Department of Clinical Pharmacy, Faculty of Pharmacy, Tehran University of Medical Sciences, 1417614411, P.O. Box:14155/6451, Enghelab Ave, Tehran, Iran,
Eur J Clin Pharmacol. 2014 Apr;70(4):399-408. doi: 10.1007/s00228-014-1642-9. Epub 2014 Jan 21.
The aim of this study was to evaluate the effectiveness of oral n-acetyl cysteine, as a potential nephroprotective agent, in preventing and/or attenuating amphotericin B-induced electrolytes imbalances.
During a one year period, patients were to receive conventional amphotericin b for any indication for at least one week and were randomly allocated to receive either placebo or 600 mg oral n-acetyl cysteine twice daily during the treatment course of amphotericin b. Demographic and clinical data of the study population were gathered. Different aspects of amphotericin b nephrotoxicity including decrease of glomerular filtration rate, hypokalemia, hypomagnesemia, renal magnesium and potassium wasting were assessed. Each patient was monitored for any adverse reaction to n-acetyl cysteine. Sixteen and 14 patients in the n-acetyl cysteine and placebo groups completed the study, 3incidences of hypokalemia (75 % versus 70 %; P = 0.724) and hypomagnesemia (30 % versus 20 %; P = 0.468) did not differ significantly between placebo and NAC groups, respectively. Although the rate of AmB nephrotoxicity was higher in the placebo than in the NAC group (60 % versus 40 %), this difference was not statistically significant (P = 0.209) even after adjusting for probable associated factors of amphotericin b nephrotoxicity (P = 0.206). The incidence as well as time of onset of electrolyte abnormalities also did not differ significantly between placebo and n-acetyl cysteine groups. About 44 % of n-acetyl cysteine recipients experienced new onset nausea and a mild unpleasant taste during the study.
Oral n-acetyl cysteine during the amphotericin B treatment course was not significantly effective in preventing or mitigating different features of its nephrotoxicity including decrease of glomerular filtration rate, hypokalemia, hypomagnesemia, and renal potassium as well as magnesium wasting.
本研究旨在评估口服 N-乙酰半胱氨酸（一种潜在的肾保护剂）预防和/或减轻两性霉素 B 引起的电解质失衡的有效性。
在一年的时间内，患者将因任何适应症接受至少一周的常规两性霉素 B 治疗，并随机分配接受安慰剂或在两性霉素 B 治疗过程中每天两次口服 600mg N-乙酰半胱氨酸。收集研究人群的人口统计学和临床数据。评估两性霉素 B 肾毒性的不同方面，包括肾小球滤过率下降、低钾血症、低镁血症、肾镁和钾丢失。监测每位患者对 N-乙酰半胱氨酸的任何不良反应。N-乙酰半胱氨酸组和安慰剂组各有 16 名和 14 名患者完成了研究，低钾血症（75%对 70%；P=0.724）和低镁血症（30%对 20%；P=0.468）的发生率在安慰剂和 NAC 组之间无显著差异。尽管安慰剂组的两性霉素 B 肾毒性发生率高于 NAC 组（60%对 40%），但即使在调整两性霉素 B 肾毒性的可能相关因素后，这种差异也无统计学意义（P=0.209）。安慰剂和 N-乙酰半胱氨酸组之间电解质异常的发生率和发生时间也无显著差异。约 44%的 N-乙酰半胱氨酸接受者在研究期间出现新发恶心和轻度不适的味觉。
在两性霉素 B 治疗过程中口服 N-乙酰半胱氨酸不能显著预防或减轻其肾毒性的不同特征，包括肾小球滤过率下降、低钾血症、低镁血症以及肾钾和镁丢失。
