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Updated: Sep 29, 2025
Simultaneous Laryngopharyngeal and Conventional Esophageal pH Monitoring
Published on: December 14, 2020
Inverse correlation between gastroesophageal reflux disease and atrophic gastritis assessed by endoscopy and serology
Yoo Min Han1, Su Jin Chung2, Seokha Yoo3
1Department of Internal Medicine and Healthcare Research Institute, Seoul National University Hospital Healthcare System Gangnam Center, Seoul 06236, South Korea.
Background:
Helicobacter pylori (H. pylori) infection is known to prevent the occurrence of gastroesophageal reflux disease (GERD) by inducing gastric mucosal atrophy. However, little is known about the relationship between atrophic gastritis (AG) and GERD.
Aim:
To confirm the inverse correlation between AG and the occurrence and severity of GERD.
Methods:
Individuals receiving health checkups who underwent upper gastrointestinal endoscopy at Seoul National University Healthcare System Gangnam Center were included. The grade of reflux esophagitis was evaluated according to the Los Angeles classification. Endoscopic AG (EAG) was categorized into six grades. Serologic AG (SAG) was defined as pepsinogen I ≤ 70 ng/mL and pepsinogen I/II ratio ≤ 3.0. The association between the extent of EAG and SAG and the occurrence and severity of GERD was evaluated using multivariate logistic regression analysis.
Results:
In total, 4684 individuals with GERD were compared with 21901 healthy controls. In multivariate logistic regression analysis, advanced age, male sex, body mass index > 23 kg/m2, presence of metabolic syndrome, current smoking, and alcohol consumption were associated with an increased risk of GERD. Seropositivity for H. pylori immunoglobulin G antibodies was associated with a decreased risk of GERD. There was an inverse correlation between the extent of EAG and occurrence of GERD: Odds ratio (OR), 1.01 [95% confidence interval (CI): 0.90-1.14] in C1, 0.87 (0.78-0.97) in C2, 0.71 (0.62-0.80) in C3, 0.52 (0.44-0.61) in O1, 0.37 (0.29-0.48) in O2, and 0.28 (0.18-0.43) in O3. Additionally, the extent of EAG showed an inverse correlation with the severity of GERD. The presence of SAG was correlated with a reduced risk of GERD (OR = 0.49, 95%CI: 0.28-0.87, P = 0.014).
Conclusion:
The extent of EAG and SAG exhibited strong inverse relationships with the occurrence and severity of GERD. AG followed by H. pylori infection may be independently protect against GERD.
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