Rifampin is a potent inducer of cytochrome P-450 oxidative enzymes. A few examples of well-documented clinically significant interactions include interactions with warfarin, oral contraceptives, cyclosporine, glucocorticoids, ketoconazole or itraconazole, theophylline, quinidine sulfate, digitoxin or digoxin, verapamil hydrochloride, human immunodeficiency virus-related protease inhibitors, zidovudine, delavirdine mesylate, nifedipine, and midazolam. Recent reports have demonstrated clinically relevant interactions with numerous other drugs, such as buspirone hydrochloride, zolpidem tartrate, simvastatin, propafenone hydrochloride, tacrolimus, ondansetron hydrochloride, and opiates. Rifabutin reduces serum concentrations of antiretroviral agents, but less so than rifampin. To avoid a reduced therapeutic response, therapeutic failure, or toxic reactions when rifampin is added to or discontinued from medication regimens, clinicians need to be cognizant of these interactions. Enhanced knowledge of known interactions will continue to develop, including research on the induction of specific cytochrome P-450 isoenzymes and on the importance of the P-glycoprotein transport system. New rifampin and rifabutin interactions will be discovered with further investigations.

To avoid a reduced therapeutic response, therapeutic failure, or toxic reactions when rifampin, rifabutin, or rifapentine are added to or discontinued from medication regimens, clinicians need to be aware of these interactions. Recent studies have indicated that other transporter systems play a role in these drug interactions. As reports of rifampin drug interactions continue to grow, this review is a reminder to clinicians to be vigilant.

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Rifampin, an antituberculosis agent, is usually administered for nine to 12 months with other antituberculosis drugs or drugs from other classes. A potential for drug interactions often exists because this drug is a potent inducer of drug metabolism. Rifampin causes a proliferation of the smooth endoplasmic reticulum and an increase in the cytochrome P-450 content in the liver. Rifampin's enzyme-induction effect is selective; therefore, it is not always clear which agents will be affected. Studies and case reports have demonstrated that rifampin accelerates the metabolism of several drugs, including oral anticoagulants, oral contraceptives, glucocorticoids, digitoxin, quinidine, methadone, hypoglycemics, and barbiturates. Rifampin interacts with other agents, but further study is needed to demonstrate the clinical importance of these interactions. In addition to inducing drug-metabolizing enzymes, rifampin may cause alterations in absorption and hepatic uptake. Future investigations will probably identify new rifampin drug interactions.

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Isoniazid inhibits the metabolism of several drugs, resulting in clinically significant interactions in some patients. Clinical trials and case reports have documented that isoniazid can cause increased phenytoin and carbamazepine serum concentrations and toxicity. In relatively high doses, isoniazid can also cause increased effect of theophylline and warfarin. Isoniazid inhibits metabolism of selected benzodiazepines and vitamin D. Inhibition of monoamine oxidase and histaminase by isoniazid can cause significant drug-food interactions. Food greatly decreases isoniazid bioavailability. Although probably best recognized as an inhibitor of drug metabolism, isoniazid has a biphasic effect of inhibition-induction on one cytochrome P450 isozyme, CYP2E1, which partially explains the interaction with acetaminophen and increased risk of hepatotoxicity. Continued investigations will likely result in discovery of new isoniazid interactions.