scholarly journals Helicobacter pylorieradication treatment for gastric carcinoma prevention in asymptomatic or dyspeptic adults: systematic review and Bayesian meta-analysis of randomised controlled trials

BMJ Open ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. e026002 ◽  
Author(s):  
Teruhiko Terasawa ◽  
Chisato Hamashima ◽  
Katsuaki Kato ◽  
Isao Miyashiro ◽  
Takaki Yoshikawa ◽  
...  

ObjectivesRecent meta-analyses of eradication therapy inHelicobacter pylori-infected adults reported significant reductions in gastric carcinoma risk. However, concerns about supporting unfocused screening and eradication programme in healthy, asymptomatic populations have arisen. We performed a systematic review and Bayesian meta-analysis to provide an accurate interpretation of randomised evidence on the preventive effectiveness of eradication therapy on gastric carcinoma risk.MethodsWe searched databases including PubMed, Cochrane Central and Embase for reference and citation tracking without language restrictions, from inception through 31 July 2018. Paired investigators independently selected randomised controlled trials (RCTs) comparing eradication therapy with placebo or no treatment for asymptomatic or dyspepticH. pylori-infected adults with no previous gastric carcinoma. The main outcome was gastric carcinoma incidence; secondary outcomes included gastric carcinoma-specific, non-gastric carcinoma and all-cause mortality.ResultsA total of 5 population-based and 2 outpatient care-based RCTs involving 7303 adults were eligible. Eradication algorithms were heterogeneous, and unsuccessful eradication and reinfection were frequently observed. A Bayesian meta-analysis with competing risk outcomes found low-certainty evidence that eradication therapy might be more likely than control to reduce gastric carcinoma risk (HR=0.65; 95% credible interval (CrI) 0.41 to 1.0;I2=11%). The CrIs included the null effects across the subgroup and sensitivity analyses, apart from those based on particular models that excluded two RCTs that enrolled subjects with specific histological findings only (HR=0.55; CrI 0.30 to 0.89;I2=14%). The uncertainty of the average 41% risk reduction in gastric carcinoma-specific mortality included a clinically important mortality risk increase (HR=0.59 favouring eradication therapy; CrI 0.25 to 1.20;I2=13%; low certainty).ConclusionsThere is insufficient evidence to support or refute the effectiveness of eradication therapy in preventing gastric carcinoma inH. pylori-infected, high-risk populations. Rigorously conducted large RCTs of healthy infected adults only would provide evidence of the true efficacy of successful eradication.PROSPERO registration number:CRD42014009245.

BMJ Open ◽  
2018 ◽  
Vol 8 (1) ◽  
pp. e019291 ◽  
Author(s):  
Shenghan Lou ◽  
Houchen Lv ◽  
Zhirui Li ◽  
Peifu Tang ◽  
Yansong Wang

IntroductionFracture healing is a complex physiological process. Impaired healing will increase the need for care and cause serious complications. Thus, identifying strategies to accelerate the rate of healing, preventing delayed unions and non-unions, is essential. Parathyroid hormone (PTH) is a key systemic regulator of calcium and phosphate metabolism. It has been determined that intermittent administration of PTH and its analogue can exert anabolic effect on bone, increase bone mass and reduce bone loss, leading to an increase in bone formation. Owing to their anabolic effect, there is an increasing interest in its potential in promoting the process of fracture healing. However, in clinical studies, the results are in conflict. This objective of this study is to determine the role of PTH analogues for fracture healing in adults.Methods and analysisMEDLINE, EMBASE and Cochrane databases will be searched to identify all randomised controlled trials (RCTs) and quasi-RCTs that compare the different effects between PTH analogues and any other treatments in adults with any type of fracture. The primary outcome is the functional recovery. And the secondary outcomes are fracture union and adverse events. The meta-analysis will be performed using a random effects model. Heterogeneity will be assessed by the P values and I² statistic. And subgroup analyses and sensitivity analyses will be used to explore the heterogeneity. Risk of bias will be assessed using the Cochrane tool and the quality of evidence will be assessed using the Grading of Recommendations Assessment, Development and Evaluation approach.Ethics and disseminationEthical approval is not required because this proposed systematic review and meta-analysis is based on published data, without including confidential personal data or data on interventions on patients. The findings of this study will be published in a peer-reviewed journaland presented at a relevant conference.PROSPERO registration numberCRD42017062093.


