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Background and aims: Factors predisposing to endoscopic ulcer formation or healing with non-steroidal anti-inflammatory drugs (NSAIDs) have not been well defined. Methods: We used multivariate analysis of data from three [...]

Background and aims: A past history of peptic ulceration increases the risk of an ulcer developing during non-steroidal anti-inflammatory drug (NSAID) use. Whether this is due to Helicobacter pylori infection [...]

The effects of transforming growth factor (TGF)-alpha on the expression of spamolytic peptides (SP) and intestinal trefoil (ITF) peptides were analyzed after gastric mucosal injury in mice. The application of glacial acetic acid to the serosal surface of the stomachs of mice with knocked out TGF-alpha genes reduced the expression of the SP andITF peptides during gastric mucosal injury. Furthermore, the reduced levels of SP and ITF expression was mediated by the increased secretion of gastric juice.

The associations between nonsteroidal anti-inflammatory drugs (NSAIDs) and the presence and complications of gastroduodenal erosions and ulcers are well established. Evidence that acid aggravates NSAID-induced injury provides a rationale for minimising such damage by acid suppression. Other strategies discussed include avoidance of NSAIDs or minimising their dosage, selecting NSAIDs known to cause less damage, and co-prescription of various agents. Cytoprotection with misoprostol, a prostaglandin analogue, has been shown to be effective in reducing NSAID-related peptic ulcers and their complications. Unfortunately, adverse effects may limit compliance in some patients. Histamine H2 antagonists have only limited efficacy in the prevention of NSAID-induced ulcers in humans, particularly in the stomach, except at higher than standard dosages. This may relate to their relatively modest effect in elevating gastric pH, especially in comparison with proton pump inhibitors. Several studies now confirm the efficacy of proton pump inhibitors in the short and longer term prevention of NSAID-induced upper gastrointestinal injury. Placebo-controlled studies suggest reductions of over 70% in gastric and duodenal ulcer rates over 3 to 6 months. The recent ASTRONAUT (Acid Suppression Trial: Ranitidine versus Omeprazole for NSAID-Associated Ulcer Treatment) study documented the greater prophylactic efficacy of omeprazole over ranitidine at standard dosages for 6 months. The OMNIUM (Omeprazole versus Misoprostol for NSAID-Induced Ulcer Management) study showed omeprazole to be slightly more effective overall than misoprostol in preventing the upper gastrointestinal adverse effects of NSAIDs, with both substantially more effective than placebo, although misoprostol was somewhat less well tolerated. Although substantial reductions in NSAID ulceration are now achievable when co-therapy with a proton pump inhibitor is given, a few patients will still develop ulcers and their complications. Hence the judicious use of NSAIDs in the first instance cannot be overemphasised. [ABSTRACT FROM AUTHOR]

Examines the hypothesis that mice with a transforming growth factor-alpha (TGF-) null mutation (knockout) would have reduced trefoil peptide expression, compared to wild-type controls after gastric ulceration. Rate of macroscopic ulcer healing; Factors which threaten the gastric mucosa; Details on the study.

Examines the therapeutic use of omeprazole for treatment of duodenal ulcers in Melbourne, Victoria. Rapid healing of patients treated with omeprazole; Adverse reactions of the drug; Assessment of serum electrolyte, urea and creatinine concentrations.