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Chin Med J (Taipei) 1996;57:S64.
Division of Gastroenterology, Department of Internal Medicine
Peking Union Medical College University
Chinese Academy of Medical Sciences
Nonsteroidal antiinflammatory drugs (NSAIDs) are commonly prescribed and have proved to be effective in the treatment of arthritic and musculoskeletal disorders. Unfortunately, the acute and chronic gastropathy is frequently associated with the use of these drugs. In our observed data, most patients receiving aspirin 6 g daily for 7 days have significant endoscopic evidence of gastric erosions, an increase in fecal blood loss and decrease in prostaglandin E2 in gastric mucosa. Among 346 patients with rheumatic disease who ingested NSAIDs more than 2 months, approximately 11% and 5% of them developed gastric ulcer and duodenal ulcer respectively. 1.2% of those long-term NSAIDs users developed upper gastrointestinal hemorrhagic complication. This is at least 4-fold increase risk of bleeding compared with non-users. The mortality of patients with bleeding ulcer due to ingestion of NSAIDs is 0.1% in our studied group. Up to 44% of chronic NSAIDs users complain of dyspeptic symptoms. However, there is poor correlation between the degree of mucosal injury and dyspeptic symptoms. 43% of NSAIDs-induced gastric ulcer patients have no symptom. In constrast, about one third of NSAIDs users with dyspepsia did not have important endoscopic mucosal abnormalities. Our observation revealed that risk factors for presentation of NSAIDs associated peptic ulcer bleeding complication are drug dose regimen, duration of therapy, previous history of peptic ulcer disease, co-administration of corticosteroids, and old age.
NSAIDs lesions reflect two modes of damage: topical versus systemic effects. The later may be more important. The mechanism by which NSAIDs induce gastric mucosal injury is likely to involve inhibition of cyclo-oxygenase and the consequent failure to produce prostaglandins. Other factors may include neutrophils adherence to the vascular endothelium, and free radical oxygen. Gastric acid also plays an prominent role in NSAIDs associated gastric mucosal lesions because of the potential therapeutic benefits of proton pump inhibitors seen in NSAIDs-induced ulceration. Our data showed that there is no statistical difference in the prevalence of Helicobacter pylori infection between NSAIDs users and non-users with peptic ulcer disease.
Colloidal bismuth subcitrate and sulcralfate are beneficial in the prophylaxis of acute NSAIDs-induced gastric lesions, but the effects of these two drugs on the healing of NSAIDs associated ulceration is insignificant. Misoprotol in dose of 800 micron g daily healed 67% and 75% of gastric ulcer after 4 and 8 weeks respectively in patients continuing NSAIDs therapy. We found that 1.1% of 48 rheumatoid arthritis patients treated with misoprostol 800 micron g daily with concomitant NSAIDs for 2 months developed gastric ulcers, compared with 9.7% of the control group. Our clinical studies indicated that the rapid symptom relief and reliable ulcer healing observed in NSAIDs-induced peptic ulcer patients treated with omeprazole. The ulcer healing rates of the patients who continued to receive NSAIDs were 69% and 83% after 4 weeks of treatment with omeprazole 20 or 40 mg daily respectively. We did a preliminary study on the prophylaxis with omeprazole in NSAIDs users. The results demonstrated that omeprazole is effective in the prevention of either in acute or in chronic gastric lesion.
[Chin Med J (Taipei) 1996; 57: S64.]
Copyright: 1996, Chinese Medical Association (Taipei)