Gastroduodenal lesions in coronary artery disease patients. Frequency, endoscopic characteristics and risk factors (CROSBI ID 135272)
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Fabijanić, Damir ; Banić, Marko ; Kardum, Duško ; Sutlić, Željko ; Radić, Mislav ; Rudež, Igor ; Biočina, Bojan
engleski
Gastroduodenal lesions in coronary artery disease patients. Frequency, endoscopic characteristics and risk factors
Our findings that cigarette smoking was associated with GD lesion could be explained with the observation that smoking delays GD lesions healing and enhances relapse after healing, affecting adversely the mucosal protective mechanisms.1 It inhibits mucus secretion, as well as mucosal prostaglandin generation, decreasing mucosal blood flow, inhibiting salivary epidermal growth factor secretion, and inhibiting pancreatic bicarbonate secretion and duodenal mucosal bicarbonate secretion.1 Data on whether H. pylori contributes to the risk of NSAID-induced GD mucosal injury have been conflicting. Although, the sum of literature reports suggest that H. pylori may have a synergistic effect to promote GD lesion in aspirin users1 our study did not confirm the importance of H. pylori in the development of GD lesion in our patients. However, we support the recommendation that H. pylori eradication is beneficial in low-dose aspirin consumers with documented peptic ulcer, especially after ulcer bleeding.1 Conclusively, our study revealed the occurrence of GD lesions in CAD patients with clinically significant frequency, especially in regard to gastric mucosal lesions. The use of low-dose aspirin was identified as the most important risk factor for GD lesions development. Interestingly, clopidogrel in standard dose (75 mg/d) added to aspirin in dose <100 mg/d did not increase risk for GD lesions development. This observation need to be tested for future prospective studies.
H. pylori; NSAID; aspirin; gastroduodenal lesion; CAD
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