Even at doses as low as 10 mg, aspirin has been shown to cause gastrointestinal damage and is associated with a greater risk of gastroduodenal ulcers and life-threatening ulcer complications. However, due to its inhibition of prostaglandin synthesis, direct cytotoxicity, and microvascular injury, aspirin is associated with upper gastrointestinal side effects, which range from mild dyspepsia to life-threatening bleeding and perforation from peptic ulcers. Currently, approximately 36% of the adult US population-more than 50 million people-is estimated to take aspirin regularly for cardiovascular disease prevention. Besides the patients requiring secondary prevention of cardiovascular events, the American Heart Association recommends prophylactic aspirin for the subjects who have a 10-year cardiovascular risk equal to or more than 10%. Low-dose aspirin (75–325 mg/day) is widely used in the prevention of myocardial infarction or ischemic stroke. Blood type O, advanced age, history of peptic ulcer, and concomitant use of NSAID are of independent significance in predicting peptic ulcer development during treatment with low-dose aspirin. The C-1676T polymorphism in the COX-1 gene promoter is not a risk factor for ulcer formation during treatment with low-dose aspirin. Multivariate analysis revealed that blood type O, advanced age, history of peptic ulcer, and concomitant use of NSAID were the independent risk factors for the development of peptic ulcer with the odds ratios of the 2.1, 3.1, 27.6, and 2.9, respectively. Univariate analysis showed no significant differences in genotype frequencies of the COX-1 gene at position -1676 between the peptic ulcer group and control group. In a case-control study including 111 low-dose aspirin users with peptic ulcers and 109 controls (asymptomatic aspirin users), the polymorphism (T-1676C) of the COX-1 gene promoter was genotyped, and blood type, H pylori status, and clinical factors were assessed. To investigate the impact of blood type, functional polymorphism (T-1676C) of the COX-1 gene promoter, and clinical factors on the development of peptic ulcer during cardiovascular prophylaxis with low-dose aspirin.
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