The effect of age and Helicobacter pylori infection on gastric epithelial cell kinetics

Summary

Background

Helicobacter pylori infection is a known risk factor for gastric cancer. The aim of the study was to determine the effect of H. pylori and age on gastric epithelial cell kinetics.

Methods

One hundred and fifty-seven patients (92 men, median age: 58.5 years, range: 18–85) who had undergone upper gastrointestinal endoscopy due to dyspeptic symptoms were enrolled into the study. Six antral biopsy samples were obtained for flow cytometric DNA analysis (expressed as proliferative index [PI], S+G2/M phase), presence of H. pylori (CLO-test, culture and histology), and histopathologic examination.

Results

Eighty-four (53.5%) patients were H. pylori positive and 93.3% of patients had diploid pattern and 6.7% expressed aneuploid pattern. The mean PI was 4.8 ± 0.2 for the whole group studied. PI were 5.14 ± 0.33 and 4.26 ± 0.36 for H. pylori (+) and H. pylori (−) patients respectively (P = 0.017). When age groups were taken into account, PI was found higher in patients over 75 years of age (n = 14, PI = 6.66 ± 1.3) compared to patients under 35 years of age (n = 25, PI = 3.83 ± 0.41, P = 0.014). There was no correlation between histological changes and PI. H. pylori (P = 0.045) and age (P = 0.082) were independent factors for PI.

Conclusion

PI of gastric antral mucosa increases in patients with H. pylori infection. Although PI increases by age, H. pylori is the only factor that significantly and independently influences the rate of epithelial cell proliferation.

Introduction

Helicobacter pylori is the main cause of chronic gastritis, peptic ulcer disease and gastric mucosa associated lymphoid tissue (MALT) lymphoma [1], [2], [3]. Further, H. pylori is now considered as a class I carcinogen and it is predicted that the absence of infection would result in at least 60% fewer cases of gastric cancer worldwide [4], [5]. Chronic gastritis induced by H. pylori may lead to atrophy and intestinal metaplasia [6], [7]. Meta-analyses have shown that H. pylori colonization of the stomach is a risk factor for gastric cancer development [8]. Although gastric cancer is thought to be a multifactorial disease, one of the suggested mechanisms of cancer development is perturbation of cellular proliferation and induction of a hyperproliferative state [9], [10]. It has been shown that H. pylori infection accelerates the proliferation of both neoplastic and non-neoplastic epithelial cells in patients with dyspepsia, peptic ulcer disease and adenocarcinoma [11], [12], [13], [14], [15], [16], [17], [18]. Similarly, proliferative activity of gastric cancer has been found to be increased and confirmed in several studies using thymidine, bromodeosyuridine, and flow cytometry [19], [20]. In the study by Chow et al., it was depicted that neither H. pylori nor age had any significant effect on gastric antral mucosal cell proliferation [21]. On the other hand, it has been shown that prevalence of H. pylori infection and chronic gastritis are both increased in the elderly population [22]. However, Baldini et al., reported that the relationship between H. pylori infection and increased gastric epithelial cell proliferation is independent from age [23]. Therefore, the aim of this study was to investigate the effect of age and H. pylori infection on gastric antral epithelial cell proliferation.