D‐thyroxine, clofibrate, and norethandrolone influence the pharmacologic effect of bishydroxycoumarin. In mice, D‐thyroxine inhibits the metabolism of bishydroxycoumarin as well as that of meperidine and pentobarbital; in man, the anticoagulant response to bishydroxycoumarin is increased at doses which do not change the rate of metabolism of the drug. Clofibrate does not affect bishydroxycoumarin metabolism in mice or in man but does increase the anticoagulant response to the drug in man. Norethandrolone also increases the anticoagulant response to bishydroxycoumarin in man without affecting the rate of metabolism of the drug. Since clinically effective doses of these three drugs do not decrease the concentration of vitamin K‐dependent clotting factors or affect the absorption, distribution, or metabolism of bishydroxycoumarin in man, it seems likely that they potentiate the pharmacologic effect of bishydroxycoumarin by increasing the affinity of the receptor site for the anticoagulant.
No takes yet. Share an insight, caveat, or question.
Schrogie et al. (1967) studied this question.