3.1. Vitamin K antagonists

The vitamin K-dependent coagulation factors II, VII, IX and X require γ-carboxylation for their procoagulant activity. Treatment with vitamin K antagonists results in the hepatic production of partially carboxylated and decarboxylated proteins with reduced coagulant activity. Among the most commonly used vitamin K antagonists are warfarin and acenocoumarol. Although vitamin K antagonists are absorbed quickly their full effect develops after about 5 days when the activity of all vitamin K-dependent coagulation factors is reduced [1].

Warfarin therapy requires regular laboratory monitoring with prothrombin time (PT). Due to different sensitivities of thromboplastin reagents used for PT measurement the results are expressed as the International Normalized Ratio (INR). For the majority of indications the target INR range falls between 2.0 and 3.0. In certain patient populations, for example, in patients with mechanical heart valves, the target range is 2.5–3.5 INR. A rare non-hemorrhagic side effect of vitamin K antagonist therapy is skin necrosis that develops at therapy initiation and is a consequence of acute thrombosis of subcutaneous venules and capillaries [1].
