Helicobacter pylori-associated exaggerated gastrin release in duodenal ulcer patients. The effect of bombesin infusion and urea ingestion

Abstract

Recent studies have shown that the exaggerated meal-stimulated gastrin release in patients with duodenal ulcer abates after eradication of Helicobacter pylori infection. Bombesin-stimulated gastrin release was compared in 11 H. pylori-infected patients with chronic duodenal ulcer and 8 uninfected healthy volunteers both before and after therapy to eradicate H. pylori. Bombesin infusion significantly increased the gastrin release both in control subjects and in patients with duodenal ulcer. Antimicrobial therapy (bismuth, tetracycline, and metronidazole) to eradicate the H. pylori infection was associated with a significant reduction in bombesin-stimulated gastrin release in patients with duodenal ulcer (from 116.9 +/- 19 pg/mL to 69.5 +/- 7 pg/mL following 50 pmol.kg-1.h-1 bombesin; and from 158 +/- 29 to 83.4 +/- 10 following 200 pmol.kg-1.h-1 bombesin: P = 0.01 for each). Antimicrobial therapy had no effect on gastrin release in uninfected volunteers, thus excluding a nonspecific effect of antimicrobial therapy on antral G-cell function. Serum gastrin was also not increased by feeding 500 mg of urea to 5 H. pylori-infected volunteers. This suggests that access of hydrogen ion to the pH-sensitive sites governing gastrin release by mucosal ammonia produced by H. pylori urease is not a critical factor. These data suggest that exaggerated gastrin release present in patients with duodenal ulcer disease is secondary to H. pylori infection.