Probiotic supplementation does not improve eradication rate of Helicobacter pylori infection compared to placebo based on standard therapy: a meta-analysis.

This meta-analysis included eligible randomized controlled trials (RCTs) with the aim of determining whether probiotic supplementation can improve H. pylori eradication rates. PUBMED, EBSCO, Web of Science, and Ovid databases were searched. We included RCTs that investigated the effect of combining probiotics, with or without a placebo, with standard therapy. A total of 21 RCTs that reported standard therapy plus probiotics were included. Compared to the placebo group, the probiotics group was 1.21(OR 1.21, 95% CI: 0.86, 1.69) and 1.28 (OR 1.28, 95% CI: 0.88, 1.86) times more likely to achieve eradication of H. pylori infection in intent-to-treat (ITT) analysis and per protocol (PP) analysis, respectively. Probiotics with triple therapy plus a 14-day course of treatment did not improve the eradication of H. pylori infection (OR 1.44, 95% CI: 0.87, 2.39) compared to the placebo. Moreover, the placebo plus standard therapy did not improve eradication rates compared to standard therapy alone (P = 0.816). However, probiotics did improve the adverse effects of diarrhea and nausea. These pooled data suggest that the use of probiotics plus standard therapy does not improve the eradication rate of H. pylori infection compared to the placebo.

Seven-day triple therapy is a better choice for Helicobacter pylori eradication in regions with low antibiotic resistance.

AIM: To investigate whether 7-d triple therapies are still valid in populations with low levels of resistance. METHODS: A total of 1106 Helicobacter pylori (H. pylori)-positive patients were divided into three groups, each of which received one type of 7-d triple therapy. Therapeutic outcomes of the patients were assessed by the (13)C-urea breath test at 8 wk after treatment. The susceptibility of H. pylori to antibiotics was determined by an agar-dilution method. Data analysis was performed by χ(2) tests. RESULTS: The eradication rates in groups A, B and C were 90.71% (332/366), 90.46% (313/346) and 90.87% (189/208), respectively (P = 0.986). The resistance rates were 8.91% for clarithromycin, 14.78% for levofloxacin and 0% for amoxicillin. The eradication rate was significantly different between clarithromycin- and levofloxacin-resistant patients (P < 0.05) in group A. Patients whose treatment failed in group A also had a higher clarithromycin resistance rate than did successive patients (P = 0.034). However, levofloxacin resistance had no obvious influence on the eradication rate. Furthermore, three main antibiotics (clarithromycin, levofloxacin and amoxicillin) had lower DID (defined daily dose per 1000 inhabitants per day) in this city. CONCLUSION: Clarithromycin resistance is the main reason for the failure of 7-d triple therapy. In populations with low levels of resistance, a 7-d triple therapy is a viable choice. The choice of therapy should not be influenced by conditions in high antibiotic resistance regions.

ω-3 Fatty acids reverse lipotoxity through induction of autophagy in nonalcoholic fatty liver disease.

OBJECTIVE: The aim of this study was to evaluate the effect of ω-3 fatty acids on nonalcoholic fatty liver disease concerning hepatocyte lipid accumulation as well as apoptosis induced by free fatty acids (FFAs) and to explore the underlying mechanism involving autophagy. METHODS: Hepatocytes were incubated with a mixture of free fatty acids (FFAs) to mimic in vitro lipotoxicity in the pathogenesis of nonalcoholic fatty liver disease, presented by lipid accumulation and cellular apoptosis. Chemical inhibitor or inducer of autophagy and genetic deficit cells, as well as ω-3 fatty acids were used as intervention. The autophagic role of ω-3 fatty acids was investigated using Western blot and immunofluorescence. The underlying mechanism of ω-3 fatty acids involving autophagy was preliminarily explored by quantitative real-time polymerase chain reaction and Western blot. RESULTS: FFAs induce lipid accumulation and apoptosis in hepatocytes. Inhibition or genetic defect of autophagy increases lipid accumulation induced by FFA, whereas induction acts inversely. ω-3 Fatty acids reduced lipid accumulation and inhibited apoptosis induced by FFA. ω-3 Fatty acids induced autophagy by downregulating stearoyl-CoA desaturase 1 expression in hepatocytes. CONCLUSION: ω-3 Fatty acids exert protective effects on hepatocytes against lipotoxicity through induction of autophagy, as demonstrated by inhibition of lipid accumulation and apoptosis.

