M. Abdelwahab et al., CELLULAR PROLIFERATION AND PLOIDY OF THE GASTRIC-MUCOSA - THE ROLE OFHELICOBACTER-PYLORI, Hepato-gastroenterology, 44(15), 1997, pp. 880-885
Background/Aims: Recently, H. pylori has been recognized as a risk fac
tor for gastric adenocarcinoma. As such, we have analyzed the DNA cont
ent of gastric epithelial cells in an attempt to reveal the role of H.
pylori in, gastric carcinogenesis. Methodology: Fifty-three subjects
presented with gastric dyspepsia, 39 males and 14 females, with a mean
. age of 42.15 (+/-13.16) years. They were referred to the out-patient
clinic to undergo endoscopic examination for the first time. Biopsy s
pecimens from the antrum of each subject were subjected to culture for
the presence of H. pylori, histologic diagnosis, and DNA flow cytomet
ry for the analysis of cellular proliferation and DNA ploidy. Results:
The endoscopic diagnoses were normal appearance (12), Gastric ulcer (
12), duodenal ulcer (29). Thirty-eight (72%) subjects were positive, a
nd 15 (28%) subjects were negative for H. pylori. Abnormal DNA-content
(aneuploidy) was found in specimens from the antrums of 3 patients, 2
patients with duodenal ulcers (DU) and one with a gastric ulcer (GU).
The cellular proliferation, as detected by flow cytometry in the form
of proliferative index: (PI; percentage of cells in the DNA S and G2M
phases) was 27.88 (+/-12.48) and 14.17 (+/-2.94) in the antrums of th
ose positive and negative for H. pylori, respectively. A very signific
ant increase in the PI (p < 0.005) was found between subjects positive
and negative for H. pylori. Patients with DU and H. pylori infection
had the highest PI, and the PI was significantly higher than in patien
ts with DU, but without infection. Regarding histology, there was a si
gnificant increase in the PI in the presence of H. pylori infection in
either CAG or dysplasia groups as compared to cases without infection
in the same groups. Conclusion: These results show that H. pylori inf
ection is associated with changes in the DNA-content and cellular prol
iferative activity, suggesting that H. pylori may be implicated in gas
tric carcinogenesis. Also, the significant increase in the PI along th
e progression of severity of the disease suggests that measuring this
parameter might allow more accurate monitoring of patients, so that a
targeted therapeutic protocol may be defined.