Department of Clinical Pharmacology, St Bartholomew's Hospital, London.
Br J Clin Pharmacol. 1974 Feb;1(1):59-66. doi: 10.1111/j.1365-2125.1974.tb00207.x.
1 Measurements have been made of steady state serum phenytoin concentration, serum half-life of (14)C-labelled phenytoin, and the urinary ratio of the major metabolite of phenytoin to the unchanged drug (p-HPPH: DPH ratio) in epileptic patients on and off sulthiame therapy. 2 Starting sulthiame treatment produced an increase in serum phenytoin concentration, a prolongation of the half-life and an increase in the p-HPPH: DPH ratio. The total urinary output of phenytoin plus p-HPPH was unaltered by sulthiame. 3 The results indicate that sulthiame or one of its metabolites inhibits the parahydroxylation of phenytoin by hepatic enzymes.
我们对正在使用和停用氨苯砜治疗的癫痫患者的稳态血清苯妥英浓度、（14）C 标记的苯妥英的血清半衰期以及苯妥英的主要代谢物与未改变的药物的尿比值（p-HPPH:DPH 比值）进行了测量。
氨苯砜治疗开始后，血清苯妥英浓度增加，半衰期延长，p-HPPH:DPH 比值增加。氨苯砜治疗并未改变苯妥英加 p-HPPH 的总尿排出量。
结果表明，氨苯砜或其代谢物之一抑制了肝酶对苯妥英的对羟化作用。
