Tsuchihashi K, Fukami K, Kishimoto H, Sumiyoshi T, Haze K, Saito M, Hiramori K
Department of Internal Medicine, National Cardiovascular Center, Osaka, Japan.
Heart Vessels. 1987;3(4):214-7. doi: 10.1007/BF02058314.
Rifampicin, an antituberculosis agent, is known to be a potent inducer of microsomal drug-metabolizing enzymes in the liver. Elimination or clearance of many drugs has been reported to be enhanced, and their effectiveness reduced; however, no report in the literature has dealt with the interaction between rifampicin and dihydropiridine calcium entry-blocking drugs such as nifedipine. We present here evidence for the possible interaction between rifampicin and nifedipine in a patient with angina pectoris, which was exacerbated during coadministration or rechallenge with rifampicin. The peak plasma level and area under the curve were reduced and the apparent oral clearance of nifedipine was increased by rifampicin, suggesting that rifampicin enhanced the elimination of nifedipine via induction of a hepatic microsomal drug-metabolizing enzyme, as has been reported on other drugs widely metabolized in the liver.
利福平是一种抗结核药物,已知它是肝脏微粒体药物代谢酶的强效诱导剂。据报道,许多药物的消除或清除会增强,其有效性会降低;然而,文献中没有关于利福平与二氢吡啶类钙通道阻滞剂(如硝苯地平)之间相互作用的报道。我们在此展示了一名心绞痛患者中利福平与硝苯地平可能存在相互作用的证据,该患者在联合使用利福平或再次使用利福平时病情加重。利福平降低了硝苯地平的血浆峰值水平和曲线下面积,并增加了硝苯地平的表观口服清除率,这表明利福平通过诱导肝脏微粒体药物代谢酶增强了硝苯地平的消除,正如其他在肝脏中广泛代谢的药物所报道的那样。