Hawkey C J
Division of Gastroenterology, University Hospital, Nottingham, UK.
Eur J Gastroenterol Hepatol. 2000 Jun;12 Suppl 1:S17-20. doi: 10.1097/00042737-200012061-00005.
Although Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) both cause peptic ulcers, they do so by different mechanisms so any interaction is not necessarily harmful. H. pylori has been shown to enhance gastric mucosal prostaglandin synthesis, while NSAIDs suppress it Pragmatically, there is no compelling evidence in favour of H. pylori eradication in all patients who take NSAIDs. As a broad generalisation, in therapeutic studies of NSAID users, those who have no ulcer at trial entry are more prone to ulcer development if they are H. pylori-positive. By contrast, in those who have ulcers at baseline, H. pylori-positive individuals are less likely to develop ulcers, particularly if taking acid-suppressive therapy. Trials of H. pylori eradication therapy tend to replicate this dichotomy. In one study of patients starting NSAIDs for the first time, with no ulcer history and no baseline ulcer, use of bismuth-based eradication therapy was associated with a lower incidence of gastric ulcer at 2 months. Conversely, in a study of patients with endoscopically proven ulcers and/or troublesome dyspepsia, proton pump inhibitor based eradication treatment had no effect on outcome (of acid suppression) over 6 months. H. pylori eradication has been associated with significantly slower healing of gastric ulcers compared with patients who did not undergo eradication. However, the effect of H. pylori eradication on healing of NSAID-associated duodenal ulcers does not appear to be so dramatic, and limited evidence suggests that it may be possible to prevent H. pylori-associated duodenal ulcer by eradicating the infection. An evidence-based approach to treatment would suggest that NSAID users should undergo H. pylori eradication therapy if they have a duodenal ulcer, whether or not they continue NSAIDs. Because COX-2 inhibitors appear not to be ulcerogenic, management of H. pylori in patients taking these drugs can be based upon the same risk assessment as in patients not taking anti-arthritis drugs. H. pylori eradication should not be used universally or in high-risk gastric ulcer patients who require management with acid suppression.
虽然幽门螺杆菌和非甾体抗炎药（NSAIDs）都会导致消化性溃疡，但它们的致病机制不同，因此任何相互作用不一定有害。幽门螺杆菌已被证明可增强胃黏膜前列腺素的合成，而NSAIDs则会抑制其合成。实际上，对于所有服用NSAIDs的患者，没有令人信服的证据支持根除幽门螺杆菌。一般来说，在NSAIDs使用者的治疗研究中，那些在试验开始时没有溃疡的人，如果感染幽门螺杆菌，则更容易发生溃疡。相比之下，在基线时有溃疡的患者中，幽门螺杆菌阳性个体发生溃疡的可能性较小，特别是在接受抑酸治疗的情况下。幽门螺杆菌根除治疗试验往往会重复这种二分法。在一项针对首次开始服用NSAIDs、无溃疡病史且无基线溃疡的患者的研究中，使用铋剂根除治疗与2个月时胃溃疡发病率较低相关。相反，在一项针对内镜证实有溃疡和/或有严重消化不良的患者的研究中，基于质子泵抑制剂的根除治疗在6个月内对（抑酸）结果没有影响。与未接受根除治疗的患者相比，根除幽门螺杆菌与胃溃疡愈合明显减慢有关。然而，根除幽门螺杆菌对NSAID相关十二指肠溃疡愈合的影响似乎没有那么显著，有限的证据表明，通过根除感染可能预防幽门螺杆菌相关十二指肠溃疡。基于证据的治疗方法表明，如果NSAIDs使用者患有十二指肠溃疡，无论他们是否继续服用NSAIDs，都应接受幽门螺杆菌根除治疗。由于COX-2抑制剂似乎不会引起溃疡，服用这些药物的患者中幽门螺杆菌的管理可以基于与未服用抗关节炎药物的患者相同的风险评估。幽门螺杆菌根除不应普遍使用，也不适用于需要抑酸治疗的高危胃溃疡患者。
