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No previous study has analyzed the impact of long-term antisecretory drugs on the precision of [13C]urea breath test (UBT). We assessed the rate of UBT conversion from positive to negative results during 60-day therapy with standard doses of ranitidine and pantoprazole. For this purpose, we recruited 60 dyspeptic patients with H. pyloriinfection ascertained on the basis of the concomitant results of CLO-test, histology, and UBT. Our patients were randomly assigned to receive ranitidine 300 mg at night or pantoprazole 40 mg in the morning for 60 days. UBT was performed at baseline and on days 14, 30, and 60, while patients were still taking antisecretory drugs. Patients with false-negative UBT on day 60 repeated the test every 3 days until conversion. After overnight fasting, duplicate breath test samples were taken from each patient before and 30 min after ingestion of 75 mg [13C]urea dissolved in 150 ml of 0.033 mol/liter citric acid. Four patients dropped out of the study. Both drugs induced similar false-negative UBTs on day 14 of dosing (P= 0.5). Afterwards, the three false-negative UBTs in the ranitidine group again became positive during therapy and particularly on day 30 of dosing. Of the four false-negative UBTs in the pantoprazole group at day 60, one became positive after 3 and three after 9 days of therapy cessation. Our findings show that the long-term use of ranitidine and pantoprazole at standard doses has different effects on the results of UBT. In the pantoprazole group patients again became positive within 3–9 days after stopping 60-day therapy, whereas in the ranitidine group patients reverted to positive on day 30 of dosing while they were still on treatment and this was likely due to development of tolerance. Therefore, patients taking pantoprazole need at least a 10-day withdrawal before UBT testing, while those taking ranitidine for at least 30 days can undergo UBT without the necessity of a wash-out period.

This study was carried out to compare the measurements and the diagnostic accuracy of the traditional expensive IRMS and the new economical LARA system using two doses of [13C]urea + two different test meals in patients undergoing upper gastrointestinal endoscopy, both before and after anti-Helicobactertreatment. A total of 354 dyspeptic patients underwent endoscopy with gastric biopsies to diagnose H. pyloriinfection by CLO-test and histology. No patients had taken antibiotics, bismuth, or antisecretory drugs in the 4 weeks before testing. After overnight fasting, breath samples were collected simultaneously in both plastic and glass tubes at baseline and at 30 and 60 min after urea ingestion. In 237 patients 100 mg [13C]urea + Ensure and in 117 patients 75 mg [13C]urea + citric acid were given. The test was also performed with the two urea dosages and meals in 67 and 64 infected patients, respectively, four weeks after anti-Helicobacter therapy. H. pyloriwas considered eradicated when both biopsy-based tests were negative. A δ value >5‰ was considered positive. Breath samples with insufficient CO2levels at both 30 and 60 min were excluded from final analysis (N = 37in pre- and N = 8in posttreatment). There was excellent agreement between overall δ values of the two machines with both [13C]urea 100 mg + Ensure and [13C]urea 75 mg + citric acid. The 95% CI of the difference against the mean was wider with the former (mean −1.3, +6.3, and −9.4) than with the latter urea dosage and test meal (mean −1.2, +5.2 and −8.1). LARA and IRMS were equally effective (P =NS) in distinguishing infected from uninfected patients before therapy using both doses of [13C]urea and test meals (sensitivity ranged from 95% to 99% and specificity from 95% to 97%). This good performance was maintained in the posttreatment phase (sensitivity ranged from 90% to 100% and specificity from 90% to 97%), without any statistical difference among the various combinations (P =NS). The LARA system is a valid alternative to IRMS in the diagnosis of H. pyloriinfection. Both machines provide highly reliable results after 30 min, so that the 60 min sample can be avoided. The dose of 75 mg + citric acid suffices to ensure an accurate UBT. The test performed with both devices and [13C]urea dosages is very effective also for posttherapy evaluation of H. pyloristatus.

Published data on the regression of the extent of duodenal gastric metaplasia (DGM) after the eradication of Helicobacter pyloriinfection and the normalization of the organism-induced alterations in gastric physiology are scanty and controversial. Therefore, we decided to assess the circadian pattern of gastric acidity and the degree of DGM before and one year after H. pylorieradication in a group of duodenal ulcer patients. Fifteen consecutive H. pylori-positive patients with endoscopically proven duodenal ulcer were recruited for this study. The diagnosis of H. pyloriinfection was based on CLO-test and histology, and DGM was assessed on four bulb biopsies taken before and one year after H. pylorieradication. At the same time, gastric pH was measured by 24-hr continuous intraluminal recording. H. pylorieradication was ascertained by means of concomitant negative CLO-test and histology performed both four weeks after the end of the eradicating treatment and at the one-year endoscopic control. After successful cure, all patients discontinued any antiulcer medication. The mean 24-hr gastric pH was 1.7 ± 0.4 before and 1.6 ± 0.4 after one year of H. pylorieradication (P = 0.75).DGM improved in three cases, worsened in four cases, and was unchanged in eight cases at the one-year control (P = 0.87).No correlation was found between 24-hr gastric pH and DGM (P =NS) both at baseline and one year after eradication. Our results show that neither circadian gastric acidity nor DGM change significantly one year after H. pylorieradication in duodenal ulcer patients. Thus, the disappearance of H. pyloriinfection does not determine any increase in gastric pH and any reversal of gastric-type epithelium in the duodenum.