Ji Kai-Yu, Hu Fu-Lian
Department of Internal Medicine and Gastroenterology, Beijing United Family Hospital, China.
World J Gastroenterol. 2006 Jun 28;12(24):3789-92. doi: 10.3748/wjg.v12.i24.3789.
According to a meta-analysis, H pylori and non-steroidal anti-inflammatory drugs (NSAID) independently and significantly increase the risk of gastroduodenal ulcer and ulcer bleeding. Their coincidence is frequent, demonstration of a possible relationship and consequent attitude is of important implications. But unfortunately, no consensus has been approved in the past years and their interactions are still controversial. H pylori and NSAID are known to share a number of pathogenic mechanisms, but there is no evidence for the significant synergic action between these two risk factors. Their relationship is independent, additive, synergistic or antagonistic without considering the influence of other factors because studies on this subject are different in almost all aspects of their methodology, including the definition of a NSAID user as well as the types, doses, duration and their indications for NSAID use, as well as their end-points, definition of dyspepsia and regimes used for eradication of H pylori. These might contribute to the conflicting results and opinions. H pylori infection in humans does not act synergistically with NSAID on ulcer healing, and there is no need to eradicate it. This notion is supported by the finding that the eradication of H pylori does not affect NSAID-induced gastropathy treated with omeprazole and that H pylori infection induces a strong cyclooxygenase-2 (COX-2) expression resulting in excessive biosynthesis of gastroprotective prostaglandin which in turn counteracts NSAID-induced gastropathy and heals the existing ulcer. Other investigators claimed that H pylori infection acts synergistically with NSAID on ulcer development, and H pylori should be eradicated, particularly at the start of long-term NSAID therapy. Eradication of H pylori prior to NSAID treatment does not appear to accelerate ulcer healing or to prevent recurrent ulcers in NSAID users. However, some recommendations can be drawn from the results of clinical trails.
一项荟萃分析表明,幽门螺杆菌和非甾体抗炎药(NSAID)分别且显著增加胃十二指肠溃疡和溃疡出血的风险。二者同时存在的情况很常见,阐明它们之间可能的关系以及相应的应对措施具有重要意义。但遗憾的是,过去几年并未达成共识,它们之间的相互作用仍存在争议。已知幽门螺杆菌和NSAID有一些共同的致病机制,但尚无证据表明这两种危险因素之间存在显著的协同作用。由于关于该主题的研究在几乎所有方法学方面都存在差异,包括NSAID使用者的定义以及NSAID的类型、剂量、疗程及其使用指征,还有研究终点、消化不良的定义以及根除幽门螺杆菌所用的方案等,所以在不考虑其他因素影响的情况下,它们之间的关系是独立、相加、协同还是拮抗并不明确。这些差异可能导致了相互矛盾的结果和观点。人类幽门螺杆菌感染与NSAID在溃疡愈合方面并无协同作用,无需根除。这一观点得到以下研究结果的支持:根除幽门螺杆菌并不影响用奥美拉唑治疗的NSAID所致胃病,而且幽门螺杆菌感染会诱导强烈的环氧化酶-2(COX-2)表达,从而导致具有胃保护作用的前列腺素过度生物合成,进而抵消NSAID所致胃病并治愈现有的溃疡。其他研究者则称,幽门螺杆菌感染与NSAID在溃疡发生方面具有协同作用,应根除幽门螺杆菌,尤其是在长期NSAID治疗开始时。在NSAID治疗前根除幽门螺杆菌似乎并不能加速溃疡愈合或预防NSAID使用者的复发性溃疡。然而,可从临床试验结果中得出一些建议。