Aspirin, Helicobacter Pylori, and Peptic Ulcer Disease

阿司匹林和其他非甾体抗炎药被广泛用于治疗疼痛和炎症，低剂量的阿司匹林也越来越多地用于心血管预防。 然而，这些药物具有显著的胃肠道毒性，并且大量患者发展为消化性溃疡和GI出血。 虽然幽门螺杆菌感染是溃疡的另一个主要危险因素，但阿司匹林和幽门螺杆菌之间的关系。幽门螺杆菌在溃疡发展中的作用仍存在很大争议。 目前还不清楚，例如，是否有一个成瘾性或协同作用，这些因素之间的相互作用，在赋予溃疡的风险，如阿司匹林与H。pylori增加溃疡并发症。 阿司匹林通过减少前列腺素的产生而损害粘膜保护机制，而H。幽门螺杆菌通过细胞因子和炎症促进粘膜损伤以形成溃疡。 过去的研究提供了与这两个因素相关的溃疡风险的相互矛盾的数据，但它们受到阿司匹林使用的回忆偏倚、选择偏倚和随访时间短的小样本量的限制。 这项研究的主要目的是确定低剂量阿司匹林和H。pylori感染、低剂量阿司匹林和H. pylori，称为cagA+ H。pylori，以及与低剂量阿司匹林和H. pylori（尤其是cagA+ H. pylori菌株）与未感染的那些相比。当比较阿司匹林的使用和溃疡形成的关系时，我们将有80%的把握度检测出比值比为1.56的差异。pylori阳性和阴性受试者。 随着美国人口的老龄化，长期使用阿司匹林预防心血管疾病和随后发生溃疡的情况可能会增加，涉及医疗保健费用。这项研究将提供重要的信息，以便对阿司匹林相关的胃肠道并发症以及是否存在H。幽门螺杆菌感染的患者在服用阿司匹林时有溃疡和胃肠道出血的风险。 这些结果可能有助于识别高风险患者，并导致减少阿司匹林使用者溃疡并发症的策略。

Aspirin and other non-steroidal anti-inflammatory drugs are widely used to treat pain and inflammation, and at low doses, aspirin is also increasingly being used for cardiovascular prophylaxis. However, these drugs have substantial gastrointestinal toxicity and a significant number of patients develop peptic ulcers and GI bleeding. Although infection with Helicobacter pylori is another major risk factor for ulcers, the relationships between aspirin and H. pylori in the development of ulcers remain highly controversial. It is unclear, for example, whether there is an addictive or synergistic interaction between these factors in conferring ulcer risk such that aspirin interacts with H. pylori to increase ulcer complications. Aspirin impairs mucosal protective mechanisms by decreasing prostaglandin production, whereas H. pylori promotes mucosal injury through cytokines and inflammation to form ulcers. Past studies have provided conflicting data on the ulcer risks associated with both factors but they have been limited by recall bias of aspirin use, selection bias, and small sample sizes with short follow-up. The primary goals of the proposed research are to determine the risk of peptic ulcers associated with the joint effects of low dose aspirin and H. pylori infection, the ulcer risk associated with low dose aspirin and a specific virulent strain of H. pylori, known as cagA+ H. pylori, and the risk of GI bleeding associated with low dose aspirin and H. pylori (especially cagA+ H. pylori strains) as compared to those without infection. We will have 80% power to detect a difference of 1.56 in the odds ratio, when comparing the association of aspirin use and ulcer formation in H. pylori positive and negative subjects. As the US population grows older, the chronic use of aspirin for cardiovascular prophylaxis and the subsequent development of ulcers are likely to increase, involving health care costs. The proposed study will provide important information to make an informed decision about aspirin related GI complications and whether H. pylori infected patients are at risk for ulcers and GI bleeding while on aspirin. These results may help identify high-risk patients and lead to strategies that will reduce ulcer complications among aspirin users.