In order to assess the prevalence of carotid artery disease in patients with arteriosclerosis obliterans (ASO) or aortic aneurysm, 142 patients underwent screening for the presence of carotid atherosclerosis (plaque) with B-mode ultrasonography. Seventy-four (87.1%) of the 85 patients with ASO and 37 (64.9%) of the 57 patients with aortic aneurysm had carotid artery lesions. Of these patients, about half had bilateral lesions. The differences in the prevalence of carotid lesions were not significantly related to age or sex. Prevalence did not differ in relation to the severity or location of the primary lesions. The majority of the carotid lesions were located in the internal carotid arteries. The prevalence of carotid lesions was higher among patients with cerebral infarction than in those without any lesions on computed tomography. These results showing high prevalence of carotid lesions in ASO and aortic aneurysm suggest the usefulness of routine carotid ultrasonographic screening and also that it is important in order to determine the correct treatment for these cases.

Background/Aims: The etiology of superficial non-ampullary duodenal epithelial tumors (SNADETs) remains unclear. Recent studies have reported conflicting associations between duodenal tumor development and Helicobacter pylori infection or endoscopic gastric mucosal atrophy. As such, the present study aimed to clarify the relationship between SNADETs and H. pylori infection and/or endoscopic gastric mucosal atrophy. Methods: This retrospective case-control study reviewed data from 177 consecutive patients with SNADETs who underwent endoscopic or surgical resection at seven institutions in Japan over a three-year period. The prevalence of endoscopic gastric mucosal atrophy and the status of H. pylori infection were compared in 531 sex- and age-matched controls selected from screening endoscopies at two of the seven participating institutions. Results: For H. pylori infection, 85 of 177 (48.0%) patients exhibited SNADETs and 112 of 531 (21.1%) control patients were non-infected (p<0.001). Non-atrophic mucosa (C0 to C1) was observed in 96 of 177 (54.2%) patients with SNADETs and 112 of 531 (21.1%) control patients (p<0.001). Conditional logistic regression analysis revealed that non-atrophic gastric mucosa was an independent risk factor for SNADETs (odds ratio, 5.10; 95% confidence interval, 2.44–8.40; p<0.001). Conclusions Non-atrophic gastric mucosa, regardless of H. pylori infection status, was a factor independently associated with SNADETs.