Warfarin is used for chronic oral anticoagulation in a variety of clinical settings. Management of warfarin therapy is usually by following the prothrombin time, rather than by measuring serum drug concentrations. Warfarin is subject to a bewildering number and variety of drug interactions, producing increased or decreased clinical effect of itself or other drugs. Many of these effects are due to changes in protein binding or hepatic metabolism. Reductions in dosage may be indicated for aging subjects treated for venous thromboembolic or coronary arterial disease, but not in those with peripheral vascular disease, deep vein thrombosis, or valvular heart disease.1,2 Warfarin is intermediate acting; a peak effect is achieved in 36-72 hours and the anticoagulant effect persists for 2-5 days. The drug is rapidly and completely absorbed from the gastrointestinal tract. The delay in achieving the peak effect results from the long half-lives of clotting factors II, IX, and X, whose levels must decline before maximal anticoagulation is reached. Warfarin is highly lipophilic and is 99% bound to albumin. Some tissue binding occurs, particularly in the liver. However, only the unbound drug is active and available for hydroxylation in the liver.
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