OBJECTIVES: Antigastric autoantibodies (AGA) can be detected in as many as 50% of adults infected with Helicobacter pylori. We investigated H pylori -associated antigastric autoimmunity in children and adolescents. STUDY DESIGN: Patients with dyspepsia (n = 78; mean age 10.9 years, range 2-21 years, SE 0.46 years) underwent gastroscopy. H pylori infection was determined by serologic and histologic features and breath tests. AGA were detected by immunohistochemistry and were characterized by immunoprecipitation with the gastric hydrogen ion, potassium ion, adenosine triphosphatase (H(+),K(+)-ATPase). In absorption assays, antibodies against H pylori were removed to determine the role of molecular mimicry. RESULTS: AGA were detected in 9 (18%) of the 51 infected patients and in 1 (4 %) of the 27 noninfected patients (P =.08; nonsignificant) and could not be absorbed to H pylori. Children with AGA were significantly older (P =.01). AGA in H pylori gastritis reacted against the gastric H(+),K(+)-ATPase in 3 (33%) of the 9 patients. CONCLUSIONS: The age of the patient or the duration of gastritis seem to be relevant factors for the formation of antigastric autoimmunity. The gastric H(+),K(+)-ATPase represents an autoantigen as early as childhood. No evidence for a role of molecular mimicry between H pylori and the host at this young age could be found.
OBJECTIVES: Antigastric autoantibodies (AGA) can be detected in as many as 50% of adults infected with Helicobacter pylori. We investigated H pylori -associated antigastric autoimmunity in children and adolescents. STUDY DESIGN:Patients with dyspepsia (n = 78; mean age 10.9 years, range 2-21 years, SE 0.46 years) underwent gastroscopy. H pylori infection was determined by serologic and histologic features and breath tests. AGA were detected by immunohistochemistry and were characterized by immunoprecipitation with the gastric hydrogen ion, potassium ion, adenosine triphosphatase (H(+),K(+)-ATPase). In absorption assays, antibodies against H pylori were removed to determine the role of molecular mimicry. RESULTS: AGA were detected in 9 (18%) of the 51 infected patients and in 1 (4 %) of the 27 noninfected patients (P =.08; nonsignificant) and could not be absorbed to H pylori. Children with AGA were significantly older (P =.01). AGA in H pylori gastritis reacted against the gastric H(+),K(+)-ATPase in 3 (33%) of the 9 patients. CONCLUSIONS: The age of the patient or the duration of gastritis seem to be relevant factors for the formation of antigastric autoimmunity. The gastric H(+),K(+)-ATPase represents an autoantigen as early as childhood. No evidence for a role of molecular mimicry between H pylori and the host at this young age could be found.