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

BACKGROUND

Helicobacter pylori induced antibodies reacting with fundal mucosa have been shown to be involved in the pathogenesis of chronic atrophic gastritis in adults. Furthermore, previous reports have indicated that Helicobacter pylori increases the risk of gastric carcinoma, suggesting that the bacterium plays a role in mucosal changes representing especially in adulthood important steps in the progression from gastritis to cancer.

PATIENTS AND

METHODS

We investigated 16 Helicobacter pylori+ children from a series of 53 dyspeptic patients. Diagnosis of Helicobacter pylori infection was based on the positivity of at least 3 of the following tests: serology, 13C-urea breath test, rapid urease test and histology. Autoreaction was detected by incubation of gastric body sections with autologous sera and revealed by immunohistochemistry. Positive sera were tested with samples of unaffected gastric body to exclude a link with residual bacterial antigens. Proliferating cell nuclear antigen immunohistostain was also performed to evaluate the epithelial proliferative state.

RESULTS

Histologically 6 out of 16 Helicobacter pylori+ patients showed chronic 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 and a clinical history of ulcer-like dyspepsia. Parietal cells, in particular, were involved and showed diffuse cytoplasm staining. Proliferating cell nuclear antigen expression demonstrated, only in this case, a zone of regeneration extending from the normal site in the neck towards the base of the glands.

CONCLUSIONS

Our finding demonstrates that an autoreaction of gastric mucosa may be found in Helicobacter pylori gastritis of childhood. Its association with some known risk factors (i.e., cytotoxic strains and increased proliferation of gastric epithelium with a changed pattern) may play a role in the progression from gastritis to atrophy and account for the increased risk of late gastric cancer when Helicobacter pylori infection occurs in paediatric age.