Editorial
Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jun 28, 2006; 12(24): 3789-3792
Published online Jun 28, 2006. doi: 10.3748/wjg.v12.i24.3789
Interaction or relationship between Helicobacter pylori and non-steroidal anti-inflammatory drugs in upper gastrointestinal diseases
Kai-Yu Ji, Fu-Lian Hu
Kai-Yu Ji, Department of Internal Medicine and Gastroenterology, Beijing United Family Hospital, Beijing 100016, China
Fu-Lian Hu, Peking University, First Hospital, Beijing 100034, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Fu-Lian Hu, Peking University, First Hospital, Beijing 100034, China. hufl@263.net
Telephone: +86-10-66551122-2618
Received: November 25, 2005
Revised: January 5, 2006
Accepted: January 14, 2006
Published online: June 28, 2006
Abstract

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.

Keywords: H pylori, Aspirin, NSAIDs, Peptic ulcer disease, Cyclooxygenase-2