwechsels in der Leber durch bestimmte Cephalosporine (z.B. NMTT-Cephalosporine).

Das Zusammenwirken dieser Faktoren führt funktionell zu einem manifesten Vitamin-K-Mangelzustand, erkenntlich an einem Abfall der Vitamin-K-abhängigen Gerinnungsfaktoren. Aufgrund dieses Mechanismus ist es verständlich, daß die Cephalosporin-induzierte HP durch prophylaktische Vitamin-K1Gaben verhindert (ca. 10 mg Vitamin K1 pro Woche) bzw. eine manifeste HP korrigiert werden kann.

Der Vollständigkeit halber sei auf die hier nicht näher erläuterten Anta-bus®-ähnlichen Reaktionen nach Alkoholzufuhr hingewiesen, die - in Analogie zu der kumarinartigen Hemmung des Vitamin-K1Stoffwechsels -ebenfalls die Gruppe der NMTT- und MTD-Cephalosporine betreffen und durch entsprechende Alkoholkarenz vermeidbar sind (60).

 
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