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High salt intake is associated with atrophic gastritis with intestinal metaplasia

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Abstract

Background: Although several studies have investigated excessive salt intake as a risk factor for gastric precancerous lesions, such as atrophic gastritis and intestinal metaplasia, the evidence is insufficient to make a conclusion. We evaluated the association between gastric precancerous lesions and salt intake. Methods: From 2008 to 2015, the medical records of 728 subjects who underwent upper gastrointestinal endoscopy and sodium excretion in 24-hour urine tests were retrospectively reviewed. Sixty-six subjects were excluded due to diuretics use (n55), diagnosis with a gastric neoplasm (n4), or the cases of intestinal metaplasia in the absence of atrophy (n 7), so 662 subjects were included. Atrophic gastritis and intestinal metaplasia were diagnosed by endoscopic findings. The subjects were grouped into three levels by tertiles of 24-hour urine sodium excretion. Results: A total of 192 (29.0%) had atrophic gastritis without intestinal metaplasia and 112 (16.9%) had atrophic gastritis with intestinal metaplasia. A total of 276 subjects (61.5%) were infected with Helicobacter pylori (H. pylori). In multivariate analyses, H. pylori infection [OR 14.17; 95% confidence interval (CI), 7.12-28.22) was associated with atrophic gastritis without intestinal metaplasia. Highest levels of sodium excretion (OR 2.870; 95% CI, 1.34-6.14), heavy smoking (20 pack-years) (OR 2.75; 95% CI, 1.02-7.39), and H. pylori infection (OR 3.96; 95% CI, 2.02-7.76) were associated with atrophic gastritis with intestinal metaplasia. Conclusions: Our endoscopy-based study suggested that high salt intake could be associated with an increased risk of atrophic gastritis with intestinal metaplasia. Impact: Low salt diet might be helpful to prevent gastric carcinogenesis.

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Song, J. H., Kim, Y. S., Heo, N. J., Lim, J. H., Yang, S. Y., Chung, G. E., & Kim, J. S. (2017). High salt intake is associated with atrophic gastritis with intestinal metaplasia. Cancer Epidemiology Biomarkers and Prevention, 26(7), 1133–1138. https://doi.org/10.1158/1055-9965.EPI-16-1024

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