Non-atrophic gastric mucosa is an independently associated factor for superficial non-ampullary duodenal epithelial tumors: a multicenter, matched, case-control study
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Background/Aims: The etiology of superficial non-ampullary duodenal epithelial tumors (SNADETs) remains unclear. Recent studieshave reported conflicting associations between duodenal tumor development and Helicobacter pylori infection or endoscopic gastricmucosal atrophy. As such, the present study aimed to clarify the relationship between SNADETs and H. pylori infection and/or endoscopicgastric mucosal atrophy. Methods: This retrospective case-control study reviewed data from 177 consecutive patients with SNADETs who underwent endoscopicor surgical resection at seven institutions in Japan over a three-year period. The prevalence of endoscopic gastric mucosal atrophyand the status of H. pylori infection were compared in 531 sex- and age-matched controls selected from screening endoscopies attwo 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 riskfactor 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.
Abstract
Background/Aims: The etiology of superficial non-ampullary duodenal epithelial tumors (SNADETs) remains unclear. Recent studieshave reported conflicting associations between duodenal tumor development and Helicobacter pylori infection or endoscopic gastricmucosal atrophy. As such, the present study aimed to clarify the relationship between SNADETs and H. pylori infection and/or endoscopicgastric mucosal atrophy. Methods: This retrospective case-control study reviewed data from 177 consecutive patients with SNADETs who underwent endoscopicor surgical resection at seven institutions in Japan over a three-year period. The prevalence of endoscopic gastric mucosal atrophyand the status of H. pylori infection were compared in 531 sex- and age-matched controls selected from screening endoscopies attwo 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 riskfactor 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.
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