Autoantibodies reacting with gastric antigens in Helicobacter pylori associated body gastritis of dyspeptic children

Background Helicobacter pylori induced antibodies reacting with fundal muco sa have been shown to be involved in the pathogenesis of chronic atrophic g astritis in adults. Furthermore, previous reports have indicated that Helic obacter pylori increases the risk of gastric carcinoma, suggesting that the bacterium plays a role in mucosal changes representing especially in adult hood important steps in the progression from gastritis to cancel: Patients and methods. We investigated 16 Helicobacter pylori+ children from a series of 53 dyspeptic patients. Diagnosis of Helicobacter pylori infect ion was based on the positivity of at least 3 of the following rests: serol ogy, C-13-urea breath test, rapid urease test and histology. Autoreaction w as detected by incubation of gastric body sections with autologous sera and revealed by immunohistochemistry. Positive sera were tested with samples o f unaffected gastric body to exclude a link with residual bacterial antigen s. Proliferating cell nuclear antigen immunohistostain was also performed t o evaluate the epithelial proliferative state. Results. Histologically 6 out of 16 Helicobacter pylori+ patients showed ch ronic pangastritis. In the remaining 10 Helicobacter pylori-related mucosal inflammation was confined to the antrum. All 6 subjects with pangastritis and 3 out of 10 with antral gastritis were anti-CagA+. The autoreaction was found in a 10-year old male child with Helicobacter pylori+ pangastritis a nd a clinical history of ulcer-like dyspepsia. Parietal cells, in particula r were involved and showed diffuse cytoplasm staining Proliferating cell nu clear antigen expression demonstrated, only in this case, a zone of regener ation extending from the normal site in the neck towards the base of the gl ands. Conclusions. Our finding demonstrates that art autoreaction of gastric muco sa may be found in Helicobacter pylori gastritis of childhood. Its associat ion with some known risk factors (i.e., cytotoxic strains and increased pro liferation of gastric epithelium with a changed pattern) may play a role in the progression from gastritis to atrophy and account for the increased ri sk of late gastric cancer when Helicobacter pylori infection occurs in paed iatric age.