Kneiseler G, Canbay A, Gerken G
Klinik für Gastroenterologie und Hepatologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstr. 55, 45122, Essen, Deutschland.
Herz. 2012 Jun;37(4):395-401. doi: 10.1007/s00059-012-3620-2.
Vitamin K antagonists are often used as oral anticoagulants for primary and secondary prevention of thromboembolic events. Vitamin K antagonists induce an anticoagulant effect by interfering with the vitamin K metabolism in the liver. Well-known complications are bleeding events and skin necrosis. Recent data indicate increasing numbers of cases with hepatic complications due to vitamin K antagonists ranging from mild hepatopathy to acute liver failure with high mortality. Hepatotoxicity is usually developed after a few months of latency, which is associated with unspecific symptoms, jaundice, elevated transaminase levels as well as cholestatic enzymes. Hepatotoxicity due to vitamin K antagonists is seldom; however, it should be considered in cases of elevated liver enzymes. In this case coumarin therapy should be discontinued. Caution is needed when changing to another coumarin derivative because cross-reactivity has been described.