Institution
Cochrane Collaboration
Nonprofit•Oxford, United Kingdom•
About: Cochrane Collaboration is a nonprofit organization based out in Oxford, United Kingdom. It is known for research contribution in the topics: Systematic review & Randomized controlled trial. The organization has 1995 authors who have published 3928 publications receiving 382695 citations.
Papers published on a yearly basis
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TL;DR: Current chemical and physical methods aimed at reducing exposure to allergens from house dust mites seem to be ineffective and cannot be recommended as prophylactic treatment for asthma patients sensitive to mites.
Abstract: Objective To determine whether patients with asthma who are sensitive to mites benefit from measures designed to reduce their exposure to house dust mite antigen in the home.
Design Meta-analysis of randomised trials that investigated the effects on asthma patients of chemical or physical measures to control mites, or both, in comparison with an untreated control group. All trials in any language were eligible for inclusion.
Subjects Patients with bronchial asthma as diagnosed by a doctor and sensitisation to mites as determined by skin prick testing, bronchial provocation testing, or serum assays for specific IgE antibodies.
Main outcome measures Number of patients whose allergic symptoms improved, improvement in asthma symptoms, improvement in peak expiratory flow rate. Outcomes measured on different scales were combined using the standardised effect size method (the difference in effect was divided by the standard deviation of the measurements).
Results 23 studies were included in the meta-analysis; 6 studies used chemical methods to reduce exposure to mites, 13 used physical methods, and 4 used a combination. Altogether, 41/113 patients exposed to treatment interventions improved compared with 38/117 in the control groups (odds ratio 1.20, 95% confidence interval 0.66 to 2.18). The standardised mean difference for improvement in asthma symptoms was −0.06 (95% confidence interval −0.54 to 0.41). For peak flow rate measured in the morning the standardised mean difference was −0.03 (−0.25 to 0.19). As measured in the original units this difference between the treatment and the control group corresponds to −3 l/min (95% confidence interval −25 l/min to 19 l/min). The results were similar in the subgroups of trials that reported successful reduction in exposure to mites or had long follow up times.
Conclusion Current chemical and physical methods aimed at reducing exposure to allergens from house dust mites seem to be ineffective and cannot be recommended as prophylactic treatment for asthma patients sensitive to mites.
215 citations
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TL;DR: This updated systematic review investigated the effect on cognitive function of the type of treatment and level of metabolic control in people with Type 2 diabetes and found that the intensity of glycaemic control may have little or no effect on all-cause mortality.
Abstract: Background
Prevention of cognitive impairment and dementia is an important public health goal. Epidemiological evidence shows a relationship between cognitive impairment and Type 2 diabetes mellitus. The risk of dementia increases with duration of disease. This updated systematic review investigated the effect on cognitive function of the type of treatment and level of metabolic control in people with Type 2 diabetes.
Objectives
To assess the effects of different strategies for managing Type 2 diabetes mellitus on cognitive function and the incidence of dementia.
Search methods
We searched ALOIS (the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (CDCIG)), the Cochrane Library, MEDLINE, Embase, PsycINFO, CINAHL and LILACS on 15 October 2016. ALOIS contains records from all major health care databases, (CENTRAL, MEDLINE, Embase, PsycINFO, CINAHL, LILACS), as well as from many trials' registers and grey literature sources.
Selection criteria
We included randomised controlled trials (RCTs) which compared two or more different treatments for Type 2 diabetes mellitus and in which cognitive function was measured at baseline and after treatment.
Data collection and analysis
Two review authors independently extracted data and assessed the quality of the included RCTs. We pooled data for comparable trials and estimated the effects of treatment by using risk ratios (RRs) and mean differences (MDs), according to the nature of the outcome. We assessed the quality of the evidence using GRADE methods.
Main results
We identified seven eligible studies but only four provided data we could include in efficacy analyses. Two of these studies compared intensive versus standard glycaemic control and two compared different pharmacological treatments. All studies were at unclear risk of bias in at least two domains and one large study was at high risk of performance and detection bias.
(a) Two studies with 13,934 participants at high cardiovascular risk provided efficacy data on intensive versus standard glycaemic control. A third study with 1791 participants provided additional data on hypoglycaemic episodes and mortality. There is probably no difference between treatment groups in the number of participants who decline by at least 3 points on the Mini–Mental State Examination (MMSE) over five years (RR 0.98, 95% CI 0.88 to 1.08; 1 study; n = 11,140; moderate-quality evidence); and there may also be little or no difference in the incidence of dementia (RR 1.27, 95% CI 0.87 to 1.85; 1 study; n = 11,140; low-quality evidence). From another study, there was probably little or no difference in MMSE score after 40 months (MD −0.01, 95% CI −0.18 to 0.16; 1 study; n = 2794; moderate quality evidence). Participants exposed to the intensive glycaemic control strategy probably experience more episodes of severe hypoglycaemia than those who have standard treatment (RR 2.18, 95% CI 1.52 to 3.14; 2 studies; n = 12,827; moderate-quality evidence). The evidence from these trials suggests that the intensity of glycaemic control may have little or no effect on all-cause mortality (RR 0.99, 95% CI 0.87 to 1.13; 3 studies; n = 15,888; low-quality evidence).
