Staatz Christine E, Tett Susan E
School of Pharmacy, The University of Queensland, Brisbane, Queensland, Australia.
Clin Pharmacokinet. 2004;43(10):623-53. doi: 10.2165/00003088-200443100-00001.
The aim of this review is to analyse critically the recent literature on the clinical pharmacokinetics and pharmacodynamics of tacrolimus in solid organ transplant recipients. Dosage and target concentration recommendations for tacrolimus vary from centre to centre, and large pharmacokinetic variability makes it difficult to predict what concentration will be achieved with a particular dose or dosage change. Therapeutic ranges have not been based on statistical approaches. The majority of pharmacokinetic studies have involved intense blood sampling in small homogeneous groups in the immediate post-transplant period. Most have used nonspecific immunoassays and provide little information on pharmacokinetic variability. Demographic investigations seeking correlations between pharmacokinetic parameters and patient factors have generally looked at one covariate at a time and have involved small patient numbers. Factors reported to influence the pharmacokinetics of tacrolimus include the patient group studied, hepatic dysfunction, hepatitis C status, time after transplantation, patient age, donor liver characteristics, recipient race, haematocrit and albumin concentrations, diurnal rhythm, food administration, corticosteroid dosage, diarrhoea and cytochrome P450 (CYP) isoenzyme and P-glycoprotein expression. Population analyses are adding to our understanding of the pharmacokinetics of tacrolimus, but such investigations are still in their infancy. A significant proportion of model variability remains unexplained. Population modelling and Bayesian forecasting may be improved if CYP isoenzymes and/or P-glycoprotein expression could be considered as covariates. Reports have been conflicting as to whether low tacrolimus trough concentrations are related to rejection. Several studies have demonstrated a correlation between high trough concentrations and toxicity, particularly nephrotoxicity. The best predictor of pharmacological effect may be drug concentrations in the transplanted organ itself. Researchers have started to question current reliance on trough measurement during therapeutic drug monitoring, with instances of toxicity and rejection occurring when trough concentrations are within 'acceptable' ranges. The correlation between blood concentration and drug exposure can be improved by use of non-trough timepoints. However, controversy exists as to whether this will provide any great benefit, given the added complexity in monitoring. Investigators are now attempting to quantify the pharmacological effects of tacrolimus on immune cells through assays that measure in vivo calcineurin inhibition and markers of immunosuppression such as cytokine concentration. To date, no studies have correlated pharmacodynamic marker assay results with immunosuppressive efficacy, as determined by allograft outcome, or investigated the relationship between calcineurin inhibition and drug adverse effects. Little is known about the magnitude of the pharmacodynamic variability of tacrolimus.
本综述的目的是批判性地分析近期关于实体器官移植受者中他克莫司临床药代动力学和药效学的文献。他克莫司的剂量和目标浓度建议因中心而异,且药代动力学变异性大,难以预测特定剂量或剂量变化会达到何种浓度。治疗范围并非基于统计学方法。大多数药代动力学研究涉及在移植后即刻对小的同质群体进行密集采血。大多数研究使用非特异性免疫测定法,且提供的药代动力学变异性信息很少。寻求药代动力学参数与患者因素之间相关性的人口统计学调查通常一次只研究一个协变量,且涉及的患者数量较少。据报道,影响他克莫司药代动力学的因素包括所研究的患者群体、肝功能不全、丙型肝炎状态、移植后的时间、患者年龄、供肝特征、受者种族、血细胞比容和白蛋白浓度、昼夜节律、食物摄入、皮质类固醇剂量、腹泻以及细胞色素P450(CYP)同工酶和P-糖蛋白表达。群体分析增进了我们对他克莫司药代动力学的理解,但此类研究仍处于起步阶段。相当一部分模型变异性仍无法解释。如果将CYP同工酶和/或P-糖蛋白表达视为协变量,群体建模和贝叶斯预测可能会得到改进。关于他克莫司低谷浓度是否与排斥反应相关的报道相互矛盾。几项研究表明高谷浓度与毒性,尤其是肾毒性之间存在相关性。药理效应的最佳预测指标可能是移植器官本身的药物浓度。研究人员已开始质疑治疗药物监测期间目前对谷浓度测量的依赖,当谷浓度在“可接受”范围内时仍会出现毒性和排斥反应的情况。通过使用非谷时间点可以改善血药浓度与药物暴露之间的相关性。然而,鉴于监测的复杂性增加,对于这是否会带来任何巨大益处仍存在争议。研究人员目前正试图通过测量体内钙调神经磷酸酶抑制作用和免疫抑制标志物(如细胞因子浓度)的测定来量化他克莫司对免疫细胞的药理作用。迄今为止,尚无研究将药效学标志物测定结果与通过移植物结果确定的免疫抑制疗效相关联,也未研究钙调神经磷酸酶抑制作用与药物不良反应之间的关系。关于他克莫司药效学变异性的程度知之甚少。