2. 病例对照研究：幽门螺杆菌感染、非甾体类抗炎药、小剂量阿司匹林、抗高血压药物引起消化性溃疡出血的风险
J Gastroenterol Hepatol. 2014 Oct 22. doi: 10.1111/jgh.12805. [Epub ahead of print]
Risk of peptic ulcer bleeding associated with Helicobacter pylori infection, NSAIDs, low-dose aspirin, and antihypertensive drugs: A case-control study.
Nagata N1, Niikura R, Sekine K, Sakurai T, Shimbo T, Kishida Y, Tanaka S, Aoki T, Okubo H, Watanabe K, Yokoi C,Akiyama J, Yanase M, Mizokami M, Uemura N.
背景：
在幽门螺杆菌感染率高的亚洲地区，仍不明确抗凝或抗高血压药物等是否为消化性溃疡出血的危险因素。本研究旨在评估抗血栓形成的药物、血管紧张素II受体拮抗剂、血管紧张素转换酶(ACE)抑制剂、钙通道阻滞剂、α受体阻断剂、β受体阻断剂引起消化性溃疡出血风险。
方法:
这是一项前瞻性的病例对照研究。包括230例经内镜证实的消化性溃疡出血患者和920例内镜下未见出血的年龄和性别匹配的对照组患者（1:4）。调整后的消化性溃疡出血风险的比值比（AOR）由条件逻辑回归分析确定。
结果：
多变量分析显示，饮酒(AOR, 2.2; p<0.001)、消化性溃疡史(AOR, 4.8; p<0.001)、幽门螺杆菌感染史(AOR, 2.1; P<0.001)、合并症指数（AOR，1.1；P = 0.089）、非甾体类抗炎药（NSAIDs）（AOR，2.0；P = 0）和低剂量阿司匹林（AOR，P = 0.003）增加消化性溃疡出血风险；而根除幽门螺杆菌（AOR，0.03；P＜0.001）质子泵抑制剂（PPIs）（AOR，0.1；P＜0.001）和组胺2受体拮抗剂（H2RA）（AOR，0.1，P＜0.001）则降低消化性溃疡出血风险。幽门螺杆菌感染与NSAIDs药物间无显著相互作用（P = 0.913）。ARBs（P = 0.564）、ACE抑制剂（P = 0.213）、钙通道阻滞剂（P = 0.215）、α-阻滞剂（P = 0.810）和β-阻滞剂（P = 0.864）与消化性溃疡出血无关。
结论：
我们发现饮酒、消化性溃疡史、幽门螺杆菌感染史、NSAIDs药物应用史及低剂量阿司匹林应用史是消化性溃疡出血的独立危险因素。幽门螺杆菌感染与NSAIDs药物间未观察到显著相互作用。抗高血压药与消化性溃疡出血无关。
译者点评：饮酒、消化性溃疡史、幽门螺杆菌感染、NSAIDs及阿司匹林应用史是消化性溃疡出血的独立危险因素
Abstract
BACKGROUND:
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), non-steroidal 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.
CONCLUSIONS:
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.