Presence of gastric autoantibodies impairs gastric secretory function in patients with Helicobacter pylori-positive duodenal ulcer

Background: Although the association between Helicobacter pylori infection and gastric autoimmunity is now well established, to date little is known a bout the significance of anticanalicular autoantibodies in patients with du odenal ulcer (DU). We therefore investigated the prevalence of serum antipa rietal cell autoreactivity in DU patients as well as the relationship betwe en these autoantibodies, gastric histopathology and gastric secretory funct ion in this setting. Methods: Forty-one consecutive patients with H. pylori -positive DU were initially recruited. In all patients, basal (BAO) and pen tagastrin stimulated acid output (PAO), fasting and meal-induced serum gast rin levels. as well as serum pepsinogen I concentrations, were measured. An tral and body gastritis was evaluated according to the Sydney system. Serum anticanalicular autoreactivity was determined by the indirect immunoperoxi dase technique. Results: Serum anticanalicular autoantibodies were found in 7 out of 34 patients (20%), The presence of these antibodies was associate d with a significantly higher grade of body gastritis (activity: 1.9 versus 0.9) as well as with significantly higher fasting and meal stimulated gast rin levels (mean fasting gastrin, 76.4 (15.2) pg/ml versus 59.3 (20.5) pg/m l). In addition, PAO values were significantly lower in patients with gastr ic autoantibodies than in those without this autoreactivity (mean 0.35 (0.1 6) mmol kg(-1) h(-1) versus 0.49 (0.16) mmol kg(-1) h(-1)). In contrast, no significant differences were found between patients with and without antic analicular autoantibodies as regards fasting serum pepsinogen I concentrati ons. Conclusions: Serum anticanalicular autoantibodies can be detected in 2 0% of patients with DU and are associated with a more severe pattern of bod y gastritis, higher gastrin levels and decreased peak acid secretion values . Their presence could account for the normal or reduced acid output which can be seen in a subset of DU patients.