Sjöqvist F, Bertilsson L
Adv Biochem Psychopharmacol. 1984;39:359-72.
There are marked interindividual differences in Css of tricyclic antidepressants. These are due mainly to corresponding differences in the rate of elimination of the drugs and hence in drug oxidation. Twin, family, and cross-over studies with NT and DMI show that their kinetics (Css, Kel, and Vd) are controlled mainly by genetic factors (in drug-free individuals). Slow hydroxylators are at risk of developing excessive plasma concentrations of NT and DMI when given per se or when formed from the tertiary amines AT and imipramine. Classic antidepressants have fairly well established concentration-effect curves in endogenous depression. Severe toxicity usually occurs at supratherapeutic plasma levels and might be prevented by tailoring the dosage according to the individual's drug hydroxylating capacity. Monitoring drug plasma levels is particularly relevant in slow hydroxylators. There is a strong association between an individual's ability to hydroxylate NT and DMI and his D hydroxylation phenotype. The ratios between D and 4-OH-D in urine after a single oral dose are bimodally distributed in the population (polymorphism), with 3 to 10% being slow hydroxylators and the remainder rapid hydroxylators. Indices of NT-hydroxylation do not sharply distinguish the two phenotypes. The D metabolic index will predict the patient's capacity to hydroxylate NT and DMI and hence Css during therapy. Possibly similar hydroxylases are involved in the 4-hydroxylation of debrisoquine, in the stereospecific E-10-hydroxylation of NT, and in the 2-hydroxylation of DMI. By contrast demethylation of AT (and probably other tertiary tricyclics) does not significantly correlate to debrisoquine hydroxylation. The increasing knowledge of the clinical pharmacokinetics of tricyclic antidepressants is a distinct advantage over that of the new generation of antidepressants, where little is known about concentration-effect relationships and factors governing their rate of metabolism.
三环类抗抑郁药的稳态血药浓度(Css)存在显著的个体间差异。这些差异主要是由于药物消除速率的相应差异,进而导致药物氧化的差异。对去甲替林(NT)和地昔帕明(DMI)进行的双生子、家族及交叉研究表明,它们的药代动力学(Css、消除速率常数[Kel]和分布容积[Vd])主要受遗传因素控制(在未用药个体中)。慢羟化者在单独使用NT和DMI或由叔胺类药物阿米替林(AT)和丙咪嗪形成NT和DMI时,有发生血浆药物浓度过高的风险。经典抗抑郁药在内源性抑郁症中有相当明确的浓度-效应曲线。严重毒性通常发生在超治疗血浆水平,可通过根据个体药物羟化能力调整剂量来预防。在慢羟化者中监测药物血浆水平尤为重要。个体羟化NT和DMI的能力与其D羟化表型之间存在很强的关联。单次口服给药后,尿中D与4-羟基-D的比值在人群中呈双峰分布(多态性),3%至10%为慢羟化者,其余为快羟化者。NT羟化指标不能清晰区分这两种表型。D代谢指标可预测患者羟化NT和DMI的能力,从而预测治疗期间的Css。参与去甲异喹胍4-羟化、NT立体特异性E-10-羟化以及DMI 2-羟化的羟化酶可能相似。相比之下,AT(可能还有其他叔胺类三环类药物)的去甲基化与去甲异喹胍羟化无显著相关性。与新一代抗抑郁药相比,对三环类抗抑郁药临床药代动力学的了解日益增多是一个明显优势,因为目前对新一代抗抑郁药的浓度-效应关系及其代谢速率的影响因素知之甚少。