Negative effect of ranitidine on the results of urea breath test for the diagnosis of Helicobacter pylori.

OBJECTIVES: In analogy with proton pump inhibitors, H2-antagonists may also be responsible for false-negative results on urea breath test for the detection of Helicobacter pylori. In this study we assessed the frequency and duration of false-negative urea breath tests in patients given different doses of ranitidine. METHODS: A total of 120 consecutive dyspeptic patients infected with H. pylori on the basis of concomitant positive results of CLO-test, histology and urea breath test were recruited for this prospective, open, parallel-group study performed in an urban university gastroenterological clinic. They were randomized to receive an acute treatment with either ranitidine 300 mg once a day in the evening, ranitidine 300 mg once a day in the morning, ranitidine 150 mg b.i.d., or ranitidine 300 mg b.i.d. for 14 days. The urea breath test was performed on day 14 while patients were still taking ranitidine, and on day 21, 1 wk after completion of therapy. The test was repeated on day 28 in those patients who were still negative on day 21. Duplicate breath samples were collected after ingestion of 75 mg 13C-urea plus citric acid. A delta value >5/1000 was considered positive. RESULTS: Of 118 patients infected with H. pylori, 15 (13%) had a negative urea breath test on day 14. The false-negative results were equally distributed among the four groups of ranitidine dosage. Nine of these patients reverted to positive at 7 days and the remaining six at 14 days after completion of therapy. CONCLUSIONS: Our study shows that ranitidine negatively affects the results of urea breath testing, independent of the given dosage. Patients undergoing this examination for H. pylori diagnosis should discontinue use of H2-antagonists 2 wk before testing.

Effect of gastric acid suppression on 13C-urea breath test: comparison of ranitidine with omeprazole.

BACKGROUND: The assessment of the effect of H2 antagonists on the results of the urea breath test has produced controversial results. AIM: To assess whether standard doses of both omeprazole and H2 blockers can adversely influence the accuracy of the urea breath test. METHODS: Sixty dyspeptic patients with ascertained Helicobacter pylori infection were recruited for this prospective, open study. They were randomized to receive either omeprazole 20 mg at 08:00 hours (n = 30) or ranitidine 300 mg at 22:00 hours (n = 30) for 14 days. The urea breath test was performed at baseline, on day 14, while patients were still taking the antisecretory drugs, and on day 21, 1 week after their cessation. Duplicate breath samples were collected after ingestion of 75 mg 13C-urea + citric acid. A delta value > 5 per thousand was considered positive. RESULTS: On day 14 the median delta values had declined, but not significantly (P = 0. 07) compared to baseline (13.79 vs. 22.39) with omeprazole, while they had increased (P = 0.27) with ranitidine (27.21 vs. 19.46). On the same day there were five out of 30 (17%) and five out of 28 (18%) false-negative results in the omeprazole and ranitidine groups, respectively. All these cases became positive again on day 21. However, in eight cases treated with omeprazole and 13 treated with ranitidine, there was an increase of 14-day delta values compared to baseline. CONCLUSIONS: Our study shows that both omeprazole and ranitidine at standard doses are able to negatively affect the results of the urea breath test. Their adverse effect resolves within 7 days of drug cessation and therefore the withdrawal of these drugs 7 days before testing seems to be sufficient to avoid false-negative results. The surprising finding that both antisecretory drugs reduce delta values in one group and increase them in another group of patients deserves further study.

24-hour gastric pH and extent of duodenal gastric metaplasia in Helicobacter pylori-positive patients.

BACKGROUND & AIMS: Gastric metaplasia (GM) is essential to explain duodenal colonization by Helicobacter pylori. It seems to be acid induced but also occurs in H. pylori-positive patients with nonulcer dyspepsia (NUD), who are not acid hypersecretors. The aim of this study was to assess the circadian gastric acidity of 47 patients with duodenal ulcers (DUs) and 32 patients with NUD, both H. pylori positive, and its correlation to duodenal GM extent. METHODS: H. pylori was detected by histology and CLOtest, and GM was diagnosed and graded on four bulb biopsy specimens. Each patient underwent 24-hour gastric pH-metry, and the relation between gastric pH and GM extent was assessed by factorial analysis. RESULTS: Gastric pH was greater in patients with NUD than in patients with DU during 24 hours, night and daytime (P < 0.03-0.005). Gastric pH differed significantly (P < 0.0002) in relation to GM extent between the two populations, whereas no difference was found among the pH values of GM degrees. A significant increase in 24-hour gastric pH was associated with greater GM in patients with DU, whereas the opposite occurred in patients with NUD (P < 0.007). CONCLUSIONS: The lower gastric acidity in patients with NUD than in patients with DU and the lack of correlation between gastric pH and the various GM degrees in the two H. pylori-positive populations suggest that gastric hyperacidity is not associated with duodenal GM.