BMJ Open ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. e036020
Author(s):  
Shuhei Murao ◽  
Hidekazu Nakata ◽  
Kazuma Yamakawa

IntroductionTranexamic acid (TXA) is a synthetic derivative of the amino acid lysine that inhibits fibrinolysis by blocking lysine-binding sites on plasminogen, which contribute to reduced bleeding, the need for transfusion and mortality. Although there is reliable evidence of the efficacy of TXA, its effects on other important outcomes, adverse events, including thrombotic events and seizure, remain uncertain.Methods and analysisWe will conduct a systematic review and meta-analysis of randomised controlled trials with the objective of evaluating the incidence of thrombotic adverse events and seizure and how the effect of TXA varies by dose and underlying disease. We will include patients with bleeding in any underlying disease. We will search MEDLINE, EMBASE and Cochrane Central Register of Controlled Trials for randomised controlled trials. The planned date of our systematic search is 1 June 2020. We will follow the recommendations of the Cochrane Collaboration and the Preferred Reporting Items for Systematic Review and Meta-Analysis statement. Subgroup and sensitivity analyses will be performed to explore residual heterogeneity and inconsistency. Meta-regression analysis will be carried out to investigate the association between the incidence of adverse events and the TXA dose. The risk of systematic errors (bias) and random errors will be assessed and the overall quality of evidence will be evaluated using the Grading of Recommendations Assessment, Development and Evaluation approach.Ethics and disseminationThis study will not involve primary data collection, and formal ethics approval will therefore not be required. We aim to publish this systematic review in a peer-review journal.Trial registration numberUMIN000039611.


2012 ◽  
Vol 201 (3) ◽  
pp. 180-185 ◽  
Author(s):  
Christopher Bridle ◽  
Kathleen Spanjers ◽  
Shilpa Patel ◽  
Nicola M. Atherton ◽  
Sarah E. Lamb

BackgroundThe prevelance of depression in older people is high, treatment is inadequate, it creates a substantial burden and is a public health priority for which exercise has been proposed as a therapeutic strategy.AimsTo estimate the effect of exercise on depressive symptoms among older people, and assess whether treatment effect varies depending on the depression criteria used to determine participant eligibility.MethodSystematic review and meta-analysis of randomised controlled trials of exercise for depression in older people.ResultsNine trials met the inclusion criteria and seven were meta-analysed. Exercise was associated with significantly lower depression severity (standardised mean difference (SMD) =–0.34, 95% CI –0.52 to –0.17), irrespective of whether participant eligibility was determined by clinical diagnosis (SMD =–0.38, 95% CI –0.67 to –0.10) or symptom checklist (SMD =–0.34, 95% CI –0.62 to –0.06). Results remained significant in sensitivity analyses.ConclusionsOur findings suggest that, for older people who present with clinically meaningful symptoms of depression, prescribing structured exercise tailored to individual ability will reduce depression severity.


BMJ Open ◽  
2017 ◽  
Vol 7 (11) ◽  
pp. e016863 ◽  
Author(s):  
Elizabeth P Neale ◽  
Linda C Tapsell ◽  
Vivienne Guan ◽  
Marijka J Batterham

ObjectivesTo examine the effect of nut consumption on inflammatory biomarkers and endothelial function.DesignA systematic review and meta-analysis.Data sourcesMEDLINE, PubMed, Cumulative Index to Nursing and Allied Health Literature and Cochrane Central Register of Controlled Trials (all years to 13 January 2017).Eligibility criteriaRandomised controlled trials (with a duration of 3 weeks or more) or prospective cohort designs conducted in adults; studies assessing the effect of consumption of tree nuts or peanuts on C-reactive protein (CRP), adiponectin, tumour necrosis factor alpha, interleukin-6, intercellular adhesion molecule 1, vascular cell adhesion protein 1 and flow-mediated dilation (FMD).Data extraction and analysisRelevant data were extracted for summary tables and analyses by two independent researchers. Random effects meta-analyses were conducted to explore weighted mean differences (WMD) in change or final mean values for each outcome.ResultsA total of 32 studies (all randomised controlled trials) were included in the review. The effect of nut consumption on FMD was explored in nine strata from eight studies (involving 652 participants), with consumption of nuts resulting in significant improvements in FMD (WMD: 0.79%(95% CI 0.35 to 1.23)). Nut consumption resulted in small, non-significant differences in CRP (WMD: −0.01 mg/L (95% CI −0.06 to 0.03)) (26 strata from 25 studies), although sensitivity analyses suggest results for CRP may have been influenced by two individual studies. Small, non-significant differences were also found for other biomarkers of inflammation.ConclusionsThis systematic review and meta-analysis of the effects of nut consumption on inflammation and endothelial function found evidence for favourable effects on FMD, a measure of endothelial function. Non-significant changes in other biomarkers indicate a lack of consistent evidence for effects of nut consumption on inflammation. The findings of this analysis suggest a need for more research in this area, with a particular focus on randomised controlled trials.PROSPERO registration numberCRD42016045424.


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