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首页> 外文期刊>Nature clinical practice. Rheumatology >Drug Insight: resistance to methotrexate and other disease-modifying antirheumatic drugs--from bench to bedside.
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Drug Insight: resistance to methotrexate and other disease-modifying antirheumatic drugs--from bench to bedside.

机译：药物洞察力：从长凳到床头对甲氨蝶呤和其他可改变疾病的抗风湿药具有耐药性。

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摘要

The chronic nature of rheumatoid arthritis (RA) means that patients require drug therapy for many years. Many RA patients, however, have to discontinue treatment because of drug-related toxic effects, loss of efficacy, or both. The underlying molecular cause for loss of efficacy of antirheumatic drugs is not fully understood, but it might be mediated, at least in part, by mechanisms shared with resistance to anticancer drugs. This Review outlines molecular mechanisms that could be involved in the onset of resistance to, or the loss of efficacy of, disease-modifying antirheumatic drugs in RA patients, including methotrexate, sulfasalazine, chloroquine, hydroxychloroquine, azathioprine, and leflunomide. The mechanisms suggested are based on findings from experimental laboratory studies of specific drug-uptake and drug-efflux transporters belonging to the superfamily of multidrug-resistance transporters, alterations in intracellular drug metabolism, and genetic polymorphisms of drug transporters and metabolic enzymes. We also discuss strategies to overcome resistance and the current clinical studies aiming to predict response and risk of toxic effects. More in-depth knowledge of the mechanisms behind these features could help facilitate a more efficient use of disease-modifying antirheumatic drugs.
机译：类风湿关节炎（RA）的慢性性质意味着患者需要药物治疗多年。但是，许多RA患者由于药物相关的毒性作用，疗效下降或两者兼而不得不中止治疗。抗风湿药疗效下降的潜在分子原因尚未完全了解，但可能至少部分地由与抗癌药耐药性共享的机制介导。这篇综述概述了可能在RA患者中对改变疾病的抗风湿药产生抗药性或丧失其疗效的分子机制，包括甲氨蝶呤，柳氮磺吡啶，氯喹，羟氯喹，硫唑嘌呤和来氟米特。所建议的机制是基于对属于多药耐药转运蛋白超家族的特定药物吸收和药物外排转运蛋白的实验实验室研究得出的结果，细胞内药物代谢的改变以及药物转运蛋白和代谢酶的遗传多态性。我们还将讨论克服耐药性的策略以及旨在预测反应和毒性作用风险的当前临床研究。这些功能背后的机制的更深入的了解可以帮助促进更有效地使用改变疾病的抗风湿药。

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