INTRODUCTION: Alterations of gut microbiota have been thought to be associated with irritable bowel syndrome (IBS). Many studies have reported significant alterations of gut microbiota in patients with IBS based on 16S ribosomal RNA-targeted sequencing. However, results from these studies are inconsistent or even contradictory. We performed a systematic review to explore the alterations of gut microbiota in patients with IBS compared with healthy controls (HCs). METHODS: The databases PubMed, Cochrane Library, Web of Science, and Embase were searched for studies published until February 28, 2018, for case–control studies detecting gut microbiota in patients with IBS. Methodological quality was assessed using the Newcastle–Ottawa Scale. The α-diversity and alterations of gut microbiota in patients with IBS compared with HCs were analyzed. RESULTS: Sixteen articles involving 777 patients with IBS and 461 HCs were included. Quality assessment scores of the studies ranged from 5 to 7. For most studies, patients with IBS had a lower α-diversity than HCs in both fecal and mucosal samples. Relatively consistent changes in fecal microbiota for patients with IBS included increased Firmicutes, decreased Bacteroidetes, and increased Firmicutes:Bacteroidetes ratio at the phylum level, as well as increased Clostridia and Clostridiales, decreased Bacteroidia and Bacteroidales at lower taxonomic levels. Results for mucosal microbiota were inconsistent. CONCLUSIONS: Alterations of gut microbiota exist in patients with IBS and have significant association with the development of IBS. Further studies are needed to draw conclusions about gut microbiota changes in patients with IBS. TRANSLATIONAL IMPACT: This knowledge might improve the understanding of microbial signatures in patients with IBS and would guide future therapeutic strategies.

Background/Aims:We conducted this meta-analysis to evaluate the prevalence of sleep disorder in irritable bowel syndrome (IBS) patients and study the association between IBS and sleep disorder.Materials and Methods:A systematic search was conducted by searching PubMed, Embase, and Cochrane library databases using the following search terms: “functional gastrointestinal disorders,” “Sleep disturbance,” “Sleep disorder,” “insomnia,” “Dysomnias,” “irritable bowel syndrome,” and “IBS.” Studies evaluating the association between IBS and sleep disorder were identified. Data analysis was conducted using meta-analysis software Comprehensive Meta-Analysis (CMA) 2.0. Heterogeneity across studies was evaluated by χ2 and I2 statistics. Publication bias was evaluated by funnel plot, Begg's test, and Egger's test. Sensitivity analysis was also performed by removing each single study separately.Results:The bibliographical search yielded a total of 2866 studies. Finally, 36 studies including 63620 participants were identified. The prevalence of sleep disorder in IBS was 37.6% (95% CI: 31.4% to 44.3%) based on this meta-analysis. The pooled odds ratio was 2.618 (95% CI: 2.052% to 3.341). Publication bias was not determined. Regarding the sensitivity analysis, the outcome was stable regardless of which study was removed.Conclusions:The prevalence of sleep disorder was higher in IBS compared to healthy controls and may be associated with the pathogenesis of IBS. The prevalence of sleep disorder in IBS may differ according to different areas, age, gender, occupation, and IBS diagnostic criteria. Further studies are needed to investigate any possible causal relationship between sleep disorder and IBS.

Background Helicobacter 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. Methods We reviewed observational studies published in English until October 2019. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were calculated for included studies. Results 46 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). Conclusions Hp, 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.

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