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对慢性丙型肝炎患者红细胞的代谢组学分析揭示了利巴韦林诱导溶血的病因。

Metabolome analysis of erythrocytes from patients with chronic hepatitis C reveals the etiology of ribavirin-induced hemolysis.

机构信息

1. Department of Gastroenterology, Yamagata University School of Medicine, Yamagata, Yamagata 990-9585;

出版信息

Int J Med Sci. 2013 Sep 9;10(11):1575-7. doi: 10.7150/ijms.6436. eCollection 2013.

DOI:10.7150/ijms.6436
PMID:24046534
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3775117/
Abstract

Ribavirin is one of the major agents used in combination therapy with interferon for chronic hepatitis C, but is often associated with hemolytic anemia as a serious adverse event. Employing metabolome analysis, we demonstrated that the concentrations of intermediate metabolites produced by glycolysis and the pentose phosphate cycle in patients' erythrocytes were significantly decreased after administration of ribavirin. Our findings suggest that hemolysis associated with ribavirin is triggered by an energy crisis and consequent oxidative stress, thus having implications for the prevention of such hemolysis.

摘要

利巴韦林是慢性丙型肝炎联合干扰素治疗的主要药物之一,但常伴有溶血性贫血等严重不良反应。采用代谢组学分析方法,我们发现利巴韦林治疗后患者红细胞中糖酵解和磷酸戊糖途径产生的中间代谢产物浓度显著降低。我们的研究结果提示,利巴韦林相关性溶血是由能量危机和随后的氧化应激引发的,因此对预防此类溶血具有重要意义。

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Metabolome analysis of erythrocytes from patients with chronic hepatitis C reveals the etiology of ribavirin-induced hemolysis.对慢性丙型肝炎患者红细胞的代谢组学分析揭示了利巴韦林诱导溶血的病因。
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Anemia management in patients with chronic viral hepatitis C.慢性丙型病毒性肝炎患者的贫血管理。
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Differential metabolomics reveals ophthalmic acid as an oxidative stress biomarker indicating hepatic glutathione consumption.差异代谢组学揭示了眼酸作为一种氧化应激生物标志物,表明肝脏谷胱甘肽的消耗。
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Glutathione peroxidase, thioredoxin, and membrane protein changes in erythrocytes predict ribavirin-induced anemia.红细胞中谷胱甘肽过氧化物酶、硫氧还蛋白和膜蛋白的变化可预测利巴韦林引起的贫血。
Clin Pharmacol Ther. 2005 Oct;78(4):422-32. doi: 10.1016/j.clpt.2005.07.002.
10
Mechanism of action of ribavirin in the combination treatment of chronic HCV infection.利巴韦林在慢性丙型肝炎病毒感染联合治疗中的作用机制。
Hepatology. 2002 May;35(5):1002-9. doi: 10.1053/jhep.2002.32672.