Cirrhosis is a severe threat to public health. Some studies have suggested that cirrhosis is associated with Helicobacter pylori infection, but the results remain controversial. This meta-analysis was conducted to quantify the association between cirrhosis and H. pylori infection. Published articles on H. pylori prevalence in patients with cirrhosis were collected to assess the potential associations between H. pylori infection and cirrhosis risk. Twenty-one eligible studies were included for the analysis. Data on publication year, geographic region, and etiology were summarized. Metaregression models and subgroup analyses were established to screen the factors for heterogeneity. Of the 322 articles retrieved, 21 met the inclusion criteria. These studies involved 6135 cases, with a total H. pylori infection rate of 52.26%. This meta-analysis showed significant difference in H. pylori infection between patients with cirrhosis and controls [odd ratio (OR)=2.05, 95% confidence interval (CI): 1.33-3.18, P<0.0001]. The subgroup analysis revealed, in contrast to Asia (OR=0.90, 95% CI: 0.48-1.66, P<0.0001), Europe (OR=2.98, 95% CI: 2.02-4.39, P<0.0001), and America (OR=4.75, 95% CI: 1.42-15.95, P=0.249), a significantly higher prevalence of H. pylori infection in patients with cirrhosis. On the basis of etiology, there was a higher prevalence of H. pylori infection due to primary biliary cirrhosis (OR=1.75, 95% CI: 1.15-2.64, P=0.147) and viral cirrhosis (OR=2.66, 95% CI: 1.24-5.71, P<0.0001) compared with alcohol cirrhosis (OR=0.77, 95% CI: 0.04-16.59, P<0.0001). The pooled data suggest that there is a significantly high prevalence of H. pylori infection in patients with cirrhosis. Large-scale and multicenter studies are needed to further investigate the relation between cirrhosis and H. pylori infection.

BackgroundEpidemiological studies have shown that gastrointestinal Helicobacter pylori (H. pylori) infection is the main cause of chronic gastritis, but the relation between oral H. pylori and chronic periodontitis (CP) remains uncertain. A meta-analysis of published papers was performed to elucidate the correlation between oral H. pylori and CP.MethodTo perform this meta-analysis, we searched papers published from 2000 to 2018 on PubMed, OVID, Springer Link, Chinese National Knowledge Infrastructure (CNKI) and Chinese Biology Medicine search engines. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) for the correlation between H. pylori and CP were estimated. Heterogeneity, publication bias and subgroup analyses were also conducted.ResultsA total of 918 papers on oral H. pylori and CP were collected, and 11 papers were in accordance with the inclusion criteria. Oral H. pylori was suggested to be correlated with CP. The results indicated that a H. pylori-positive state significantly increased the risk of CP 3.42 times (OR = 3.42; 95% CI = 2.71–4.31). A diagnostic test using polymerase chain reaction (PCR) showed a higher prevalence of H. pylori (OR = 3.70; 95% CI = 2.66–5.14) than did that using the rapid urease test (RUT) (OR = 3.13; 95% CI = 2.26–4.34).ConclusionsThis paper demonstrated that CP was potentially correlated with oral H. pylori in adults and that oral H. pylori may be a possible risk factor for CP.

Chronic hepatitis B (CHB) is a worldwide infectious disease caused by hepatitis B virus (HBV). HBV mainly damages liver cells through immune response. The purpose of this study was to determine whether there were dynamic changes of Treg and Th17 cells and to judge the value of these indicators to antiviral treatment. Twenty-two CHB patients and selected 30 healthy adults were enrolled. Results showed that the expression of Treg (5.72±0.46 vs. 4.42±0.17, p=0.0019) and Th17 (3.94±0.64 vs. 2.66±3.12, p=0.0436) cells was significantly increased in CHB patients, as well as the level of interleukin-17 (IL-17) (16.88±5.37 vs. 8.59±3.31; p=0.004). Then, we monitored longitudinally the impact of the treatment with interferon-α and found that the suppression of viral replication induced by interferon-α resulted in a decrease in Treg, Th17 cells, and IL-17; we also found that the percentage of Treg and Th17 cells went up without clear evidence of clinical autoimmune disease at the end of treatment. Thus, Treg and Th17 cells might play an important role in interferon-α treatment to eliminate HBV. The level of changes may be served to determine the antiviral efficacy of interferon-α therapy.