Endoscopic Evaluation of Gastroduodenal Mucosal Injury in Asymptomatic Japanese Patients with Antiplatelet Agents

Abstract

Introduction: In consideration of increasing patients with arteriosclerosing diseases, gastroduodenal mucosal injury due to antiplatelet therapy has become a large clinical problem. Some epidemiological studies have suggested that not only aspirin but other antiplatelets (APs) might have gastrotoxicity which increase risk for upper gastrointestinal bleeding. However, there is inadequate endoscopic information regarding gastroduodenal mucosal injury in such patients. Our previous study suggested that APs did not cause mucosal injury so as to aspirin, although it might add risk for bleeding when used with aspirin. Here we conducted the present retrospective study to estimate the incidence of gastroduodenal mucosal injury in asymptomatic patients with APs, including low-dose aspirin, and other non-steroidal anti-inflammatory drugs (NSAIDs) in Japan. Aims and Methods: From January through December 2005, a total of 2986 patients underwent upper gastrointestinal endoscopy at the Department of Internal Medicine of Teikyo University Hospital (Tokyo, Japan). At first, the prescribed medications and reasons for undergoing examination in all of these cases were investigated, and asymptomatic patients who underwent endoscopy for screening purpose were selected. Finally, 128 patients with low-dose aspirin (less than 100 mg/day), 15 with cilostazol and 23 with ticlopidine were enrolled as subjects. Also 90 asymptomatic patients with NSAIDs other than low-dose aspirin were examined for comparison. The subjects' records were evaluated to judge for the presence of gastroduodenal mucosal injury which was defined as obvious findings of gastroduodenal mucosal defects (ulcer or erosion). Results: In 128 patients with low-dose aspirin, 30 patients (23.4%) had gastric erosions or ulcers. Four of 23 patients with ticlopidine (17.3%) and 2 of 15 with cilostazol (13.3%) had mucosal injury, and 24 patients (26.7%) showed mucosal injury in 90 NSAIDs consumers. Concomitant use of ticlopidine or cilostazol with NSAIDs seemed not to be a risk for mucosal injury, but aspirin with other NSAIDs were regarded as the significant risk. Most of lesions were located at gastric antrum in aspirin or other NSAIDs users. On the other hand, mucosal injury appeared at any part of the stomach in patients with cilostazol or ticlopidine. Conclusion: Concomitant use of APs and NSAIDs seemed not to add the risk for gastroduodenal mucosal injury. Now further investigation has been made regarding patients who underwent endoscopy in 2006.