Interactions between Helicobacter pylori and other risk factors for peptic ulcer bleeding

Aim:To investigate the role of Helicobacter pylori, expressing the virulence marker CAGA (cytotoxin associated gene product A) in ulcer complications and its interaction with nonsteroidal anti‐inflammatory drugs (NSAIDs) and other risk factors.Design:Case control study using conditional logistic regression analysis.Setting:University and City Hospitals, Nottingham.Subjects:203 consecutive patients with ulcer bleeding and 203 age‐ and sex‐matched controls.Results:Ulcer bleeding was more likely with positive H. pylori serology (odds ratio = 3.3, 95% CI: 1.7–6.6 for CagA positive, but only OR = 1.6, 95% CI: 0.7–3.7 for CagA negative serology), current smoking (OR 2.2, 95% CI: 1.04–4.7), aspirin ≤ 300 mg daily (OR 7.7, 95% CI: 2.8–20.6), all other nonsteroidal anti‐inflammatory drugs (NSAIDs: OR 10.6, 95% CI: 3.1–35.7 for ≤ 1 defined daily dose lower and OR 22.6, 95% CI: 6.2–82.0 for higher doses) and past ulcer history (OR 5.6, 95% CI: 2.3–14.1). Aspirin ≤ 300 mg daily was used by 25.1% of patients vs. 7.4% of controls. Smoking only enhanced risk in the presence of H. pylori, with a synergistic interaction (interaction odds ratio = 4.9, 2.4–9.9, P=0.002). Conversely, risks with non‐aspirin NSAIDs were reduced in the presence of H. pylori, particularly if CagA‐positive (interaction odds ratio=0.21, 0.05–0.9, P=0.03).Conclusions:CagA positive H. pylori infection is associated with an increased risk of ulcer bleeding. The risk from non‐aspirin NSAIDs is even higher, but is less in H. pylori infected people. Low‐dose aspirin is now commonly associated with ulcer bleeding.