An associatioin of cagA+ helicobacter pylori infection with cell proliferation in gastric mucosae of gastritis and gastric cancer patients.
- Author:
Geum Am SONG
1
;
Yang Jung KIM
;
Tae Oh KIM
;
Hyong Wook KIM
;
Seung Keun PARK
;
Dae Hwan KANG
;
Chul Soo SONG
;
Mong CHO
;
Ung Suk YANG
Author Information
1. Department of Internal Medicine, College of Medicine, Pusan National University, Pusan, Korea.
- Publication Type:Original Article
- Keywords:
Helicobacter pylori;
cagA;
Cell proliferation
- MeSH:
Biopsy;
Carcinogenesis;
Cell Proliferation*;
Gastric Mucosa*;
Gastritis*;
Gastrointestinal Diseases;
Hand;
Helicobacter pylori*;
Helicobacter*;
Humans;
Ki-67 Antigen;
Polymerase Chain Reaction;
Prevalence;
Stomach Neoplasms*;
Urea
- From:Korean Journal of Medicine
1999;57(2):158-167
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: It has been suggested that cytotoxin associated gene A (cagA) is a marker of more virulent strains of H. pylori and cagA bearing H. pylori is more pathogenic in the gastrointestinal diseases. On the other hand, according to several reports H. pylori causes the cell proliferation, which may be an important mechanism of gastric carcinogenesis. So, we studied to elucidate whether there is the association of the cagA positive H. pylori infection with cell proliferation on the gastric mucosae of the patients with gastritis and gastric cancer or not. METHODS: In this study, 27 gastritis and 35 gastric cancer patients were included. PCR assay for the detection of H. pylori(ureA PCR) and cagA bearing H. pylori(eagA PCR) were performed on the gastric mucosal biopsy specimen. Immunohistochemical study using the MIB 1 Ab against Ki 67 antigen was carried out to evaluate the cell proliferation. RESULTS: The prevalence of H. pylori infection was 85.2%(23/27) in the patients with gastritis and 54.3%(19/ 35) in the patients with gastric cancer. The prevalence of cagA+ strain of H. pylori was 52.2%(12/23) and 47.4%(9/ 19) in the patients with gastritis and gastric cancer. In the patients with gastritis, the degree of cell proliferation was not different in the ureA positive(24.8%) and ureA negative(21.7%) gastric mucosae. Moreover, the difference of cell proliferation was not observed according to the presence or absence of cagA gene(29.4% vs 19.9%) among the ureA positive gastric mucosae. In the patients with gastric cancer, cell proliferation indices were 25.5% and 27.5% in the ureA postive and cagA negative gastric mucosae, 28.1% and 22.2% in the cagA positive and cagA negative group among the ureA positive gastric mucosae. There was no significant difference statistically. CONCLUSIONS: There was no association of cagA+ strain of H. pylori with cell proliferation in the gastric mucosae of the patients with gastritis and gastric cancer. It was presumed that more studies are needed to elucidate the role of H. pylori infection in the gastric carcinogenesis.
