Aspirin irreversibly inhibits the enzyme cyclooxygenase-1 and depresses the production of thromboxane A2, and also exerts antiplatelet effects. On the other hand, it also depresses the production of prostaglandin E2 (PGE2) and induces gastroduodenal lesions, which are often seen in patients taking aspirin. The aim of this study was to clarify the degree of gastroduodenal lesions induced by low-dose aspirin. We investigated the incidence rate of such lesions induced by aspirin and non-steroidal anti-inflammatory drugs (NSAIDs), and performed theoretical evaluations in a retrospective study. The incidence rates of gastroduodenal lesions in the low-dose aspirin (n=1103) and NSAIDs (n=1856) groups were 2.54% and 0.27%, respectively, which was significantly greater in the aspirin group. Furthermore, the calculated value of inhibition rate of gastric PGE2 was significantly correlated with the actual value after administration of aspirin or NSAIDs (r=0.902, p<0.05), which suggested that the calculated value reflected the actual value. The calculated value of aspirin (98.9%) was higher than that of NSAIDs (3.67-70.8%) after administration of the drugs with the standard doses. Our findings indicate that the incidence rate of gastroduodenal lesions induced by low-dose aspirin was higher than that of those induced by NSAIDs. Therefore, we were able to perform a theoretical evaluation of the occurrence of gastroduodenal lesions.
