The effect of ammonia on omeprazole-induced reduction of gastric acidity in subjects with Helicobacter pylori infection

OBJECTIVE: Omeprazole produces a higher intragastric pH during Helicobacter pylori (H. pylori) infection than after cure. We tested the hypothesis tha t this difference is due to the production of ammonia by H. pylori. METHODS: Gastric acidity and acid output (AO) were measured overnight in 12 subjects, with and without omeprazole, before and 1 and 6 months after cur e of H. pylori infection. Gastric ammonia ([NH3]), total bile acid ([TBA]) and protein concentrations and plasma omeprazole levels were measured. RESULTS: During omeprazole, median AO were 0.0 mmol/h before, 0.86 mmol/h ( p = 0.003 vs before cure) at 1 month, and 0.34 mmol/h (p = 0.02) at 6 month s after cure; median NH3 output was 0.17 mmol/h before, 0.03 mmol/h (p = 0. 002) at 1 month, and 0.02 mmol/h (p = 0.005) at 6 months after cure. AO and NH3 output were similar 1 and 6 months after cure. When corrected for [NH3 ], AO and gastric pH curves were similar before and after cure. Omeprazole plasma levels increased after cure and gastric [TBA] were unchanged. CONCLUSIONS: The higher pH observed before cure of H. pylori during omepraz ole administration is attributable, in large part, to ammonia production. O ther acid-neutralizing substances and changes in acid secretion may also be important, but duodenogastric reflux and omeprazole pharmacokinetics are n ot involved. (C) 2000 by Am. Cell. of Gastroenterology.