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首页> 外文期刊>Therapeutic Drug Monitoring >Amikacin Pharmacokinetics in Terminal Stage of Hematological Malignancy
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Amikacin Pharmacokinetics in Terminal Stage of Hematological Malignancy

机译：Amikacin药代动力学在血液恶性肿瘤终阶段

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Background: The influence of cancer cachexia on the pharmacokinetics of and kidney injury caused by amikacin remains unclear. This study investigated whether the pharmacokinetics of amikacin and the risk of kidney injury are altered with the progression of cancer cachexia. Methods: A retrospective analysis was conducted using therapeutic drug monitoring data obtained from 52 cancer patients who received amikacin intravenously for infection(s). The patients were classified into 2 groups based on the status of cachexia using a consensus definition: noncachexia group (n = 31) and cachexia group (n = 21). Differences in amikacin pharmacokinetics and occurrence of kidney injury were compared between the 2 groups. Amikacin pharmacokinetics was calculated based on a 1-compartment model using peak and trough concentrations measured clinically for therapeutic drug monitoring. In addition, intrapatient analysis was conducted based on patients who received amikacin treatments more than once during the study period to examine the alteration in amikacin pharmacokinetics with the progression of cancer cachexia. Results: Systemic clearance of amikacin [median (range)] was significantly (P , 0.05) lower in the cachexia group [37.3 (11.2-87.3) (mL/min)] than in the noncachexia group [52.0 (19.1-133.4) (mL/min)]. In contrast, volume of distribution was significantly (P , 0.05) increased in the cachexia group [0.47 (0.20-1.45) L/kg] compared with the noncachexia group [0.32 (0.21-1.00) L/kg]. There was no difference in the occurrence of kidney injuries between the 2 groups. In an intrapatient analysis of the longitudinal alteration of amikacin pharmacokinetics, an approximately 50% reduction in clearance and 30% increase in volume of distribution were observed as cancer cachexia progressed. Conclusions: The present study suggests that progression of cancer cachexia may reduce amikacin clearance and increase the volume of distribution, but cancer cachexia does not increase amikacin-induced kidney injury.
机译：背景：癌症恶化对Amikacin引起的药代动力学的影响尚不清楚。本研究调查了Amikacin的药代动力学和肾损伤的风险是否随着癌症恶化的进展而改变。方法：使用从52名癌症患者获得的治疗药物监测数据进行回顾性分析，静脉内接受Amikacin进行感染。根据同意定义在2组之间比较了Amikacin药代动力学和肾损伤的发生差异。基于使用峰值和谷粒浓度的1室模型计算Amikacin药代动力学，用于治疗药物监测。此外，基于在研究期间接受Amikacin治疗的患者进行脑内分析，以检查Amikacin药代动力学的改变与癌症恶病症的进展。结果：疟原虫组中Amikacin [中位数（范围）]的全身间隙显着（p，0.05），比在非生物疾病组中较低（11.2-87.3）（ml / min）[52.0（19.1-133.4）（ ml / min）]。相比之下，与非生物抑制基团相比，分布体积显着（p，0.05）增加[0.47（0.20-1.45）L / kg] [0.32（0.21-1.00）L / kg]。 2组肾脏损伤的发生没有差异。在对阿米卡星药代动力学的纵向改变的纵向改变的内部分析中，随着癌症恶化的进展，观察到分布的约50％和30％的分布量增加。结论：本研究表明，癌症恶化的进展可能会降低Amikacin清除并增加分布的体积，但癌症恶病症不会增加Amikacin诱导的肾损伤。

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