September 1970

Studies of the Epidemiology of Anticoagulant-Drug Interactions

Author Affiliations

Rochester, NY

From the University of Rochester School of Medicine, Rochester, NY. Dr. Kleinman is now with the University of Pittsburgh School of Medicine, Pittsburgh. Dr. Griner is a fellow of the Life Insurance Foundation in Health Care Administration.

Arch Intern Med. 1970;126(3):522-523. doi:10.1001/archinte.1970.00310090152022

In recent years, a number of drugs have been identified which may alter the response to oral anticoagulants in man. Phenylbutazone and its congeners are probably the most widely recognized drugs capable of enhancing the hypoprothrombinemic action of oral anticoagulants. Other drugs which may enhance the anticoagulant response include acetaminophen, antibiotics, clofibrate, diphenylhydantoin, disulfiram, indomethacin, methylphenidate hydrochloride, methandrostenolone and norethandrolone, phenyramidol hydrochloride, quinidine and quinine, salicylates, thiouracils, and dextrothyroxine sodium. Conversely, barbiturates may decrease the anticoagulant effect of coumarin drugs and necessitate larger doses for effective anticoagulation. The failure to anticipate a reduced coumarin requirement when the barbiturate is discontinued may result in excessive anticoagulation. A similar effect has been demonstrated for the following drugs: antacids, chloral hydrate, cholestyramine resin, corticosteroids, ethchlorvynol, glutethimide, griseofulvin, haloperidol, meprobamate, and contraceptives administered orally. Mechanisms responsible for these interactions have been elucidated for a number of drugs.1-10 Numerous case reports confirm bleeding complications

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