Effect of increasing Helicobacter pylori ammonia production by urea infusion on plasma gastrin concentrations.

Abstract

It has been proposed that the hypergastrinaemia in subjects with Helicobacter pylon infection is caused by the action of the ammonia produced by the organism's urease activity on the antral G cells. To investigate this hypothesis we examined the effect on plasma gastrin of increasing the bacterium's ammonia production by infusing urea intragastrically to eight H pylori positive duodenal ulcer patients. After a 60 minute control intragastric infusion of dextrose solution at 2 ml/ minute, a similar infusion containing urea (50 mmol/l) was continued for four hours. During the urea infusion, the median gastric juice urea concentration rose from 1.1 mmoVI (range 0.3-1.6) to and this resulted in an increase in the ammonium concentration from 2-3 mmol/l (range 1.3-5.9) to 6*1 mmoil/ (range 4.2-11.9) (p<001). This appreciable rise in ammonia production did not result in any change in the plasma gastrin concentration. The experiment was repeated one month after eradication of H pylori, at which time the median basal gastrin was 20 ng/l (range 15-25), significantly less than the value before eradication (30 ng/l range 15-60) (p<005). On this occasion, the gastric juice ammonium concentration was considerably reduced at 0 4 mmolIl (range 0.1-0.9) and the urea infusion did not raise the ammonium concentration or change the plasma gastrin concentration. In conclusion, augmenting H pylori ammonia production does not cause any early change in plasma gastrin.

Effect of Helicobacter pylori on Parietal Cell Sensitivity to Pentagastrin in Duodenal Ulcer Subjects

“…(13) noted that healthy volunteers with H . pylori had increased basal and meal-stimulated gastrin concentrations compared with uninfected volunteers, yet there was no difference between the two groups with regard to (5)(6)(7). basal, maximal, or meal-stimulated acid outputs.…”

Role of apoptosis induced by Helicobacter pylori infection in the development of duodenal ulcer

“…H pylori has a remarkably high urease activity by which it hydrolyses urea to ammonia and carbon dioxide 17. As a result, patients with this infection have reduced concentrations of urea and increased concentrations of ammonia in their gastric juice 18. Several investigators have shown ammonia to be deleterious to the gastric mucosa, suggesting the importance of urease and ammonia in the pathophysiology of gastroduodenal diseases in H pylori infected patients 8…”

Helicobacter pyloriand Disturbance of Gastric Function Associated with Duodenal Ulcer Disease and Gastric Cancer

“…Levi et al postulated that ammonia produced by H. pylori might raise the pH of the antral mucosal surface, blocking the normal stimulation of somatostatin and the consequent inhibition of gastrin (17). However, neither increasing production of ammonia by H. pylori by intragastric infusion of urea (18), nor inhibiting ammonia production with acetohydroxamic acid (19) or 24 hours of triple antibacterial therapy (10) alters serum gastrin levels in H. pylori-infected individuals. The lack of an acute effect does not, however, exclude an effect from long-term production of ammonia by H. pylori on D cells and gastrin release.…”