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High prevalence of clarithromycin resistance and effect on Helicobacter pylori eradication in a population from Santiago, Chile: cohort study and meta-analysis.
Arenas, A, Serrano, C, Quiñones, L, Harris, P, Sandoval, M, Lavanderos, M, Sepúlveda, R, Maquilón, S, Echeverría, A, Ríos, C, et al
Scientific reports. 2019;(1):20070
Abstract
Helicobacter pylori (H. pylori) eradication using standard triple therapy (STT) with proton pump inhibitors (PPI), amoxicillin and clarithromycin (CLA) has been the standard in Latin America. However, CLA resistance is a rising problem affecting eradication rates. Genetic polymorphisms of CYP2C19, a PPI metabolizer may also affect eradication. The primary aims of this study were to evaluate the effect of clarithromycin resistance on H. pylori eradication in a population from Santiago, and to establish the pooled clarithromycin resistance in Santiago, Chile. Symptomatic adult patients attending a tertiary hospital in Santiago were recruited for this study. CLA resistance and the polymorphisms of CYP2C19 were determined on DNA extracted from gastric biopsies, using PCR. The STT was indicated for 14 days and eradication was determined by a urea breath test 4-6 weeks after therapy. A meta-analysis of CLA resistance studies among adult residents in Santiago was performed. Seventy-three out of 121 consecutive patients had positive rapid urease test (RUT) and received STT. Sixty-nine patients (95%) completed the study. The H. pylori eradication rate was 63% and the prevalence of CLA resistance was 26%. According to the CYP2C19 polymorphisms, 79.5% of the RUT-positive patients were extensive metabolizers. Multivariable analyses showed that only CLA resistance was significantly and inversely associated with failure of eradication (OR: 0.13; 95% confidence interval [95% CI], 0.04-0.49). A meta-analysis of two previous studies and our sample set (combined n = 194) yielded to a pooled prevalence of CLA resistance of 31.3% (95% CI 23.9-38.7). Our study shows that CLA resistance is associated with failure of H. pylori eradication. Given the high pooled prevalence of CLA resistance, consideration of CLA free therapies in Santiago is warranted. We could recommend bismuth quadruple therapy or high-dose dual therapy, according to bismuth availability. Further studies need to evaluate the best therapy.
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The effect of synbiotics in improving Helicobacter pylori eradication: A systematic review and meta-analysis.
Pourmasoumi, M, Najafgholizadeh, A, Hadi, A, Mansour-Ghanaei, F, Joukar, F
Complementary therapies in medicine. 2019;:36-43
Abstract
BACKGROUND Helicobacter pylori is a common human infection, presenting in half of the world's population. The failure of the Helicobacter pylori eradication rate necessitates the assessment of new options. The aim of the present meta-analysis was therefore to assess the role of synbiotics in Helicobacter pylori eradication therapy. METHODS A comprehensive literature search was conducted using PubMed, Google Scholar, Scopus, and Web of Knowledge up to June 2018 to identify all randomized controlled trials assessing the effect of synbiotics on the treatment of Helicobacter pylori. A random-effects model was applied for pooling analysis to compensate for the heterogeneity of included studies. The Cochrane Risk of Bias Tool was applied to assess potential bias risks. RESULTS A total of 6 randomized controlled trials were found which assessed the effect of synbiotics on Helicobacter pylori eradication rate. The pooled effect size of the intention-to-treat showed that synbiotics can improve eradication rate (RR: 1.28; 95% CI: 1.15-1.43; I2 = 0%). Also, common adverse events resulting from antibiotics therapy were significantly reduced by adding synbiotics to conventional antibiotics treatments (RR: 0.47; 95% CI: 0.25-0.90; I2 = 36%). However, no difference in eradication rate was observed from per-protocol treatment between intervention and control groups (RR: 0.90; 95% CI: 0.69-1.16; I2 = 88%). CONCLUSION The present systematic review and meta-analysis suggested synbiotics might improve Helicobacter pylori eradication rates, and reduce adverse effects. However, these findings assessed a low number of studies, and further high-quality studies are needed to confirm these results.
