Beszłej Jan Aleksander, Grzesiak Magdalena, Milejski Piotr
Katedra i Klinika Psychiatrii AM we Wrocławiu.
Psychiatr Pol. 2007 Jul-Aug;41(4):495-501.
The authors describe the case of a female patient with the diagnosis of schizophrenia and the CYP2D6 poor metaboliser phenotype (PM phenotype), who experienced severe extrapyramidal side effects, including acute dystonia, while being treated with chloropromazine at 100 mg per day (in the third day of therapy). The CYP2D6 phenotype was determined using the sparteine test before and after 3 days of treatment. Metabolic ratio increased 12 times during treatment, from initial 30 to 355. The authors conclude that CYP2D6 poor phenotype leading to slow chloropromazine metabolism, which was further inhibited by chloropromazine during treatment (as chlorpromazine is a strong CYP2D6 enzyme inhibitor) had significant importance on the occurrence of acute extrapyramidal side effects. Most likely the antidopaminergic influence of the drug on the CNS was much more marked due to an inhibition of chlorpromazine metabolism leading probably to an increase of the chlorpromazine blood level.
作者描述了一名被诊断为精神分裂症且具有细胞色素P450 2D6(CYP2D6)慢代谢型(PM型)的女性患者的病例。该患者在每天服用100毫克氯丙嗪治疗期间(治疗第三天)出现了严重的锥体外系副作用,包括急性肌张力障碍。在治疗前及治疗3天后,通过司巴丁试验确定CYP2D6表型。治疗期间代谢率从最初的30增加到355,增加了12倍。作者得出结论,CYP2D6慢代谢型导致氯丙嗪代谢缓慢,而氯丙嗪在治疗期间进一步抑制了其代谢(因为氯丙嗪是一种强效的CYP2D6酶抑制剂),这对急性锥体外系副作用的发生具有重要意义。很可能由于氯丙嗪代谢受到抑制,导致氯丙嗪血药浓度升高,药物对中枢神经系统的抗多巴胺能作用更加明显。