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杜氏利什曼原虫野外分离株对米替福新和两性霉素B的体外敏感性：与葡萄糖酸锑钠敏感性的相关性及对流行地区治疗的意义

In vitro susceptibility of field isolates of Leishmania donovani to Miltefosine and amphotericin B: correlation with sodium antimony gluconate susceptibility and implications for treatment in areas of endemicity.

作者信息

Kumar Dhiraj, Kulshrestha Arpita, Singh Ruchi, Salotra Poonam

机构信息

Institute of Pathology, Safdarjung Hospital Campus, New Delhi, India.

出版信息

Antimicrob Agents Chemother. 2009 Feb;53(2):835-8. doi: 10.1128/AAC.01233-08. Epub 2008 Nov 17.

DOI:10.1128/AAC.01233-08
PMID:19015344
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2630609/
Abstract

Indian Leishmania donovani isolates (n = 19) from regional zones representing various levels of antimony resistance displayed significantly (P < 0.01) correlated results with respect to in vitro susceptibility to the antileishmanial drugs sodium antimony gluconate, amphotericin B, and Miltefosine, raising the possibility of cross-resistance mechanisms operating in the field isolates. The results of gene expression analysis of LdMT and LdRos3 were suggestive of alternate mechanisms of Miltefosine susceptibility in the isolates.

摘要

来自代表不同锑抗性水平的区域的19株印度杜氏利什曼原虫分离株，在体外对抗利什曼原虫药物葡萄糖酸锑钠、两性霉素B和米替福新的敏感性方面显示出显著（P < 0.01）相关的结果，这增加了野外分离株中存在交叉抗性机制的可能性。LdMT和LdRos3的基因表达分析结果提示了分离株中米替福新敏感性的替代机制。

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本文引用的文献

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Miltefosine in the treatment of leishmaniasis: Clinical evidence for informed clinical risk management.米替福新治疗利什曼病：知情临床风险管理的临床证据。
Ther Clin Risk Manag. 2007 Oct;3(5):733-40.
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Possibility of membrane modification as a mechanism of antimony resistance in Leishmania donovani.膜修饰作为杜氏利什曼原虫抗锑机制的可能性。
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A proteomics screen implicates HSP83 and a small kinetoplastid calpain-related protein in drug resistance in Leishmania donovani clinical field isolates by modulating drug-induced programmed cell death.一项蛋白质组学筛选表明，热休克蛋白83（HSP83）和一种小型动基体钙蛋白酶相关蛋白通过调节药物诱导的程序性细胞死亡，参与杜氏利什曼原虫临床现场分离株的耐药性。
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Visceral leishmaniasis, or kala azar (KA): high incidence of refractoriness to antimony is contributed by anthroponotic transmission via post-KA dermal leishmaniasis.内脏利什曼病，即黑热病（KA）：通过黑热病后皮肤利什曼病的人传人传播导致对锑难治性的高发生率。
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Mechanisms of experimental resistance of Leishmania to miltefosine: Implications for clinical use.利什曼原虫对米替福新产生实验性耐药的机制：对临床应用的启示
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Phospholipid translocation and miltefosine potency require both L. donovani miltefosine transporter and the new protein LdRos3 in Leishmania parasites.磷脂转运和米替福新效力在利什曼原虫中既需要杜氏利什曼原虫米替福新转运蛋白，也需要新蛋白LdRos3。
J Biol Chem. 2006 Aug 18;281(33):23766-75. doi: 10.1074/jbc.M605214200. Epub 2006 Jun 19.
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Unresponsiveness to AmBisome in some Sudanese patients with kala-azar.一些苏丹黑热病患者对两性霉素B脂质体无反应。
Trans R Soc Trop Med Hyg. 2007 Jan;101(1):19-24. doi: 10.1016/j.trstmh.2006.02.005. Epub 2006 May 26.
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Drug resistance in leishmaniasis.利什曼病中的耐药性。
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Availability of miltefosine for the treatment of kala-azar in India.在印度可获得用于治疗黑热病的米替福新。
Bull World Health Organ. 2005 May;83(5):394-5. Epub 2005 Jun 24.