The role of ursodeoxycholic acid in non-alcoholic steatohepatitis: a systematic review.

BACKGROUND: Non-alcoholic steatohepatitis (NASH) is a condition that occurs during the progression of non-alcoholic fatty liver disease. Effective therapy for NASH is still lacking. In this study, we investigated the effects of Ursodeoxycholic acid (UDCA) in the treatment of NASH. METHODS: Western and Chinese databases were searched by independent investigators using appropriate MESH headings to identify randomized, controlled Western and Chinese clinical trials, published between January 1990 and October 2012, testing the effects of UDCA in patients with NASH. Patient characteristics and trial endpoints were analyzed, with quality assessment according to widely acknowledged criteria. P < 0.05 was defined as statistically significant in all trials. RESULTS: Twelve qualified randomized clinical trials, including six from China and involving 1160 subjects, were selected. Seven of these trials assessed the effects of UDCA Monotherapy, with the other five testing combinations of UDCA with vitamin E, polyene phosphatidylcholine, silymarin, glycyrrhizin and tiopronin. The duration of therapy ranged from 3 to 24 months, with two studies using high doses of UDCA (23-35 mg/kg/d). The average quality point was 2.69, and was significantly lower in articles from China than in those from Western countries (2.2 ± 0.4 vs. 3.8 ± 1.1, respectively, p < 0.05). UDCA Monotherapy significantly improved liver function in five studies and improved steatosis and fibrosis in two studies. All five studies assessing UDCA combination therapy showed significant improvements liver function, while two studies also improved steatosis and inflammation. One study of high-dose UDCA showed significant improvements in ALT, γGT and liver fibrosis, whereas the other study showed no significant change in ALT and liver pathology. CONCLUSIONS: UDCA therapy is effective in NASH, especially when combined with other drugs. However, the low quality of these studies and the heterogeneity of their results precluded further meta-analysis. Additional carefully designed clinical trials are needed, especially in China.

[T lymphocyte subgroups and serum levels of trace elements in patients with diarrhea type of irritable bowel syndrome].

OBJECTIVE: To investigate the T lymphocyte subgroups and the levels of serum zinc (Zn), selenium (Se), iron (Fe), copper (Cu) in patients with diarrhea type of irritable bowel syndrome (D-IBS). METHODS: A total of 30 D-IBS patients and 30 control subjects were enrolled in this study, and their peripheral blood samples were collected. The percentage of peripheral CD3, CD4, CD8 T lymphocytes were analyzed by flow cytometry, and the ratio of CD4/CD8 was calculated. Serum Zn, Fe and Cu levels were determined by atomic absorption spectrometry(AAS), and the Se level by atomic fluorometry. RESULT: Compared with control group,the percentage of CD4 T lymphocyte and the ratio of CD4/CD8 in D-IBS group were significantly lower (P<0.01). However, there was no significant difference in serum Zn, Se, Fe, Cu levels between two groups (P>0.05). CONCLUSION: The declines of peripheral blood CD4 T lymphocytes and the ratio of CD4/CD8 may suggest a cellular immune abnormality in D-IBS patients. There was no significant difference in trace elements levels between the two groups.

Green tea consumption and liver disease: a systematic review.

OBJECTIVES: To present the effect of green tea consumption against liver disease. DATA SOURCES: Interventional and observational studies both in Western countries and in China and published between the years 1989 and December 2007. REVIEW METHODS: The articles were retrieved from Medline, Embase database, Chinese biomedicine web database and Chinese scientific journal's database using proper MESH headings and assessed by two independent investigators according to established inclusion criteria. The characteristics and outcomes of the chosen articles were displayed for further analysis and the quality of each study was also evaluated according to the widely acknowledged criteria. P<0.05 was defined as statistically significant in all enrolled trials. RESULTS: Ten qualified studies (eight from China, one from Japan and the other from the USA) with various outcomes such as liver cancer, cirrhosis and fatty liver disease were finally chosen. Among them, study designs differed in that there were four randomized-controlled clinical trials, two cohort, one case-control and three cross-sectional studies. The heterogeneity in the study design, outcomes, cofounders and amount of tea consumption precluded further meta-analysis. Nevertheless, eight studies showed a significant protective role of green tea against various liver diseases as determined by relative risk/odds ratio or P-value and among them, four studies showed a positive correlation between green tea intake and attenuation of liver disease. Moreover, the other two studies also presented the protective tendency of green tea against liver disease. CONCLUSIONS: An increased consumption of green tea may reduce the risk of liver disease.

