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DOI: 10.1055/s-0037-1619499
Hämostasestörungen durch Antibiotika
Disturbed hemostasis subsequent to antibioticsPublikationsverlauf
Publikationsdatum:
27. Dezember 2017 (online)

Zusammenfassung
Hämostasestörungen durch Antibiotika können sowohl die plasmatischen Komponenten des Gerinnungssystems als auch die Thrombozyten betreffen. Ersteres beinhaltet eine verminderte Bildung von Vitamin-K-abhängigen Gerinnungsfaktoren durch Zerstörung der Vitamin-K-bildenden Darmflora (z.B. ß-Laktamantibiotika) und/oder Hemmung der Vitamin-K-Epoxidhydrolase (NMMT-substituierte Zephalosporine) mit nachfolgender Hypoprothrombinämie. Eine Immunthrombozytopenie tritt vor allem nach Trimethoprim/Sulfmethoxazol und anderen Sulfonamidantibiotika auf, ist aber auch für andere Antibiotika gut dokumentiert. Darüber hinaus wird eine direkte Hemmung der Plättchenfunktion durch Interferenz mit der Bindung von Agonisten (ADP, Adrenalin) vorwiegend für Penizilline und einige Zephalosporine beschrieben. Das klinische Bild dieser erworbenen Hämostasestörungen ist zusätzlich durch Risikofaktoren seitens des Patienten bestimmt. Erschwerend wirken schlechter Ernährungsszustand (Hypalbuminämie), parenterale Ernährung (niedriger Vitamin-K-Plasmaspiegel), Niereninsuffizienz (reduzierte Antibiotika-Clearance) und Komedikation zytotoxischer Substanzen (Zytostatika). Therapieoptionen sind neben dem Absetzen der Substanz in Abhängigkeit von Ursache und Schweregrad der Hämostasestörung Vitamin K1, Plättchenkonzentrate oder Frisch-(gefrorenes)Plasma.
Summary
Disturbed hemostasis subsequent to intake of antibiotics might affect both the plasmatic coagulation as well as platelet aggregation. Disturbed plasmatic coagulation is caused by reduced generation of vitamin K-dependent clotting factors subsquent to elimination of vitamin K-producing microorganisms in the gut (e. g. ß-lactam antibiotics) and/or inhibition of the vitamin K-epoxyidhydrolase (NMMT-substituted cephalosporins), eventually resulting in hypoprothrombinemia. Immunthrombocytopenias are observed particularly with the use of trimethoprime/sulfmethoxazole and other sulfonamides, but have also been described for a variety of other antibiotics. In contrast, direct inhibition of platelet function caused by interference with platelet agonists (ADP, adrenaline) appears to be specific for penicillines and several cephalosporins. The clinical picture of these acquired disorders in hemostasis is additionally determined by risk factors at the patient´s site. Aggravation is seen in malnutrition (hypalbuminemia), parenteral nutrition (reduced vitamin K-plasma level), renal failure (reduced antibiotic clearance) and comedication of cytotoxic drugs (cytostatics). Therapeutic options besides removal of the drug in dependency on cause and severity of the disease include vitamin K1 administration, administration of platelet concentrates and of fresh-frozen plasma.
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