» Articles » PMID: 7698690

Cell Proliferation in Helicobacter Pylori Associated Gastritis and the Effect of Eradication Therapy

Overview
Journal Gut
Specialty Gastroenterology
Date 1995 Mar 1
PMID 7698690
Citations 42
Authors
Affiliations
Soon will be listed here.
Abstract

Helicobacter pylori causes chronic (type B) gastritis. The 'intestinal' form of gastric cancer arises against a background of chronic gastritis, and prospective epidemiological studies have shown that H pylori is a major risk factor for this. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging where there is chronic epithelial cell injury associated with H pylori gastritis. In vitro bromodeoxyuridine labelling of endoscopic antral biopsy specimens was used to measure mucosal cell proliferation in H pylori associated gastritis before and after therapy for H pylori triple infection. Cell proliferation was increased in H pylori associated gastritis patients compared with normal controls and patients with H pylori negative chronic gastritis (p = 0.0001; Tukey's Studentised range). There was no difference in antral epithelial cell proliferation between duodenal ulcer and non-ulcer subjects infected with H pylori (p = 0.62; Student's t test). Antral mucosal cell proliferation fell four weeks after completing triple therapy, irrespective of whether or not H pylori had been eradicated (p = 0.0001). At retesting six to 18 months later (mean = 12 months), however, those in whom H pylori had not been successfully eradicated showed increased mucosal proliferation compared with both H pylori negative subjects at a similar follow up interval and all cases (whether H pylori positive or negative) four weeks after completion of triple therapy (p = 0.024). These findings suggest that H pylori infection causes increased gastric cell proliferation and in this way may play a part in gastric carcinogenesis.

Citing Articles

Impact of Helicobacter pylori on the healing process of the gastric barrier.

Mnich E, Kowalewicz-Kulbat M, Sicinska P, Hinc K, Obuchowski M, Gajewski A World J Gastroenterol. 2016; 22(33):7536-58.

PMID: 27672275 PMC: 5011668. DOI: 10.3748/wjg.v22.i33.7536.


Epigenetic regulation of DNA repair machinery in Helicobacter pylori-induced gastric carcinogenesis.

Santos J, Ribeiro M World J Gastroenterol. 2015; 21(30):9021-37.

PMID: 26290630 PMC: 4533035. DOI: 10.3748/wjg.v21.i30.9021.


Helicobacter pylori protein JHP0290 exhibits proliferative and anti-apoptotic effects in gastric epithelial cells.

Tavares R, Pathak S PLoS One. 2015; 10(4):e0124407.

PMID: 25879227 PMC: 4400171. DOI: 10.1371/journal.pone.0124407.


Helicobacter pylori Infection Activates the Akt-Mdm2-p53 Signaling Pathway in Gastric Epithelial Cells.

Shu X, Yang Z, Li Z, Chen L, Zhou X, Xie Y Dig Dis Sci. 2014; 60(4):876-86.

PMID: 25480405 DOI: 10.1007/s10620-014-3470-2.


Magnifying narrow-band imaging of surface maturation in early differentiated-type gastric cancers after Helicobacter pylori eradication.

Kobayashi M, Hashimoto S, Nishikura K, Mizuno K, Takeuchi M, Sato Y J Gastroenterol. 2013; 48(12):1332-42.

PMID: 23420575 DOI: 10.1007/s00535-013-0764-7.


References
1.
MORSON B . Intestinal metaplasia of the gastric mucosa. Br J Cancer. 1955; 9(3):365-76. PMC: 2073705. DOI: 10.1038/bjc.1955.35. View

2.
Sobala G, Schorah C, Shires S, Lynch D, Gallacher B, Dixon M . Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. Gut. 1993; 34(8):1038-41. PMC: 1374349. DOI: 10.1136/gut.34.8.1038. View

3.
Hart-Hansen O, Johansen A, Larsen J, Svendsen L . Cell proliferation in normal and diseased gastric mucosa. Autoradiography after in vitro continuous labelling with tritiated thymidine. Acta Pathol Microbiol Scand A. 1979; 87A(3):217-22. View

4.
Rauws E, Langenberg W, Houthoff H, Zanen H, Tytgat G . Campylobacter pyloridis-associated chronic active antral gastritis. A prospective study of its prevalence and the effects of antibacterial and antiulcer treatment. Gastroenterology. 1988; 94(1):33-40. View

5.
Mackerness C, Leach S, Thompson M, Hill M . The inhibition of bacterially mediated N-nitrosation by vitamin C: relevance to the inhibition of endogenous N-nitrosation in the achlorhydric stomach. Carcinogenesis. 1989; 10(2):397-9. DOI: 10.1093/carcin/10.2.397. View