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  • Risk of peptic ulcer bleeding associated with Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, low-dose aspirin, and antihypertensive drugs: a case-control study.

Risk of peptic ulcer bleeding associated with Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, low-dose aspirin, and antihypertensive drugs: a case-control study.

Journal of gastroenterology and hepatology (2014-10-24)
Naoyoshi Nagata, Ryota Niikura, Katsunori Sekine, Toshiyuki Sakurai, Takuro Shimbo, Yoshihiro Kishida, Shohei Tanaka, Tomonori Aoki, Hidetaka Okubo, Kazuhiro Watanabe, Chizu Yokoi, Junichi Akiyama, Mikio Yanase, Masashi Mizokami, Naomi Uemura
ZUSAMMENFASSUNG

The associations between antithrombotic or antihypertensive drugs and peptic ulcer bleeding (PUB) remain unknown, particularly in Asia, where Helicobacter pylori infection is prevalent. This study aims to evaluate the risks of PUB from antithrombotic drugs, angiotensin II receptor blockers (ARBs), angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, α-blockers, and β-blockers. This prospective hospital-based case-control study included 230 patients with endoscopically verified PUB and 920 age and sex-matched controls (1:4) without bleeding on screening endoscopy. Adjusted odds ratios (AOR) for the risk of PUB were determined by conditional logistic regression analysis. In multivariate analysis, alcohol consumption (AOR, 2.2; P < 0.001), history of peptic ulcer (AOR, 4.8; P < 0.001), H. pylori infection (AOR, 2.1; P < 0.001), comorbidity index (AOR, 1.1; P = 0.089), nonsteroidal anti-inflammatory drugs (NSAIDs) (AOR, 2.0; P = 0.025), and low-dose aspirin (AOR, 2.8; P = 0.003) increased the risk of PUB, whereas H. pylori eradication (AOR, 0.03; P < 0.001), proton pump inhibitors (PPIs) (AOR, 0.1; P < 0.001), and histamine 2-receptor antagonists (H2RA) (AOR, 0.1; P < 0.001) reduced it. No significant interactions were observed between H. pylori infection and NSAIDs use for PUB (P = 0.913). ARBs (P = 0.564), ACE inhibitors (P = 0.213), calcium channel blockers (P = 0.215), α-blockers (P = 0.810), and β-blockers (P = 0.864) were not associated with PUB. We found that alcohol consumption, history of peptic ulcer, H. pylori infection, NSAIDs use, and low-dose aspirin use were independent risk factors for PUB, whereas H. pylori-eradication, PPIs use, and H2RA use reduced its risk. Interactions between H. pylori and NSAIDs use in PUB were not observed. No antihypertensive drug was associated with PUB.

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