CHANGES IN THE INTRAGASTRIC DISTRIBUTION OF HELICOBACTER-PYLORI DURING TREATMENT WITH OMEPRAZOLE

Omeprazole is a powerful inhibitor of gastric acid and may suppress He licobacter pylori by effecting the pKa of H pylori urease, by altering the pattern of infection, or by promoting overgrowth of other bacteri a. At routine endoscopy H pylori was detected by histology and culture before and after four weeks' treatment with omeprazole, 40 mg each mo rning. A C-13-urea breath test was also done at t=0, 2, 4, and 6 weeks . Thirty nine patients with duodenal ulcer (n=25) or reflux oesophagit is (n=14) were studied, of whom 29 of 39 had H pylori infection. Durin g omeprazole treatment, C-13-urea breath test values fell significantl y - mean (SEM) values before treatment and at four weeks were 23.0 (2. 1) and 15.5 (2.7) per mil respectively, p<0.001. Before treatment H py lori was seen in 28 of 29 antral, 29 of 29 corpus, and 28 of 29 fundic biopsy specimens. After four weeks of omeprazole treatment, the histo logical density of H pylori in the antrum and corpus was reduced (p<0. 001), while that in the fundus was increased. The migration of H pylor i from the antrum to the fundus was associated with a corresponding de crease in the activity of antral gastritis. H pylori was not seen in a ntral biopsy specimens from 12 of 29 patients whose median excess 6 (C O2)-C-13, excretion fell from 23.0 to 9.9 per mil. In the body mucosa, 26 of 29 specimens were still positive for H pylori and there was no significant change in the gastritis type. Two weeks after finishing tr eatment, the mean (SEM) excess 6 (CO2)-C-13 excretion returned to leve ls before treatment. Omeprazole decreases antral H pylori colonisation but increases that in the fundus. The changes in the intragastric dis tribution of the organism are associated with concomitant changes in t he activity of gastritis and are matched by a progressive fall in the excretion of delta (CO2)-C-13.