[Effect of tea polyphenols on alcoholic liver injury].

OBJECTIVE: To reproduce an experimental model of alcoholic liver disease in rats and to investigate the preventive and treatment effects of tea polyphenols on alcoholic liver disease. METHODS: 68 male Sprague-Dawley rats were randomly divided into 3 groups: alcohol group (gastrically infused with 56% of ethanol once a day with a dose of 7 g/kg body weight for 4, 12 and 24 weeks), tea polyphenols group (gastric infusion with alcohol same as in the alcohol group and with tea polyphenols at 0.25 g/kg bw) and control group (gastric infusion with normal saline). At the end of 4, 12 and 24 weeks, blood samples were collected and then the rats were sacrificed. Liver samples were obtained for routine histological examination and the degree of hepatic steatosis and alcoholic hepatitis were examined. Blood specimens were used for evaluation of alanine transaminase (ALT) and aspartate aminotransferase (AST). RESULTS: (1) The levels of the two transaminases were elevated with the increase of the duration of ethanol feeding and the difference is significant. TP significantly mitigated the increase of ALT and AST activities induced by the alcohol. (2) Histological changes of the liver injury indicated that piecemeal or focal necrosis of hepatocytes was present in the centrilobular area. As fibrosis advanced, broader septa were formed with central-central and centra-portal bridging necrosis. In the TP infusion group, the severity of the pathological changes was significantly milder. CONCLUSION: The results of this study revealed that TP mitigated the development of alcoholic liver disease, and TP may be a potential drug for treatment of alcoholic liver disease.

Effects of tea polyphenols on hepatic fibrosis in rats with alcoholic liver disease.

BACKGROUND: As an anti-oxidation agent, tea polyphenols may have the effect of anti-fibrosis. This study was designed to observe the effect of tea polyphenols on hepatic fibrosis in rats with alcoholic liver disease and to explore the related mechanisms. METHODS: Sixty healthy Sprague-Dawley rats were divided randomly into normal control group, single alcohol group, and three alcohol groups given different doses of tea polyphenols. Alcohol or isovolumic normal saline and corresponding doses of tea polyphenols were given daily to the rats separately. The rats were sacrificed at the end of the 24th week. Masson staining was performed to observe liver fibrosis, serum endotoxin, and oxidant and anti-oxidant activity. RESULTS: Hepatic fibrosis was less severe in the rats of the alcohol groups given tea polyphenols than in the single alcohol group. Tea polyphenols increased the serum anti-oxidant capacity and decreased the endotoxin level. CONCLUSION: Tea polyphenols show anti-fibrosis effect in rats with alcoholic liver disease, and the mechanism may be related to the clearance of overall oxidant and decrease of the endotoxin level.

[Effect of tea polyphenol on liver fibrosis in rats and related mechanism].

OBJECTIVE: To investigate the effect of tea polyphenol (TP)'s on liver fibrosis in rats and its possible mechanism. METHOD: Rats were divided into 5 groups, 4 groups of which were stomach perfused with alcohol resulting in alcoholic liver fibrosis, and 3 groups of which were stomach perfused with TP simultaneously. Another group was normal control one. Histological change of rat liver was investigated and quantitative analysis was made in 24 weeks, and rat liver anti-oxidation index and serum endotoxin were determined at the same time. RESULT: Liver fibrosis in TP group was slight, and anti-oxidize index and endotoxin level were markedly improved in comparison with those of alcohol groups. CONCLUSION: Tea polyphenol can protect hepatocytes from fibrosis. Its mechanism is possibly due to cleaning up overfull lipid per-oxidation and reducing the level of endotoxin.