Warfarin-induced changes in procoagulant and anticoagulant proteins.

Dicoumarol was found to be the causative agent of a haemorrhagic disease in cattle following the ingestion of spoiled sweet clover. Vitamin K deficiency in chickens caused bleeding. Dicoumarol was later determined to be a vitamin K antagonist. A more potent form of the drug was produced synthetically and, following its initial use as rat poison, was recognized as a potential anti-thrombotic treatment in humans. The mode of action of a coumarin derivative (i.e. warfarin) is described. The overall effect of high-dose and low-dose warfarin and the possibility of a transient state of hypercoagulability on the introduction and withdrawal of treatment is considered.