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Association Between Helicobacter pylori Exposure and Decreased Odds of Eosinophilic Esophagitis-A Systematic Review and Meta-analysis.
Shah, SC, Tepler, A, Peek, RM, Colombel, JF, Hirano, I, Narula, N
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2019;(11):2185-2198.e3
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Abstract
BACKGROUND & AIMS Previous or current infection with Helicobacter pylori (exposure) has been reported to protect against eosinophilic esophagitis (EoE), perhaps owing to H pylori-induced immunomodulation. However, findings vary. We performed a systematic review and meta-analysis of comparative studies to define the association between H pylori exposure and EoE more clearly. METHODS We searched 4 large databases to identify comparative clinical studies that included sufficient detail to determine the odds or risk of EoE (primary outcome) or esophageal eosinophilia (secondary outcome) among individuals exposed to H pylori (exposed) vs individuals who were tested and found to be unexposed. Estimates were pooled using a random-effects model. Meta-regression and sensitivity analyses were planned a priori. Studies were evaluated for quality, risk of bias, publication bias, and heterogeneity. RESULTS We analyzed 11 observational studies comprising data on 377,795 individuals worldwide. H pylori exposure vs nonexposure was associated with a 37% reduction in odds of EoE (odds ratio, 0.63; 95% CI, 0.51-0.78) and a 38% reduction in odds of esophageal eosinophilia (odds ratio, 0.62; 95% CI, 0.52-0.76). Fewer prospective studies found a significant association between H pylori exposure and EoE (P = .06) than retrospective studies. Effect estimates were not affected by study location, whether the studies were performed in pediatric or adult populations, time period (before vs after 2007), or prevalence of H pylori in the study population. CONCLUSIONS In a comprehensive meta-analysis, we found evidence for a significant association between H pylori exposure and reduced odds of EoE. Studies are needed to determine the mechanisms of this association.
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Systematic review with meta-analysis: association between Helicobacter pylori CagA seropositivity and odds of inflammatory bowel disease.
Tepler, A, Narula, N, Peek, RM, Patel, A, Edelson, C, Colombel, JF, Shah, SC
Alimentary pharmacology & therapeutics. 2019;(2):121-131
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Abstract
BACKGROUND Accumulating data support a protective role of Helicobacter pylori against inflammatory bowel diseases (IBD), which might be mediated by strain-specific constituents, specifically cagA expression. AIM: To perform a systematic review and meta-analysis to more clearly define the association between CagA seropositivity and IBD. METHODS We identified comparative studies that included sufficient detail to determine the odds or risk of IBD, Crohn's disease (CD) or ulcerative colitis (UC) amongst individuals with vs without evidence of cagA expression (eg CagA seropositivity). Estimates were pooled using a random effects model. RESULTS Three clinical studies met inclusion criteria. cagA expression was represented by CagA seropositivity in all studies. Compared to CagA seronegativity overall, CagA seropositivity was associated with lower odds of IBD (OR 0.31, 95% CI 0.21-0.44) and CD (OR 0.25, 95% CI 0.17-0.38), and statistically nonsignificant lower odds for UC (OR 0.68, 95% CI 0.35-1.32). Similarly, compared to H pylori non-exposed individuals, H pylori exposed, CagA seropositive individuals had lower odds of IBD (OR 0.26, 95% CI 0.16-0.41) and CD (OR 0.23, 95% CI 0.15-0.35), but not UC (OR 0.66, 0.34-1.27). However, there was no significant difference in the odds of IBD, CD or UC between H pylori exposed, CagA seronegative and H pylori non-exposed individuals. CONCLUSION We found evidence for a significant association between CagA seropositive H pylori exposure and reduced odds of IBD, particularly CD, but not for CagA seronegative H pylori exposure. Additional studies are needed to confirm these findings and define underlying mechanisms.