AIM:To study the effect of Helicobacter pylori (H. pylori) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS: Gastric biopsy specimens from normal controls (n = 11), superficial gastritis (n = 32), atrophic gastritis with intestinal metaplasia (n= 83), dysplasia (n= 25) and gastric carcinoma (n = 10) were studied by immunohistochemical stianing of proliferating cell nuclear antigen (PCNA). RESULTS: The gastric epithelial proliferation, expressed as PCNA labeling index (LI)%, was progressively increased in successive stages from normal mucosa to gastric carcinoma regardless of H. pylori status. There was significant difference in PCNA LI% among all groups (P <0.01). The analysis pursuing the effect of H. pylori infection on gastric epithelial proliferation in the progression from normal mucosa to gastriccarcinoma showed that in superficial gastritis and mild atrophic gastritis groups, PCNA LI% in H. pylori positive patients were 13.14 ± 1.6 and 19.68 ± 2.22 respectively, significantly higher than 6.95 ± 0.78 and 11.34 ± 1.89 in H. pylori negative patients (P <0.01); but there was no such difference in other groups (P >0.05). CONCLUSION: H. pylori infection causes increased gastric epithelial proliferation in the stages of superficial and mild atrophic gastritis and may play a part in triggering gastric carcinogenesis.
AIM:To study the effect of Helicobacter pylori (H. pylori) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS: Gastric biopsy specimens from normal controls (n = 11), superficial gastritis (n = 32), atrophic gastritis with intestinal metaplasia (n= 83), dysplasia (n= 25) and gastric carcinoma (n = 10) were studied by immunohistochemical stianing of proliferating cell nuclear antigen (PCNA). RESULTS: The gastric epithelial proliferation, expressed as PCNA labeling index (LI)%, was progressively increased in successive stages from normal mucosa to gastric carcinoma regardless of H. pylori status. There was significant difference in PCNA LI% among all groups (P <0.01). The analysis pursuing the effect of H. pyloriinfection on gastric epithelial proliferation in the progression from normal mucosa to gastriccarcinoma showed that in superficial gastritis and mild atrophic gastritis groups, PCNA LI% in H. pylori positive patients were 13.14 ± 1.6 and 19.68 ± 2.22 respectively, significantly higher than 6.95 ± 0.78 and 11.34 ± 1.89 in H. pylori negative patients (P <0.01); but there was no such difference in other groups (P >0.05). CONCLUSION:H. pyloriinfection causes increased gastric epithelial proliferation in the stages of superficial and mild atrophic gastritis and may play a part in triggering gastric carcinogenesis.
Authors: G M Sobala; B Pignatelli; C J Schorah; H Bartsch; M Sanderson; M F Dixon; S Shires; R F King; A T Axon Journal: Carcinogenesis Date: 1991-02 Impact factor: 4.944