Effect of Helicobacter pylori‐Induced Cyclooxygenase‐2 on Gastric Epithelial Cell Kinetics: Implication for Gastric Carcinogenesis

Document Type



Internal Medicine (East Africa)


Background. Cyclooxygenase (COX)‐2 induced by Helicobacter pylori is thought to enhance gastric carcinogenesis by affecting the maintenance of epithelial homeostasis.

Materials and Methods. Gastric biopsies from 160 subjects, 97 with nonulcer dyspepsia (47 H. pylori negative, 50 H. pylori positive) and 63 with gastric cancer were examined immunohistochemically for COX‐2 expression, cell proliferation and apoptotic indices.

Results. COX‐2 expression in corpus was significantly higher in H. pylori positive than in negative non‐ulcer dyspepsia (NUD) (p < .05). Regardless of site, gastric cancer subjects had higher COX‐2 expression in both antrum and corpus compared with H. pylori negative and positive NUD (p < .005). Proliferation was higher in cancer and H. pylori positive than in negative NUD (p < .0001). Moreover, cancer had enhanced proliferation than H. pylori positive NUD in corpus greater (p = .0454) and antrum lesser (p = .0215) curvatures. Apoptosis was higher in H. pylori positive than in negative NUD (p < .05). However, both had a higher index than the cancer subjects (p < .0001). Apoptosis : proliferation ratio was higher in corpus of H. pylori negative than in positive NUD in greater (p = .0122) and lesser (p = .0009) curvatures. However, both had a higher A:P ratio than cancer cases (p = .0001). A negative correlation between COX‐2 expression and A:P ratio was found in corpus greater (r = –.176, p= .0437) and lesser (r = –.188, p= .0312) curvatures.

Conclusion. The expression of COX‐2 is associated with disruption in gastric epithelial kinetics and hence may play a role in gastric carcinogenesis.


This work was published before the author joined Aga Khan University.