Unit for Pharmacokinetics and Drug Metabolism, Department of Pharmacology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Department of Pharmacy, School of Medicine and Pharmacy, University of Rwanda, Kigali, Rwanda.
Antimicrob Agents Chemother. 2021 Jun 17;65(7):e0004621. doi: 10.1128/AAC.00046-21.
Pyrazinamide is a first-line drug used in the treatment of tuberculosis. High exposure to pyrazinamide and its metabolites may result in hepatotoxicity, whereas low exposure to pyrazinamide has been correlated with treatment failure of first-line antitubercular therapy. The aim of this study was to describe the pharmacokinetics and metabolism of pyrazinamide in patients coinfected with tuberculosis and HIV. We further aimed to identify demographic and clinical factors which affect the pharmacokinetics of pyrazinamide and its metabolites in order to suggest individualized dosing regimens. Plasma concentrations of pyrazinamide, pyrazinoic acid, and 5-hydroxypyrazinamide from 63 Rwandan patients coinfected with tuberculosis and HIV were determined by liquid chromatography-tandem mass spectrometry followed by nonlinear mixed-effects modeling. Females had a close to 50% higher relative pyrazinamide bioavailability compared to males. The distribution volumes of pyrazinamide and both metabolites were lower in patients on concomitant efavirenz-based HIV therapy. Furthermore, there was a linear relationship between serum creatinine and oral clearance of pyrazinoic acid. Simulations indicated that increasing doses from 25 mg/kg of body weight to 35 mg/kg and 50 mg/kg in females and males, respectively, would result in adequate exposure with regard to suggested thresholds and increase probability of target attainment to >0.9 for a MIC of 25 mg/liter. Further, lowering the dose by 40% in patients with high serum creatinine would prevent accumulation of toxic metabolites. Individualized dosing is proposed to decrease variability in exposure to pyrazinamide and its metabolites. Reducing the variability in exposure may lower the risk of treatment failure and resistance development.
吡嗪酰胺是治疗结核病的一线药物。高暴露于吡嗪酰胺及其代谢物可能导致肝毒性,而低暴露于吡嗪酰胺与一线抗结核治疗失败有关。本研究旨在描述结核和 HIV 合并感染患者中吡嗪酰胺的药代动力学和代谢情况。我们还旨在确定影响吡嗪酰胺及其代谢物药代动力学的人口统计学和临床因素,以便为个体化给药方案提供建议。通过液相色谱-串联质谱法测定了来自 63 名卢旺达结核和 HIV 合并感染患者的吡嗪酰胺、吡嗪酸和 5-羟基吡嗪酰胺的血浆浓度,并进行了非线性混合效应建模。女性的相对吡嗪酰胺生物利用度比男性高近 50%。同时接受依非韦伦为基础的 HIV 治疗的患者中,吡嗪酰胺和两种代谢物的分布容积较低。此外,血清肌酐与吡嗪酸的口服清除率之间存在线性关系。模拟表明,女性和男性分别将剂量从 25mg/kg 体重增加到 35mg/kg 和 50mg/kg,将导致根据建议的阈值达到足够的暴露,并将目标达成率提高到 >0.9,MIC 为 25mg/L。此外,在血清肌酐较高的患者中降低 40%的剂量可防止有毒代谢物的积累。建议个体化给药以降低吡嗪酰胺及其代谢物的暴露变异性。降低暴露的变异性可能降低治疗失败和耐药发展的风险。