Interaction or relationship between Helicobacter pylori and non-steroidal anti-inflammatory drugs in upper gastrointestinal diseases.
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.
Ji
Kai-Yu
KY
Department of Internal Medicine and Gastroenterology, Beijing United Family Hospital, China.
Hu
Fu-Lian
FL
D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D001241:Aspirin / Q000009:adverse effects / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000517:prevention & control; D051546:Cyclooxygenase 2 / Q000502:physiology; D052246:Cyclooxygenase 2 Inhibitors / Q000627:therapeutic use; D004415:Dyspepsia / Q000139:chemically induced / Q000188:drug therapy / Q000382:microbiology / Q000503:physiopathology; D005767:Gastrointestinal Diseases / Q000139:chemically induced* / Q000188:drug therapy / Q000382:microbiology* / Q000503:physiopathology; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D009853:Omeprazole / Q000627:therapeutic use; D010437:Peptic Ulcer / Q000139:chemically induced / Q000188:drug therapy / Q000382:microbiology / Q000503:physiopathology; D012216:Rheumatic Diseases / Q000188:drug therapy; D012307:Risk Factors
D000900:Anti-Bacterial Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D000897:Anti-Ulcer Agents; D052246:Cyclooxygenase 2 Inhibitors; D051546:Cyclooxygenase 2; D009853:Omeprazole; D001241:Aspirin