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Abstract
BackgroundHelicobacter pylori (Hp) is a class I carcinogen in gastric carcinogenesis, but its role in Barrett’s esophagus (BE) is unknown. Therefore, we aimed to explore the possible relationship.MethodsWe reviewed observational studies published in English until October 2019. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were calculated for included studies.Results46 studies from 1505 potential citations were eligible for inclusion. A significant inverse relationship with considerable heterogeneity was found between Hp (OR = 0.70; 95% CI, 0.51–0.96; P = 0.03) and BE, especially the CagA-positive Hp strain (OR = 0.28; 95% CI, 0.15–0.54; P = 0.0002). However, Hp infection prevalence was not significantly different between patients with BE and the gastroesophageal reflux disease (GERD) control (OR = 0.99; 95% CI, 0.82–1.19; P = 0.92). Hp was negatively correlated with long-segment BE (OR = 0.47; 95% CI, 0.25–0.90; P = 0.02) and associated with a reduced risk of dysplasia. However, Hp had no correlated with short-segment BE (OR = 1.11; 95% CI, 0.78–1.56; P = 0.57). In the present infected subgroup, Hp infection prevalence in BE was significantly lower than that in controls (OR = 0.69; 95% CI, 0.54–0.89; P = 0.005); however, this disappeared in the infection history subgroup (OR = 0.88; 95% CI, 0.43–1.78; P = 0.73).ConclusionsHp, especially the CagA-positive Hp strain, and BE are inversely related with considerable heterogeneity, which is likely mediated by a decrease in GERD prevalence, although this is not observed in the absence of current Hp infection.
Highlights
Helicobacter pylori (Hp) is a class I carcinogen in gastric carcinogenesis, but its role in Barrett’s esopha‐ gus (BE) is unknown
A significant inverse relationship with considerable heterogeneity was found between Hp (OR = 0.70; 95% Confidence interval (CI), 0.51–0.96; P = 0.03) and BE, especially the cytotoxin-associated gene A (CagA)-positive Hp strain (OR = 0.28; 95% CI, 0.15–0.54; P = 0.0002)
Hp was negatively correlated with long-segment BE (OR = 0.47; 95% CI, 0.25–0.90; P = 0.02) and associated with a reduced risk of dysplasia
Summary
Helicobacter pylori (Hp) is a class I carcinogen in gastric carcinogenesis, but its role in Barrett’s esopha‐ gus (BE) is unknown. Owing to improvements in hygiene and living conditions, the prevalence of Helicobacter pylori (Hp) has continued to fall in developed countries, along with the incidence of gastric cancer and peptic ulcer, it remains high in some developing countries, such as 70.1% in Africa [1, 2]. Hp is classified by the World Health Organization as a class 1 carcinogen, since it promotes gastric cancer, and is regarded as a commensal organism that confers some protection against asthma, allergies, and even obesity [9, 10]. Hp seems to have a protective influence on BE, the relationship between Hp and BE remains controversial
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