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The objective of this study was to investigate the prevalence of gastric mucosal injury induced by nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with rheumatoid arthritis (RA). Upper gastrointestinal endoscopy was performed on 100 RA patients treated with NSAIDs. Patient factors potentially contributing to the development of NSAID-induced gastric mucosal injury were identified by logistic regression analysis; gastric mucosal injury and ulcers were used as objective variables. Gastric mucosal injury was detected in 62 of 100 patients, and eight of these patients had ulcers. Previous history of ulcers, lifestyle, NSAID dosage, and body mass index were associated with the development of gastric mucosal injury,and the use of diclofenac and steroid dose were associated with the development of ulcers. Disease-modifying antirheumatic drugs (DMARDs) did not appear to influence the risk of NSAID-induced gastric mucosal injury. RA patients treated for long periods with NSAIDs for RA symptoms should be controlled with DMARDs, without consideration of increased doses of steroids, in terms of risk for NSAID-induced gastric mucosal injury. Simultaneously, concomitant use of histamine-2 receptor antagonists (H2RA) such as famotidine should be considered.

Background: An increase in gastric mucosal lesions due to nonsteroidal antiinflammatory drugs (NSAIDs) has been reported along with the aging of society; even orthopedic surgeons can no longer remain unconcerned about this disease. However, no study has accurately examined the incidence of gastric mucosal lesions; therefore, adequate evidence has not been established. In this study, endoscopic examinations were performed to determine the status of gastric mucosal lesions in patients receiving long-term NSAID therapy., Methods: In 261 patients receiving NSAIDs other than aspirin for more than 28 days, excluding external application, upper gastrointestinal endoscopy was performed regardless of any subjective symptoms after obtaining the patient's medical history. The severity of the gastric mucosal lesions was evaluated using the modified Lanza score. Patient factors involved in the development of lesions were examined using a logistic regression analysis with criterion variables of gastric mucosal lesions and ulcers and the factors of sex, age, Helicobacter pylori infection, and type of NSAID as candidates for the explanatory variable., Results: Gastric mucosal lesions were observed in 164 patients (62.8%); 27 (10.3%) had ulcers. The use of diclofenac, subjective symptoms, irregular lifestyle, and increased body mass index (BMI) were four factors associated with the development of gastric mucosal lesions; the odds ratios were 2.99, 1.92, 1.80, and 1.09, respectively. Also, the use of diclofenac, presence of H. pylori, irregular lifestyle, alcohol consumption, and aging were five factors associated with the development of ulcers; the odds ratios were 6.40, 6.07, 2.62, 2.06, and 1.05, respectively., Conclusions: Diclofenac can cause gastric mucosal lesions, including ulcers, more easily than other NSAIDs. H. pylori infection is a high-risk factor for ulcers in patients receiving long-term NSAIDs therapy. In NSAID-treated patients, subjective symptoms are not grounds for a diagnosis of gastric mucosal lesions, especially ulcers.

Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori infection are major causes of gastric mucosal lesions. In Japan, histamine-2 receptor antagonists are frequently prescribed, but the literature regarding their efficacy is limited. In this study, we compare the effects of famotidine and rebamipide on NSAID-associated gastric mucosal lesions using upper gastrointestinal endoscopy., Methods: This study examined 112 patients taking NSAIDs for either gastric hemorrhage or erosion. Before treatment, the patients were assessed by endoscopy. Using blind randomization, patients were divided into two groups: group F (famotidine, 20 mg/day) and group R (rebamipide, 300 mg/day). Efficacy was examined 4 weeks later using endoscopy., Results: After treatment, the Lanza score decreased significantly in group F (P < 0.001) but not in group R (P = 0.478). The change in the Lanza score in group F was significantly greater (P = 0.002) than that in group R., Conclusions: Famotidine was superior to rebamipide in treating NSAID-associated mucosal lesions.

We investigated the relation between gastric mucosal lesions and substance P (SP) in 64 patients with rheumatoid arthritis (RA) taking nonsteroidal antiinflammatory drugs (NSAIDs). In these patients, the incidence of gastric mucosal lesions was as high as 53.1%. Serum SP levels were significantly higher in patients with gastric mucosal lesions than in those without gastric lesions. Erythrocyte sedimentation rate, serum C-reactive protein and rheumatoid factor (RF) levels were also higher in patients with gastric mucosal lesions. A positive correlation between serum SP and RF levels was found in patients with RA. Experimental gastric mucosal lesions induced by an oral administration of indomethacin in rats were significantly enhanced by an additional intraperitoneal injection of SP. From these observations, it is suggested that, in addition to the effect of NSAIDs, SP elevation in blood has a role in the development of gastric mucosal lesion in patients with RA.