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针对非甾体抗炎药所致胃十二指肠损伤的挽救策略。

Rescue strategies against non-steroidal anti-inflammatory drug-induced gastroduodenal damage.

作者信息

Lim Yun Jeong, Lee Jeong Sang, Ku Yang Suh, Hahm Ki-Baik

机构信息

Department of Internal Medicine, Dongguk University Ilsan Hospital, Dongguk University College of Medicine, Goyang, Korea.

出版信息

J Gastroenterol Hepatol. 2009 Jul;24(7):1169-78. doi: 10.1111/j.1440-1746.2009.05929.x.

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) are the most commonly prescribed drugs worldwide, which attests to their efficacy as analgesic, antipyretic and anti-inflammatory agents as well as anticancer drugs. However, NSAID use also carries a risk of major gastroduodenal events, including symptomatic ulcers and their serious complications that can lead to fatal outcomes. The development of "coxibs" (selective cyclooxygenase-2 [COX-2] inhibitors) offered similar efficacy with reduced toxicity, but this promise of gastroduodenal safety has only partially been fulfilled, and is now dented with associated risks of cardiovascular or intestinal complications. Recent advances in basic science and biotechnology have given insights into molecular mechanisms of NSAID-induced gastroduodenal damage beyond COX-2 inhibition. The emergence of newer kinds of NSAIDs should alleviate gastroduodenal toxicity without compromising innate drug efficacy. In this review, novel strategies for avoiding NSAID-associated gastroduodenal damage will be described.

摘要

非甾体抗炎药(NSAIDs)是全球处方量最多的药物,这证明了它们作为止痛、退热、抗炎药物以及抗癌药物的功效。然而,使用NSAIDs也存在发生严重胃十二指肠事件的风险,包括有症状的溃疡及其可能导致致命后果的严重并发症。“昔布类药物”(选择性环氧化酶-2 [COX-2] 抑制剂)的研发显示出相似的疗效且毒性降低,但胃十二指肠安全性方面的这一前景仅部分得以实现,如今又因心血管或肠道并发症的相关风险而受到影响。基础科学和生物技术的最新进展使人们对NSAIDs诱导的胃十二指肠损伤的分子机制有了更深入的了解,超出了COX-2抑制的范畴。新型NSAIDs的出现应能减轻胃十二指肠毒性,同时又不损害药物固有的疗效。在这篇综述中,将描述避免NSAIDs相关胃十二指肠损伤的新策略。

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