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首页> 外文期刊>Human psychopharmacology: clinical and experimental >No evidence of increased adverse drug reactions in cytochrome P450 CYP2D6 poor metabolizers treated with fluoxetine or nortriptyline.
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No evidence of increased adverse drug reactions in cytochrome P450 CYP2D6 poor metabolizers treated with fluoxetine or nortriptyline.

机译：没有证据表明增加药物不良反应细胞色素P450 CYP2D6可怜的代谢治疗与氟西汀或去甲替林。

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摘要

The polymorphic enzyme cytochrome P450 CYP2D6 is involved in the metabolism of many antidepressants, including nortriptyline and fluoxetine. Some 7%-10% Caucasians have inactivating mutations in both alleles of the CYP2D6 gene, and are referred to as poor metabolizers (PMs). Several case reports and clinical studies suggest that CYP2D6 PMs are at a greater risk of developing adverse drug reactions (ADRs) on antidepressant medication than extensive metabolizers (EMs). However, few clinical trials have investigated whether CYP2D6 PM genotype is predictive of ADRs during antidepressant treatment. This paper explores the link between CYP2D6 genotype and antidepressant-associated ADRs in outpatients being treated for major depression with either nortriptyline or fluoxetine. Patients were randomized to fluoxetine (n=65) or nortriptyline (n=60) for the 6 week trial. CYP2D6 genotypes predicted that of these patients 115 were EM and the remaining 10 were PMs. ADRs attributed to antidepressant usage were recorded over the 6-week trial. Although the type of ADR was, as expected, different between drugs, the frequency of ADRs experienced did not differ significantly between the two antidepressants or between CYP2D6 PMs and EMs. In addition, the frequency at which PMs discontinued antidepressant medication was not noticeably different from EMs, although with only 10 PMs the study is under powered to detect moderate or small differences. These findings suggest that inability to efficiently metabolize antidepressants that are CYP2D6 substrates does not necessarily lead to increased occurrence of antidepressant-associated ADRs. Thus, for clinicians prescribing antidepressant monotherapy, CYP2D6 polymorphisms are probably not of relevance to antidepressant side effects and therapy.
机译：多态CYP2D6酶细胞色素P450参与许多代谢抗抑郁药物,包括去甲替林和氟西汀。灭活突变的等位基因CYP2D6基因,被称为差的代谢(PMs)。临床研究表明,CYP2D6在经前综合症大的发展中国家药品不良反应风险抗抑郁药物比(adr)广泛的代谢(EMs)。临床试验是否CYP2D6调查基因型是下午预测期间的adr抗抑郁药物治疗。CYP2D6基因型之间的联系antidepressant-associated adr在门诊接受治疗的抑郁症去甲替林、氟西汀。随机氟西汀(n = 65)或去甲替林6周(n = 60)试验。115 EM和预测,这些病人剩下的10 pm。抗抑郁药物使用记录的六周的审判。预期,不同药物、频率adr的经历没有显著差异两者之间的抗抑郁药物或CYP2D6之间经前综合症和EMs。PMs停用抗抑郁药物没有明显不同于EMs,虽然只有10 pm动力检测下的研究中等或小的差异。表明,无法有效地代谢抗抑郁药CYP2D6的基质不一定会增加发生的antidepressant-associated adr。临床医生处方抗抑郁单一疗法,CYP2D6多态性可能是不相关的抗抑郁药物的副作用和治疗。

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