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非甾体抗炎药(NSAIDs)导致的胃肠道和心血管损伤。

NSAID-induced gastrointestinal and cardiovascular injury.

机构信息

Institute of Digestive Disease, Chinese University of Hong Kong, Department of Medicine and Therapeutics, Prince of Wales Hospital, Shalin, NT, Hong Kong.

出版信息

Curr Opin Gastroenterol. 2010 Nov;26(6):611-7. doi: 10.1097/MOG.0b013e32833e91eb.

DOI:10.1097/MOG.0b013e32833e91eb
PMID:20948372
Abstract

PURPOSE OF REVIEW

To review recent publications related to NSAID-induced adverse effects on the gastrointestinal and cardiovascular systems.

RECENT FINDINGS

This paper explores novel mechanisms of NSAID-induced gastrointestinal injury, highlights new composite endpoints evaluating adverse events of NSAIDs in the entire gastrointestinal tract, and combines published data to establish evidence-based guidance on the best use of NSAIDs to achieve optimal clinical outcomes whilst minimizing cardiovascular and gastrointestinal injuries.

SUMMARY

NSAIDs can induce peptic ulcers via epithelial cell membrane disruption and the renin angiotensin system, independent of the cyclooxygenase (COX) pathways, whereas mast cells and bile acid sensors may have a protective effect on NSAID-induced gastrointestinal damage. Patients with arthritis treated with a COX-2 inhibitor are less likely to develop upper and lower gastrointestinal complications than those who are treated with diclofenac plus a proton pump inhibitor (PPI). PPI therapy is recommended in patients receiving dual antiplatelet treatment but observational studies show that clopidogrel users taking PPIs have an increased risk of cardiovascular events. Until further reliable controlled data are available, this potential, but currently unproven, clinical interaction can be minimized by widely separating the dosing of clopidogrel and PPI. Histamine-2 antagonists may be an alternative to PPI for the prevention of peptic ulcers in patients taking low-dose aspirin.

摘要

目的综述

回顾近期有关 NSAID 对胃肠道和心血管系统不良影响的相关文献。

最近的发现

本文探讨了 NSAID 诱导胃肠道损伤的新机制,强调了新的综合终点来评估 NSAID 在整个胃肠道的不良事件,并结合已发表的数据为 NSAID 的最佳使用提供循证指导,以实现最佳的临床效果,同时将心血管和胃肠道损伤的风险最小化。

总结

NSAID 可通过上皮细胞膜破坏和肾素-血管紧张素系统诱导消化性溃疡,这与环氧化酶(COX)途径无关,而肥大细胞和胆酸感受器可能对 NSAID 诱导的胃肠道损伤具有保护作用。与使用双氯芬酸加质子泵抑制剂(PPI)的患者相比,接受 COX-2 抑制剂治疗的关节炎患者发生上消化道和下消化道并发症的可能性较小。建议接受双重抗血小板治疗的患者使用 PPI 治疗,但观察性研究表明,使用氯吡格雷的患者服用 PPI 会增加心血管事件的风险。在有进一步可靠对照数据之前,为尽量减少这种潜在但目前尚未证实的临床相互作用,可以广泛错开氯吡格雷和 PPI 的用药时间。对于服用小剂量阿司匹林的患者,组胺 2 拮抗剂可能是预防消化性溃疡的 PPI 替代药物。

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