The effects of Helicobacter pylori infection and cyclooxygenase-2 expression during the gastric carcinogenesis

Objective To clarify the role of Helicobacter pylori (H. Pylori) that induced cyclooxygenase (COX)-2 expression during the gestric carcinogenesis. Methods A total of 138 gastric biopsies, including 30 cases with chronic non-atrophic gastritis, 85 cases with chronic atrophic gastritis (accompanying moderate or severe intestinal metaplasia 45 cases and dysplasia 12 cases), and 23 cases with gastric carcinoma were studied. H. pylori infection was assessed by rapid urease test and histological examination (modified Giemsa staining). Expression of COX-1 and COX-2 was detected by immunohistochemical stain. Results H. pylori infection rate was 69.6% in gastric carcinoma, significantly higher than 36.7% in chronic non-atrophic gastritis (P0.05). The positive expression rates of COX-2 were 10.0%, 37.6%, 37.8%, 41.7% and 69.6% in chronic non-atrophic gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia and gastric carcinoma respectively. From chronic non-atrophic gastritis to chronic atrophic gastritis to intestinal metaplasia to dysplasia to gastric carcinoma, expression of COX-2 showed as ascending tendency, whereas COX-1 expression did not change significantly in the gastric mucosa. COX-2 expression in chronic atrophic gastritis, intestinal metaplasia and dysplasia were significantly higher in H. pylori-positive than in H. pylori-negative subjects (P0.01). Conclusion COX-2 expression induced by H. pylori infection is a relatively early event during carcinogenesis in the stomach.