The clinical pathological characteristics of 3969 adult patients with chronic atrophic gastritis were retrospectively studied. The positivity of intestinal metaplasia and dysplasia in atrophic gastric specimens increased with age; however, H. pylori positivity and inflammatory activity decreased significantly with increased age. H. pylori infection was present in 21.01% of chronic atrophic gastritis patients, and 92.33% of the subjects with H. pylori infection were found to have simultaneous inflammatory activity. The intestinal metaplasia and dysplasia positivity markedly increased as the degree of gastric atrophy increased. In conclusion, the incidence of H. pylori infection decreased with age and correlated significantly with inflammatory activity in atrophic gastritis patients. The intestinal metaplasia and dysplasia positivity notably increased as the degree of gastric atrophy increased. Large population-based prospective studies are needed to better understand the progression of CAG. 1. Introduction Chronic atrophic gastritis (CAG) is a histopathologic entity characterized by chronic inflammation of the gastric mucosa with loss of gastric glandular cells. CAG, intestinal metaplasia (IM), and epithelial dysplasia (ED) of the stomach are common and are associated with an increased risk of gastric cancer. CAG and IM are considered to be precancerous conditions. ED represents the penultimate stage of the gastric carcinogenesis sequence, defined as histologically unequivocal neoplastic epithelium without evidence of tissue invasion, and is thus a direct neoplastic precancerous lesion. ED is characterized by cellular atypia reflective of abnormal differentiation and disorganized glandular architecture. Helicobacter pylori are Gram-negative bacteria that colonize the human gastric epithelium and represent one of the most common human infections worldwide. H. pylori infection is usually contracted in the first few years of life, and its prevalence increases with older age and lower socioeconomic status during childhood [1]. This infection is the primary inducer of CAG, IM, and ED. More than half of all humans have H. pylori colonies in their stomachs; however, only a minority of H. pylori-infected individuals develop cancer of the stomach [2]. Haziri et al. [3] reported that the prevalence of H. pylori infection was high in patients with CAG (66.0%), IM (71.7%), and gastric dysplasia (71.4%). In the present study, the clinical and histopathological characteristics of 3969 CAG patients from our hospital were retrospectively studied, and the relationship
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