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吸烟与艾司西酞普兰的剂量校正血清浓度降低有关。

Smoking Is Associated With Lower Dose-Corrected Serum Concentrations of Escitalopram.

机构信息

From the Department of Psychiatry, Psychosomatics and Psychotherapy, University Hospital of Würzburg, Würzburg, Germany.

出版信息

J Clin Psychopharmacol. 2019 Sep/Oct;39(5):485-488. doi: 10.1097/JCP.0000000000001080.

Abstract

BACKGROUND

Tobacco smoking rates in depressive patients are higher compared with the general population. Smoking was demonstrated to accelerate the metabolism of different drugs metabolized by CYP1A2, but possibly also by CYP2C19 and CYP3A4. The principle aim of the present investigation from 2015 to 2018 was to determine the differences in the pharmacokinetics of escitalopram between smokers and nonsmokers.

METHODS

A group of nonsmokers (n = 88) was compared with smokers (n = 36), both receiving escitalopram, using the Mann-Whitney U test. Linear regression analysis was used to account for the impact of escitalopram dose, age, and sex in addition to smoking on the steady-state serum concentration of escitalopram.

RESULTS

Smokers received by mean 17.6% higher doses of escitalopram (P = 0.026) but showed 31.9% lower serum concentrations (P = 0.031). To control for confounders, linear regression analysis showed that dose (P < 0.001), sex (P = 0.03), and smoking tobacco (P = 0.027) did significantly influence serum concentrations of escitalopram with higher levels in women and nonsmokers.

CONCLUSIONS

Notwithstanding higher daily doses, smokers had significantly lower serum concentrations of escitalopram. In concordance with previous results, besides CYP1A2, a possible induction of CYP2C19 and CYP3A4 by tobacco smoke, resulting in lower serum concentrations of escitalopram in smokers than in nonsmokers, is suggested. Therefore, to provide personalized therapy, clinicians should consider smoking status and inform patients on the interactions of smoking and escitalopram metabolism.

摘要

背景

与普通人群相比,抑郁患者的吸烟率更高。吸烟被证明可以加速不同由 CYP1A2 代谢的药物的代谢,但也可能由 CYP2C19 和 CYP3A4 代谢。本研究于 2015 年至 2018 年进行,旨在确定吸烟与非吸烟患者之间艾司西酞普兰的药代动力学差异。

方法

使用曼-惠特尼 U 检验将一组非吸烟者(n = 88)与吸烟者(n = 36)进行比较,两组均接受艾司西酞普兰治疗。线性回归分析用于考虑艾司西酞普兰剂量、年龄和性别以及吸烟对艾司西酞普兰稳态血清浓度的影响。

结果

吸烟者接受的艾司西酞普兰剂量平均高 17.6%(P = 0.026),但血清浓度低 31.9%(P = 0.031)。为了控制混杂因素,线性回归分析表明剂量(P < 0.001)、性别(P = 0.03)和吸烟(P = 0.027)显著影响艾司西酞普兰的血清浓度,女性和不吸烟者的水平更高。

结论

尽管每日剂量较高,但吸烟者的艾司西酞普兰血清浓度明显较低。与先前的结果一致,除了 CYP1A2 外,烟草烟雾可能诱导 CYP2C19 和 CYP3A4,导致吸烟者的艾司西酞普兰血清浓度低于非吸烟者,因此,为了提供个体化治疗,临床医生应考虑吸烟状况,并告知患者吸烟和艾司西酞普兰代谢的相互作用。

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