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To test the hypothesis that Helicobacter pylon1 infection is associated with a decreased intragastric acidity during omeprazole therapy, ambulatory 24 hour dual point gastric pH recordings were performed in 18 H pyloni positive and 14 H pylori negative subjects. There was a four to six week washout period between the two pH recordings made in each subject after one week courses of placebo or omeprazole, 20 mg daily. During placebo, median 24 hour pH values were not different in the corpus (H pylori positive=1.5, negative=1-4; p=0*9) or antrum (H pyloni positive= 13, negative= 12; p=0 1). However, during omeprazole treatment, median 24 hour pH values were higher in H pylori positive subjects, both in the corpus (H pylori positive=5 5, negative=4*0; p=0.001) and antrum (H pylorn positive=5.5, negative=3.5; p=0.0004). During placebo treatment, the only difference between the two groups was a higher later nocturnal pH in the antrum in the H pylorn positive group. During omeprazole treatment, gastric pH was higher both in the corpus and in the antrum in the H pylon positive group for all periods, except for mealtime in the corpus. These data indicate that omeprazole produces a greater decrease in gastric acidity in subjects with H pylon infection than in those who are H pylon negative. It is not, however, known whether there is a causal relationship between H pylorn infection and increased omeprazole efficacy. (Gut 1995; 36: 539-543) Keywords: Acid inhibition, Helicobacter pylori, omeprazole, intragastric pH-metry.Omeprazole has been shown to have both direct1 and indirect23 effects on Helicobacter pylori, but it is not known whether infection with the organism may itself influence gastric acidity during omeprazole therapy. It has been reported that during treatment with omeprazole, the intragastric pH is higher in patients with duodenal ulceration than in healthy controls.4 5 It is unclear whether this reduction in gastric acidity is observable in all subjects with H pylori infection, or whether it is confined to a subset of patients who develop peptic ulceration. If the increased susceptibility to omeprazole is related solely to Hpylori infection then Hpyloni negative subjects and H pylori positive subjects without ulceration should show different degrees of acid suppression in response to an equal dose of omeprazole.To test the hypothesis that Hpylori infection is associated with decreased intragastric acidity during treatment with omeprazole, we have conducted gastric pH-metry in H pylori positive individuals and compared the pH data with those obtained previously in 14 H pylori negative individuals. Methods SUBJECTSFourteen H pylon negative healthy subjects (seven men and seven women, age range: 22-46 years) and 18 H pylori positive subjects (1 1 men and seven women, age range: 22-45 years) were studied. Students and employees of a university hospital who had volunteered for an H pylori screening programme were also invited to participate in the present study. H pylori status was determined using the ...

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Background-In healthy subjects, continuous infusions of high dose ranitidine and omeprazole produce high intragastric pH values. Aim-To test the hypothesis that both drugs also maintain high intragastric pH values in patients with bleeding ulcers. Patients and Methods-In two parallel studies, 20 patients with bleeding duodenal ulcers and 20 patients with bleeding gastric ulcers were randomly assigned to receive either ranitidine (0.25 mg/kg/hour after a bolus of 50 mg) or omeprazole (8 mg/hour after a bolus of 80 mg) for 24 hours. Intragastric pH was continuously recorded with a glass electrode placed 5 cm below the cardia. Results-Both drugs rapidly raised the intragastric pH above 6. During the second 12 hour period, however, the percentage of time spent below a pH of 6 was 0-15% with omeprazole and 20.1% with ranitidine (p=0.0015) in patients with duodenal ulcer; in patients with gastric ulcer it was 001% with omeprazole and 46-1% with ranitidine (p=0-002). Conclusions-Primed infusions of omeprazole after a bolus produced consistently high intragastric pH values in patients with bleeding peptic ulcers, whereas primed infusions with ranitidine were less effective during the second half of a 24 hour treatment course. This loss of effectiveness may be due to tolerance. (Gut 1997; 40: 36-41)

Background and aims-Treatment of functional dyspepsia with acid inhibitors is controversial and it is not known if the presence of Helicobacter pylori infection influences the response. Methods-After a complete diagnostic workup, 792 patients with functional dyspepsia unresponsive to one week of low dose antacid treatment were randomised to two weeks of treatment with placebo, ranitidine 150 mg, omeprazole 10 mg, or omeprazole 20 mg daily. Individual dyspeptic and other abdominal symptoms were evaluated before and after treatment according to H pylori status. Results-The proportions of patients considered to be in remission (intention to treat) at the end of treatment with placebo, ranitidine 150 mg, omeprazole 10 mg, and omeprazole 20 mg were, respectively, 42%, 50%, 48%, and 59% in the H pylori positive group and 66%, 73%, 64%, and 71% in the H pylori negative group. In H pylori positive patients, the therapeutic gain over placebo was significant for omeprazole 20 mg (17.6%, 95% confidence intervals (CI) 4.2-31.0; p<0.014 using the Bonferroni-adjusted p level of 0.017) but not for omeprazole 10 mg (6.8%, 95% CI −6.7-20.4) or ranitidine 150 mg (8.9%, 95% CI −4.2-21.9). There was no significant therapeutic gain from active treatment over placebo in H pylori negative patients. Complete disappearance of symptoms and improvement in quality of life also occurred most frequently with omeprazole 20 mg and was significant in both H pylori positive and H pylori negative groups. The six month relapse rate of symptoms requiring treatment was low (<20%) in all groups. Conclusions-Omeprazole 20 mg per day had a small but significant favourable eVect on outcome in H pylori positive patients. The diVerential response in these patients may be explained by an enhanced antisecretory response in the presence of H pylori. The eVect of weaker acid inhibition was unsatisfactory. (Gut 2000;47:473-480)