| Literature DB >> 16188503 |
Abstract
In developed countries at least, ulcers related to Helicobacter pylori infection are becoming rarer. However, ulcers associated with the use of non-steroidal anti-inflammatory drugs (NSAIDs) remain a major clinical problem, which has not been solved through the introduction of selective inhibitors of cyclooxygenase (COX)-2. Recent studies suggest that NSAID-induced ulcers can be prevented largely through co-administration of a proton pump inhibitor to block acid secretion in the stomach. In patients requiring aspirin therapy to prevent cardiovascular diseases, co-administration of aspirin plus a proton pump inhibitor was found to be safer than using another anti-platelet therapy that does not block gastric prostaglandin production (e.g. clopidogrel). Several recent papers have clarified further the contribution of COX-2 to gastric mucosal defence and to the healing of ulcers. In some circumstances, COX-2 produces a highly potent gastroprotective substance (15-R-lipoxin A(4)), and analogues of this substance could have therapeutic value for preventing gastric ulceration. Nitric oxide-releasing NSAIDs continue to show promise in terms of limiting damage to the gastrointestinal tract, even when given in combination with aspirin. Recent studies support the notion that platelets make a major contribution to ulcer healing, and the release of several key growth factors from platelets appears to be regulated by proteinase-activated receptors.Entities:
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Year: 2005 PMID: 16188503 DOI: 10.1016/j.coph.2005.06.004
Source DB: PubMed Journal: Curr Opin Pharmacol ISSN: 1471-4892 Impact factor: 5.547