Helicobacter pylori infection accelerates human gastric mucosal cell proliferation
Helicobacter pylori causes chronic atrophic gastritis and intestinal type gastric cancer arises against a background of atrophic gastritis. Increased proliferation of epithelial cells is an important indicator of increased risk for gastric adenocarcinoma. We investigated gastric mucosal cell proliferation inH. pylori-associated gastritis and the effect of eradication therapy on this proliferation in 45 patients endoscopically diagnosed (31 with persistent eradication and 14 in whomH. pylori) recurred.H. pylori status was determined by culture and histology in biopsied specimens from the gastric antrum and corpus. Eradication of the infection was defined as reversal to negative on both tests. In vitro Ki-67 immunostaining of endoscopic biopsy specimens was used to measure mucosal cell proliferation inH. pylori-associated gastritis before and after therapy. The proliferative zone was defined as the distance of Ki-67-positive gastric epithelial cells between the highest and the lowest cells. In patients in whomH. pylori was eradicated, cell proliferation in both the antral and corpus mucosa had decreased 4 weeks after completion of the eradication therapy (P<0.01,P<0.001), and 6 months later, it had markedly decreased (P<0.05,P<0.05) and returned to normal. In patients in whomH. pylori recurred, only antral epithelial cell proliferation was reduced 4 weeks after eradication therapy, but whenH. pylori recurred, determined by culture and histology, cell proliferation level was the same as that before eradication. These results suggest thatH. pylori infection accelerates cell proliferation in gastric mucosa and may play a causal role in the chain of events leading to gastric carcinoma.
Key wordsHelicobacter pylori gastric cancer cell proliferation Ki-67 eradication therapy
Unable to display preview. Download preview PDF.
- 2.Wyatt JI.Campylobacter pylori, duodenitis and duodenal ulceration. In: Rathbone BJ, Heatley RV (eds)Campylobacter pylori and gastroduodenal disease. Oxford: Blackwell Scientific, 1989:117–124.Google Scholar
- 4.Correa P. The gastric precancerous process. Cancer Surv 1983;2:437–450.Google Scholar
- 5.Hart-Hansen O, Johansen A, Larsen JK, et al. Cell proliferation in normal and diseased gastric mucosa: Autoradiography after in vitro continuous labelling with titrated thymidine. Acta Pathol Microbiol Scand A 1979;87:217–222.Google Scholar
- 13.Raus EAJ, Langenberg W, Houthoff HJ, et al.Campylobacter pyloridis-associated chronic active gastritis. A prospective study of its prevalence and effects of antibacterial and antiulcer treatment. Gastroenterology 1988;94:33–40.Google Scholar
- 14.Gerdes J, Lemke H, Baisch H, et al. Cell cycle analysis of a cell proliferation-associated human nuclear antigen defined by the monoclonal antibody Ki-67. J Immunol 1983;133:1710–1715.Google Scholar
- 16.Lott M, Wright NA Epithelial kinetics control, and consequences of alterations in disease. In: Whitehead R (ed) Gastrointestinal and oesophageal pathology, 1st ed. Edinburgh: Churchill Livingstone, 1992:93–105.Google Scholar
- 19.Ken WC, Simmy B, John ADO, et al.Helicobacter pylori infection does not increase gastric antrum mucosal cell proliferation. Am J Gastroenterol 1995;90:64–66.Google Scholar