Impact of Blood Type, Functional Polymorphism (T-1676C) of theCOX-1Gene Promoter and Clinical Factors on the Development of Peptic Ulcer during Cardiovascular Prophylaxis with Low-Dose Aspirin

Abstract

Aims. 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. Methods. 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. Results. 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. 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. Conclusion. The C-1676T polymorphism in the COX-1 gene promoter is not a risk factor for ulcer formation during treatment with low-dose aspirin. 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.

AGT A-20C (rs5050) gene polymorphism and ulcer occurrence in patients treated with low-dose aspirin: a case-control study / Polimorfismul AGT A-20C și ulcerele gastro-duodenale la pacienții sub tratament cu aspirină în doze antiagregante: studiu caz-control

“…Our study proved the role of infection in mucosal damage in aspirin consumers. In our study, more than 50% of patients with ulcer were H. pylori positive, a percentage higher than in the majority of similarly published papers [20]. Concurrent use of NSAIDs, frequently with no medical prescriptions (data not showed), was a significant risk factor for ulcer, in our study.…”

Epoxidase inhibitor-aspirin resistance and the relationship with genetic polymorphisms: a review

“…22 At present, the common mutation sites in the 5 terminal non-coding regions of the COX-1 gene are A-842G, 1676 T-C, G-1498A, A1201G, T1794C, G-10006A, A-918G and A-807G. [23][24][25][26][27][28] The -842 A-G allele mutation was present in 60% of aspirin-resistant patients, while only 17% of non-aspirin-resistant patients had the mutation at the above site, suggesting that the A-842G allele mutation is closely related to aspirin resistance. 25 It was further found that the polymorphic changes at this gene locus could significantly increase the expression level of thrombin B2 and stimulate platelet aggregation, leading to an increased risk of thrombosis.…”

MALT lymphoma and erosive and ulcerative lesions of the stomach: modern diagnostic approaches and own clinical observation

“…Так, применение НПВП или аспирина с селективными ингибиторами обратного захвата серотонина, кортикостероидами, антагонистами альдостерона или антикоагулянтами существенно увеличивает риск развития желудочно-кишечного кровотечения [19]. Результаты некоторых исследований показали связь использования аспирина с повышенным риском язвенной болезни у пациентов с генетическими полиморфизмами (T-1676C, PSCA rs2 294 008), но клиническая значимость этих исследований до конца не ясна [20].…”