Journal of gastroenterology and hepatology · 2015
Risk of peptic ulcer bleeding associated with Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, low-dose aspirin, and antihypertensive drugs: a case-control study.
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Nagata Naoyoshi, Niikura Ryota, Sekine Katsunori, Sakurai Toshiyuki, Shimbo Takuro, Kishida Yoshihiro, Tanaka Shohei, Aoki Tomonori, Okubo Hidetaka, Watanabe Kazuhiro, Yokoi Chizu, Akiyama Junichi, Yanase Mikio, Mizokami Masashi, Uemura Naomi
Аннотация
BACKGROUND AND AIM: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.