比较etodolac和布洛芬对肾脏血液动力学的影响,管式功能,肾素,血管加压素和尿白蛋白排泄,在健康受试者alpha-glutathione-S-transferase:一项安慰剂对照交叉研究。

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斯文森主持KB,贝克约,索伦森结核病,皮德森EB

56欧元中国新药杂志。2000年8月;(5):383 - 8。

PubMed ID

11009046 (在PubMed

]

文摘

背景:非甾体抗炎药(非甾体抗炎药),其肾毒性可能代理。非甾体抗炎药抑制酶cyclo-oxygenase的前列腺素的合成,从而阻止肾脏。Cyclo-oxygenase存在于两个亚型(COX-1和cox - 2)。已经提出,非甾体抗炎药与优惠cox - 2选择性肾的副作用少于与优惠COX-1选择性药物。Etodolac相对选择性的cox - 2抑制剂,而布洛芬对COX-1效力高于cox - 2。目的:在这项研究中,我们比较了etodolac和布洛芬对肾功能的影响,血浆肾素、血浆精氨酸加压素和尿白蛋白排泄和alpha-glutathione-S-transferase (alpha-GST)。方法:在一个随机、双盲、三方交叉研究与安慰剂相比我们2周的治疗的效果与布洛芬和etodolac肾脏血液动力学(肾小球滤过率(GFR),肾血浆流量(RPF)和滤过分数(FF)],管状功能和血浆中肾素的激素浓度(中华人民共和国)和精氨酸加压素(AVP)在18个健康受试者。此外,我们研究了影响尿白蛋白排泄和alpha-GST肾损伤的标志。结果:未发现差异之间的三个治疗,安慰剂,布洛芬和etodolac,肾小球滤过率(GFR)的影响,RPF, FF,自由水的间隙,尿输出或部分钾和钠的排泄。导致etodolac相反,然而,布洛芬,在锂间隙明显降低(-16%和安慰剂)和锂的分数排泄(-17%和安慰剂),建议增加近端tubuli再吸收。 PRC was reduced significantly by ibuprofen (-32% versus placebo) but not etodolac. None of the drugs changed AVP. Fourteen days of treatment with ibuprofen caused a significant decrease (-47% versus placebo) in the urinary excretion of alpha-GST, while no changes were seen after etodolac. None of the drugs changed the urinary excretion of albumin. CONCLUSION: In conclusion, a 14-day administration of etodolac or ibuprofen in therapeutic doses did not affect the renal haemodynamics, the net excretion of electrolytes or the urinary excretion of albumin in healthy subjects. However, ibuprofen, in contrast to etodolac, caused a reduction in PRC, suggesting that COX-1 is involved in basal renin release in humans. Furthermore, ibuprofen decreased lithium excretion suggesting that COX-1 is involved in the re-absorption of sodium and/or water in the proximal tubuli. The reduction in the urinary excretion of alpha-GST by ibuprofen may be caused by an inhibition of the detoxification enzyme by ibuprofen. Overall the study indicates that only small differences in the effects of the two drugs on renal function in healthy subjects exist during a treatment period of 2 weeks.

DrugBank数据引用了这篇文章

药物靶点

药物	目标	类	生物	药理作用	行动
Etodolac	前列腺素合成酶2 G / H	蛋白质	人类	是的	抑制剂	细节