Prevention and treatment of gastrointestinal symptoms and complications due to NSAIDs.Best Pract Res Clin Gastroenterol. 2001 Oct; 15(5):755-73.BP
The mechanisms by which aspirin(ASA) and non-steroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal symptoms are poorly understood. They probably arise from several causes, including direct and indirect mucosal injury, exacerbation of underlying peptic ulcer disease or non-ulcer dyspepsia, exacerbation of Helicobacter pylori gastritis, and possibly motility disorders. No single form of therapy has been generally successful. Because, in most cases, symptoms abate fairly rapidly with continued treatment, there is little evidence that benefit associated with any symptom-directed drug therapy is superior to placebo beyond 4 weeks. Exceptions may be the subsets of patients with pre-existing ulcer disease or heartburn, exacerbated by the NSAID therapy, who usually benefit from acid-suppressive drug treatment. Different NSAIDs vary in the frequency with which their use leads to gastrointestinal(GI) complications such as haemorrhage, perforation, obstruction, or the symptomatic ulcers from which about 40% of the complications arise. Most gastroduodenal ulcers heal over time, albeit more slowly, with conventional doses of any of the available anti-ulcer drugs. Maintenance therapy may be needed in many patients who continue NSAID therapy. Anti-ulcer drugs have not, thus far, been shown to be more effective than placebo in preventing ulcer complications or their recurrence. The use of COX-2-selective inhibitors appears, in outcome studies, to reduce gastrointestinal bleeding, including bleeding from ulcers, but it is not established that the ulcers protected were caused by NSAIDs, as distinct from ulcers exacerbating or recurring from antecedent peptic ulcer disease. To-date, perforation or obstruction have not been shown to be affected by selective COX-2 inhibitor drugs. If the major problem giving rise to severe NSAID complications is pre-existing peptic ulcer disease, it may yet emerge that the most effective approach will be the use of proton pump inhibitor drugs, for the duration of NSAID therapy, in a small subset of high-risk patients. Most other low-risk patients may not need any special care. Co-morbid conditions have a major impact on outcome of NSAID therapy. Morbidity or even death attributable solely to NSAIDs is probably small in normal patients, and requires little in the way of prophylaxis.