Oral anticoagulants

Vitamin K antagonists (oral anticoagulants)

Vitamin K antagonists of oral anticoagulants or coumarin derivatives diminish the availability of vitamin K. Synthesis of various coagulation factors in the liver is dependent on vitamin K. During carboxylation of glutamic acid residues (Glu) of these factors into gamma-carboxyglutamic acid (Gla) residues reduced vitamin K (hydroquinone) acts as a co-factor and is oxidized to vitamin K epoxide. Subsequently, vitamin K epoxide is reduced again in two steps to vitamin K hydroquinone. Coumarin derivatives inhibit the enzymes responsible for the reduction process (vitamin K epoxide reductase or VKOR), resulting in less available reduced vitamin K, decreased gamma-carboxylation and impaired function of these coagulation factors. The Gla-residues are necessary for binding calcium ions resulting in conformational change and binding to phospholipid surfaces through which the efficacy

of the coagulation process is increased.

Coumarin derivatives (acenocoumarol, fenprocoumon) are widely used for the prevention and treatment of arterial and venous thromboembolism (deep vein thrombosis, pulmonary embolism, atrial fibrillation, artificial heart valves). Bleeding is the major adverse effect of coumarin treatment. Coumarins have important interactions with many other drugs. Examples of drugs that potentiate the action of coumarins are amiodarone, miconazol, metronidazole, and thyroxin. Other drugs inhibit the action of coumarins (aminoglutethimide, barbiturates, carbamazepin, phenytoin, rifampicin).


What is true about acenocoumarol?


What is true about acenocoumarol? 


The monitoring of the effect of coumarins is best done by