C Sostres1, P Carrera-Lasfuentes2, R Benito3, P Roncales4, M Arruebo4, M T Arroyo1, L Bujanda5, L A García-Rodríguez6, A Lanas7. 1. Universitary Hospital Lozano Blesa, Gastroenterology Unit, Zaragoza, Spain. 2. CIBERehd, Madrid, Spain. 3. Universitary Hospital Lozano Blesa, Microbiology Unit, Zaragoza, Spain. 4. Health Science Institute of Aragon, Zaragoza, Spain. 5. Universitary Hospital of Donostia, San Sebastian, Spain. 6. CEIFE, Madrid, Spain. 7. 1] Universitary Hospital Lozano Blesa, Gastroenterology Unit, Zaragoza, Spain [2] CIBERehd, Madrid, Spain [3] Health Science Institute of Aragon, Zaragoza, Spain.
Abstract
OBJECTIVES: Helicobacter pylori (H. pylori) infection and NSAID/low-dose aspirin (ASA) use are associated with peptic ulcer disease. The risk of peptic ulcer bleeding (PUB) associated with the interaction of these factors remains unclear. The objective of this study was to determine the risk of PUB associated with the interaction between H. pylori infection and current nonsteroidal anti-inflammatory drugs (NSAIDs) or low-dose ASA use. METHODS: This was a case-control study of consecutive patients hospitalized because of PUB. Controls were matched by age, sex, and month of admission. H. pylori infection status was determined in all cases and controls by serology. Drug use was determined by structured questionnaire. Adjusted relative risk (RR) associated with different factors, and the interaction between NSAID/ASA and H. pylori infection was estimated by logistic regression analysis. RESULTS: The study included 666 cases of PUB and 666 controls; 74.3% cases and 54.8% controls (RR: 2.6; 95% confidence interval (CI): 2.0-3.3) tested positive for H. pylori infection; 34.5% of cases had current NSAID use compared with 13.4% of controls (RR: 4.0; 95% CI: 3.0-5.4). Respective proportions for low-dose ASA use were 15.8 and 12%, respectively (RR: 1.9; 95% CI: 1.3-2.7). The RR of PUB for concomitant NSAID use and H. pylori infection suggested an additive effect (RR: 8.0; 95% CI: 5.0-12.8), whereas no interaction was observed with ASA use (RR: 3.5; 95% CI: 2.0-6.1). CONCLUSIONS: NSAID, low-dose ASA use, and H. pylori infection are three independent risk factors for the development of PUB, but there were differences in the interaction effect between low-dose ASA (no interaction) or NSAID (addition) use and H. pylori infection, which may have implications for clinical practice in prevention strategies.
OBJECTIVES:Helicobacter pylori (H. pylori) infection and NSAID/low-dose aspirin (ASA) use are associated with peptic ulcer disease. The risk of peptic ulcer bleeding (PUB) associated with the interaction of these factors remains unclear. The objective of this study was to determine the risk of PUB associated with the interaction between H. pyloriinfection and current nonsteroidal anti-inflammatory drugs (NSAIDs) or low-dose ASA use. METHODS: This was a case-control study of consecutive patients hospitalized because of PUB. Controls were matched by age, sex, and month of admission. H. pyloriinfection status was determined in all cases and controls by serology. Drug use was determined by structured questionnaire. Adjusted relative risk (RR) associated with different factors, and the interaction between NSAID/ASA and H. pyloriinfection was estimated by logistic regression analysis. RESULTS: The study included 666 cases of PUB and 666 controls; 74.3% cases and 54.8% controls (RR: 2.6; 95% confidence interval (CI): 2.0-3.3) tested positive for H. pyloriinfection; 34.5% of cases had current NSAID use compared with 13.4% of controls (RR: 4.0; 95% CI: 3.0-5.4). Respective proportions for low-dose ASA use were 15.8 and 12%, respectively (RR: 1.9; 95% CI: 1.3-2.7). The RR of PUB for concomitant NSAID use and H. pyloriinfection suggested an additive effect (RR: 8.0; 95% CI: 5.0-12.8), whereas no interaction was observed with ASA use (RR: 3.5; 95% CI: 2.0-6.1). CONCLUSIONS: NSAID, low-dose ASA use, and H. pyloriinfection are three independent risk factors for the development of PUB, but there were differences in the interaction effect between low-dose ASA (no interaction) or NSAID (addition) use and H. pyloriinfection, which may have implications for clinical practice in prevention strategies.
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