Eichelbaum M, Köthe K W, Hoffman F, von Unruh G E
Clin Pharmacol Ther. 1979 Sep;26(3):366-71. doi: 10.1002/cpt1979263366.
The kinetics of carbamazepine using 15N-carbamazepine were investigated in epileptic patients during combined anticonvulsant therapy. The 15N-carbamazepine plasma half-lives ranged from 5.0 to 13.6 hr with a mean of 8.2 hr. These half-lives are appreciably shorter than reported during chronic carbamazepine monotherapy. Predicted steady-state plasma levels and observed plasma levels of carbamazepine were in excellent agreement. Between 32% and 61% of the dose administered is excreted in the urine as carbamazepine-trans-diol, 5.2% to 8.8% as 9-hydroxymethyl-10-carbamoyl acridane, 1% to 1.4% as 10,-11-carbamazepine epoxide, and 0.5% as carbamazepine. The data indicate that it is the epoxide-diol pathway which is induced during long-term treatment. Concomitant therapy with primidone, phenytoin, phenobarbital, ethosuximide, or methsuximide further induces carbamazepine metabolism.
在癫痫患者联合抗惊厥治疗期间，使用15N-卡马西平研究了卡马西平的动力学。15N-卡马西平的血浆半衰期为5.0至13.6小时，平均为8.2小时。这些半衰期明显短于慢性卡马西平单药治疗期间报告的半衰期。卡马西平的预测稳态血浆水平与观察到的血浆水平高度一致。给药剂量的32%至61%以卡马西平反式二醇的形式经尿液排泄，5.2%至8.8%以9-羟甲基-10-氨甲酰吖啶的形式排泄，1%至1.4%以10,11-卡马西平环氧化物的形式排泄，0.5%以卡马西平的形式排泄。数据表明，长期治疗期间诱导的是环氧化物-二醇途径。与扑米酮、苯妥英、苯巴比妥、乙琥胺或甲琥胺联合治疗可进一步诱导卡马西平代谢。
