Drugs may interact with warfarin through pharmacodynamic or pharmacokinetic 
mechanisms. Examples of the former include alteration of the bioavailability of 
vitamin K by antibiotics, mineral oils or cholestyramine; oestrogens, diuretics 
and hypolipidaemic agents such as clofibrate may influence vitamin K-dependent 
clotting factor synthesis, and drugs which affect haemostasis, e.g. via platelet 
function, will enhance the anticoagulant effect of warfarin. Pharmacokinetic 
interactions are better understood. Few drugs have been shown to alter warfarin 
absorption, the importance of protein binding displacement has been exaggerated, 
and since warfarin is not eliminated to any extent unchanged by the kidney, the 
most important kinetic interactions are those due to inhibition or induction of 
its hepatic metabolism. Isomeric differences in metabolism form an important 
basis for stereoselective metabolic interactions, especially inhibition; this 
has been demonstrated with phenylbutazone, metronidazole and co-trimoxazole. 
Enzyme induction, although recognised for many years, may still pose problems in 
therapeutics, usually on withdrawal of the inducing agent.