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.
Stirling
Y
Y
MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, Medical College of St Bartholomew's Hospital, London, UK.
D000818:Animals; D000925:Anticoagulants / Q000009:adverse effects* / Q000627:therapeutic use; D001779:Blood Coagulation Factors / Q000378:metabolism*; D003374:Coumarins / Q000009:adverse effects / Q000494:pharmacology; D006487:Hemostasis / Q000187:drug effects; D006801:Humans; D011486:Protein C / Q000378:metabolism; D017293:Protein S / Q000378:metabolism; D014812:Vitamin K / Q000502:physiology; D014813:Vitamin K Deficiency / Q000139:chemically induced; D014859:Warfarin / Q000008:administration & dosage / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use
D000925:Anticoagulants; D001779:Blood Coagulation Factors; D003374:Coumarins; D011486:Protein C; D017293:Protein S; D014812:Vitamin K; D014859:Warfarin