INTRODUCTION: Helicobacter pylori is a definite risk factor for the development of gastric cancer, especially in the context of corpus-predominant gastritis. The infection is usually acquired in early childhood, implying lifelong exposure to this carcinogen if untreated. Our objective was to analyze the prevalence of H. pylori induced corpus-predominant gastritis in children. MATERIAL AND METHODS: We analyzed the results of 265 esophagogastroduodenoscopies (EGD) in children performed between February 2006 and August 2008; 34 endoscopies were excluded (24 with follow-up investigations, 5 with incomplete data, 5 adults). H. pylori gastritis was defined by the presence of H. pylori in histology or by a positive rapid urease test. Grade of inflammation was rated according to the updated Sydney Scoring System. Gastritis was classified as corpus-predominant when the degree of chronic inflammation was higher in the corpus than in the antrum and vice versa for antrum-predominant gastritis. RESULTS: Two hundred thirty-one patients (128 female; mean age ± SEM: 10.5 ± 3.5 years) were analyzed. Eighty-four (36%) were H. pylori positive, 147 (64%) patients were negative for H. pylori. In H. pylori positive patients, 39 (46%) patients had pangastritis (one patient with mucosal atrophy, which is regarded as precancerous lesion), 42 (50%) had antrum-predominant gastritis and 3 (4%) had corpus-predominant gastritis. One female patient (15.6 years old) with severe (grade 3) pangastritis had focal mucosal atrophy in both antrum and corpus, but no patient had intestinal metaplasia. CONCLUSIONS: Corpus-predominant gastritis develops in H. pylori infected children, while mucosal atrophy and intestinal metaplasia develop later in the course of the infection.
INTRODUCTION:Helicobacter pylori is a definite risk factor for the development of gastric cancer, especially in the context of corpus-predominant gastritis. The infection is usually acquired in early childhood, implying lifelong exposure to this carcinogen if untreated. Our objective was to analyze the prevalence of H. pylori induced corpus-predominant gastritis in children. MATERIAL AND METHODS: We analyzed the results of 265 esophagogastroduodenoscopies (EGD) in children performed between February 2006 and August 2008; 34 endoscopies were excluded (24 with follow-up investigations, 5 with incomplete data, 5 adults). H. pylorigastritis was defined by the presence of H. pylori in histology or by a positive rapid urease test. Grade of inflammation was rated according to the updated Sydney Scoring System. Gastritis was classified as corpus-predominant when the degree of chronic inflammation was higher in the corpus than in the antrum and vice versa for antrum-predominant gastritis. RESULTS: Two hundred thirty-one patients (128 female; mean age ± SEM: 10.5 ± 3.5 years) were analyzed. Eighty-four (36%) were H. pylori positive, 147 (64%) patients were negative for H. pylori. In H. pylori positive patients, 39 (46%) patients had pangastritis (one patient with mucosal atrophy, which is regarded as precancerous lesion), 42 (50%) had antrum-predominant gastritis and 3 (4%) had corpus-predominant gastritis. One female patient (15.6 years old) with severe (grade 3) pangastritis had focal mucosal atrophy in both antrum and corpus, but no patient had intestinal metaplasia. CONCLUSIONS: Corpus-predominant gastritis develops in H. pylori infected children, while mucosal atrophy and intestinal metaplasia develop later in the course of the infection.