Background:The impact of probiotics on non-Helicobacter pylori gastric microbiota and its role in microbial restoration after eradication were relatively unknown. We aimed to explore the effect of H. pylori eradication and probiotic intervention on gastric microbiota in young adults.Methods: Fifty-six H. pylori-negative and 95 H. pylori-positive subjects aged 19-30 were included in this study. H. pylori-infected individuals were randomly assigned to quadruple therapy, probiotics supplemented quadruple therapy, or probiotics monotherapy group. Gastric mucosa and gastric juice samples were collected before and 2 months after treatment for 16SrRNA gene sequencing.
Results:The gastric microbial community structure and composition differed from H. pylori-negative subjects 2 months after successful H. pylori eradication. The α diversity of gastric mucosal microbiota significantly increased and was higher than H. pylorinegative subjects, while the α diversity of gastric juice microbiota decreased and was lower than the H. pylori-negative. After probiotics supplemented eradication treatment, Bifidobacterium was enriched in gastric mucosa, Lactobacillus was enriched in gastric juice, potentially pathogenic bacteria such as Fusobacterium and Campylobacter decreased, and the microbial diversity was closer to that of H. pylori-negative subjects compared to quadruple therapy group. Probiotics monotherapy significantly altered the diversity, community structure, and composition of gastric microbiota but showed no advantage in H. pylori inhibition and upregulating beneficial bacteria such as Bifidobacterium and Lactobacillus and related metabolism pathways. Certain potentially pathogenic bacteria such as Fusobacterium increased after probiotic monotherapy.
Conclusion:H. pylori eradication significantly disrupted gastric microbiota in young adults and could not be restored in a short time. Probiotics supplementation partially helped restore the gastric dysbiosis caused by eradication therapy, but it might be unnecessary for H. pylori-infected young adults to take probiotics alone.
Background and AimEndoscopic examination of gastric atrophy has been developed to determine the extent of atrophy by identifying the atrophic border of gastric mucosa, but its value in predicting the risk of developing gastric neoplasms is not quantified. Thus, this systematic review and meta‐analysis aim to assess the incidence risk of gastric neoplasms on the basis of endoscopic grading of gastric atrophy.MethodsTwo authors independently searched the electronic databases (PubMed, Embase, and the Cochrane Library) from inception through December 31, 2019, without language restriction. The effect size on study outcomes is calculated using random‐effects model and presented as risk ratio (RR) with 95% confidence interval (CI). Heterogeneity, publication bias, and quality of included studies were also assessed.ResultsFourteen retrospective studies are identified to perform systematic review and meta‐analysis, 11 were cohort studies, and three were cross‐sectional research. The pooled RR for developing gastric neoplasms is 3.89 (95% CI 2.92–5.17) among general patients with severe endoscopic atrophy. For patients who underwent endoscopic resection for early gastric neoplasms, nearly two times increased risk of synchronous or metachronous neoplasms is pooled (RR = 1.96, 95% CI 1.39–2.75). In terms of the type of endoscopic atrophy, patients with open‐type endoscopic atrophy have a higher risk of gastric cancer development (RR 8.02; 95% CI 2.39–26.88) than those with close type. [Correction added on 22 December 2020, after first online publication: ‘(RR = 7.27; 95% CI 1.64–32.33)’ has been corrected to ‘(RR 8.02; 95% CI 2.39–26.88)’]ConclusionsGrading endoscopic atrophy according to the Kimura–Takemoto classification can assess the risk of gastric neoplasia development. Patients with severe or open‐type endoscopic gastric atrophy at baseline should undergo rigorous surveillance to early detect premalignant lesions and cancer.
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