Research Information System
Turkish Journal of Gastroenterology, vol.10, no.4, pp.396-402, 1999 (SCI-Expanded)
Serious adverse events can be seen in the gastrointestinal tract and kidneys of patients treated with NSAIDs. The purpose of this study was to demonstrate whether a relationship exists between NSAID induced gastrointestinal mucosal injury and the presence of H. pylori and correlation of serum gastrin and pepsinogen-1 levels with the development of mucosal injury. The study included 30 patients (11 female and 9 male) with a mean age of 36.6 (18-65) years. Who were randomised into three comparable groups and either aspirin 300 mg/day, nabumetone, 1000 mg/day, or placebo was given orally for 10 days. Upper gastrointestinal tract endoscopy was performed and symptoms evaluated in each group before and after the treatment period. H. pylori was found to be positive in 24 (80%), patients prior to treatment. Gastrointestinal symptoms before and after 10 days of NSAID treatment were not significantly different (p>0.05) but patients treated with either aspirin (COX1 inhibitor) or nabumetone (COX-2 inhibitor) had a significant (p < 0.05) increase in mucosal injury as demonstrated by endoscopy, when compared to pretreatment findings. No difference was found between the severity or type of mucosal lesions induced either by aspirin or nabumetone. Fasting serum gastrin and pepsinogen-1 levels before and after NSAID treatment were found to be similar. NSAID induced mucosal changes were seen more frequently (p < 0.O5)in patients with H. pylori positivity when compared to those with negative values. In summary, short term NSAID treatment induces asymptomatic mucosal changes. The presence of H. pylori has a role in the development of NSAID induced mucosal changes but pathophysiologic mechanism is not through changes in serum gastrin or pepsinogen-1 levels.