Helicobacter pylori and bleeding duodenal ulcer: Prevalence of the infection and role of non-steroidal anti-inflammatory drugs

Background: Several authors have reported low prevalence of Helicobacter py lori infection in patients with upper gastrointestinal bleeding (UGIB). Our aim was to study the prevalence of H. pylori in bleeding duodenal ulcer (D U), with both invasive and non-invasive methods, and to assess the role of non-steroidal anti-inflammatory drugs (NSAIDs). Methods: Ninety-two patient s with bleeding DU were prospectively studied. The use of NSAIDs was evalua ted by specific questionnaire. As a control group. 328 patients undergoing outpatient evaluation for the investigation of dyspepsia and found to have a DU at endoscopy were included. At endoscopy, two antral biopsies were obt ained (H&E stain). A C-13-urea breath test was carried out in all patients. Breath rest was repeated in patients treated with omeprazole during the ho spitalization if H. pylori was not detected with the first test. Results: G astric biopsies could be obtained in 39 patients with UGIB. Three patients with UGIB treated with omeprazole and being H. pylori-negative with the fir st breath test were finally considered infected with the second test. Overa ll. 92.4% (95% CI, 85%-96%) of the patients with UGIB were infected (89.7% with histology and 92.4% with breath test (P = 0.15)). Concordance kappa va lue for both diagnostic tests was 0.63. NSAID intake was more frequent in p atients with UGIB (34%) than in those without UGIB (5.6%) (P < 0.001), whil e H. pylori infection was less frequent in patients with UGIB (92.4% (85%-9 6%)) than in those without UGIB (99.1% (98%-100%); P < 0.001). Even in pati ents with UGIB. NSAID intake was the only risk factor in 5% of cases. The p roportion of cases without H. pylori infection and without NSAID intake was very low in both bleeding and non-bleeding ulcers (2% and 0.5%, respective ly; P = 0.146). H. pylori prevalence in bleeding ulcers was of 84% (67%-93% ) in patients with NSAID intake, and 96.7% (89%-99%) when patients taking N SAIDs were excluded. In the multivariate analysis. NSAID intake (odds ratio , 9.8 (5.2-18.4)) correlated with UGIB: however, neither H. pylori status n or the interaction between H. pylori infection and NSAID intake correlated with UGIB. In the multivariate analysis in the subgroup of patients with UG IB, NSAID use was the only variable which correlated with H. pylori prevale nce (odds ratio, 0.18 (0.03-0.97)). Conclusions: The most important factor associated with H. pylori-negative bleeding DU is NSAID use, and if this fa ctor is excluded prevalence of infection is almost 100% (97%). similar to t hat found in patients with non-bleeding DU land without NSAID intake). Blee ding DU patients with neither H. pylori infection nor NSAID use are extreme ly rare (only 2%), which suggests that the pathogenesis of bleeding DU is s imilar to that of non-complicated DU disease.