Spina E, Martines C, Caputi A P, Cobaleda J, Piñas B, Carrillo J A, Benitez J
Institute of Pharmacology, School of Medicine, University of Messina, Italy.
Eur J Clin Pharmacol. 1991;41(5):467-70. doi: 10.1007/BF00626371.
The debrisoquine oxidation phenotype was determined in 91 schizophrenic patients on monotherapy with different neuroleptics and in 67 untreated healthy volunteers. The prevalence of poor metabolizers of debrisoquine was significantly higher in the patients (46.2%) than in the healthy subjects (7.5%). Treatment with phenothiazine antipsychotics (chlorpromazine, levomepromazine and thioridazine) was associated with a higher debrisoquine metabolic ratio than treatment with haloperidol. On the other hand, treatment with clothiapine appeared not to interfere with debrisoquine oxidation. Oral administration of 50 mg thioridazine daily to 8 healthy subjects resulted in a marked increase in the debrisoquine metabolic ratio and 4 of them were transformed into phenotypically poor metabolizers. The results confirm the fact that phenothiazines, and to a lesser extent haloperidol, inhibit the oxidative metabolism of debrisoquine. They show also that clothiapine administration does not disturb the debrisoquine metabolic ratio.
对91例接受不同抗精神病药物单一疗法的精神分裂症患者以及67名未经治疗的健康志愿者进行了异喹胍氧化表型测定。异喹胍代谢不良者在患者中的患病率(46.2%)显著高于健康受试者(7.5%)。与使用氟哌啶醇治疗相比,使用吩噻嗪类抗精神病药物(氯丙嗪、左美丙嗪和硫利达嗪)治疗时异喹胍代谢率更高。另一方面,使用氯氮平治疗似乎不会干扰异喹胍氧化。每天给8名健康受试者口服50mg硫利达嗪导致异喹胍代谢率显著增加,其中4人转变为表型代谢不良者。结果证实了吩噻嗪类药物以及在较小程度上氟哌啶醇会抑制异喹胍氧化代谢这一事实。研究还表明,服用氯氮平不会干扰异喹胍代谢率。