(b) One study with 156 participants compared glibenclamide (glyburide) with repaglinide. There may be a small advantage of glibenclamide on global cognitive function measured with the MMSE after 12 months (MD −0.90, 95% CI −1.68 to −0.12; low-quality evidence). No data were reported on the incidence of dementia, hypoglycaemic events or all-cause mortality.
(c) One study with 145 participants compared rosiglitazone plus metformin to glibenclamide (glyburide) plus metformin over 24 weeks. It reported only on cognitive subdomains and not on global cognitive function, incidence of MCI or dementia, hypoglycaemic events or all causes of mortality.
Authors' conclusions
We found no good evidence that any specific treatment or treatment strategy for Type 2 diabetes can prevent or delay cognitive impairment. The best available evidence related to the comparison of intensive with standard glycaemic control strategies. Here there was moderate-quality evidence that the strategies do not differ in their effect on global cognitive functioning over 40 to 60 months.
215 citations
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TL;DR: The effect of including unpublished trial outcome data obtained from the Food and Drug Administration on the results of meta-analyses of drug trials varies by drug and outcome.
Abstract: Objective To investigate the effect of including unpublished trial outcome data obtained from the Food and Drug Administration (FDA) on the results of meta-analyses of drug trials. Design Reanalysis of meta-analyses. Data sources Drug trials with unpublished outcome data for new molecular entities that were approved by the FDA between 2001 and 2002 were identified. For each drug, eligible systematic reviews containing at least one meta-analysis were identified by searches of Medline, Embase, and the Cochrane Library in November 2010. Selection criteria Eligible systematic reviews were done after FDA approval of the drug, were published in English, and had outcomes and comparators that were the same as those of the trials with unpublished FDA trial outcomes, and the characteristics of participants in the systematic reviews were consistent with the FDA approved indication for the drug. Clinical guidelines, conference proceedings, duplicate systematic reviews, and systematic reviews in which included trials were not referenced or that combined trials across multiple drug classes were excluded. Systematic reviews using non-standard meta-analytic techniques (such as Bayesian or network meta-analyses) and those that used inappropriate or invalid methods for calculation of summary statistics (such as unweighted pooled analyses) were also excluded. Data extraction Two authors independently extracted data from both the published systematic reviews and the FDA’s medical and statistical reviews of the trials submitted to FDA. Main outcome measure Summary statistics (risk ratios, odds ratios, or weighted mean differences) for relevant outcomes with and without unpublished FDA trial data. Results 42 meta-analyses (41 efficacy outcomes, one harm outcome) for nine drugs across six drug classes were reanalysed. Overall, addition of unpublished FDA trial data caused 46% (19/41) of the summary estimates from the meta-analyses to show lower efficacy of the drug, 7% (3/41) to show identical efficacy, and 46% (19/41) to show greater efficacy. The summary estimate of the single harm outcome showed more harm from the drug after inclusion of unpublished FDA trial data. Conclusion The effect of including unpublished FDA trial outcome data varies by drug and outcome. Unpublished FDA trial outcome data should be available and included in meta-analysis. Making these data easily accessible is particularly important because the effects of including unpublished data vary.
214 citations
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TL;DR: The findings suggest that for a woman with a 32 % chance of achieving a live birth using placebo or other treatment, the corresponding chance using metformin treatment would be between 28% and 53%.
Abstract: Background
The use of insulin-sensitising agents, such as metformin, in women with polycystic ovary syndrome (PCOS) who are undergoing ovulation induction or in vitro fertilisation (IVF) cycles has been widely studied. Metformin reduces hyperinsulinaemia and suppresses the excessive ovarian production of androgens. As a consequence, it is suggested that metformin could improve assisted reproductive techniques (ART) outcomes, such as ovarian hyperstimulation syndrome (OHSS), pregnancy and live birth rates.
Objectives
To determine the effectiveness and safety of metformin as a co-treatment during IVF or intracytoplasmic sperm injection (ICSI) in achieving pregnancy or live birth in women with PCOS.
Search methods
We searched the Cochrane Menstrual Disorders and Subfertility Group Trials Register, Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library), MEDLINE, EMBASE, LILACS, the metaRegister of Controlled Trials and reference lists of articles (up to 15 October 2014).
Selection criteria
Types of studies: randomised controlled trials (RCTs) comparing metformin treatment with placebo or no treatment in women with PCOS who underwent IVF or ICSI treatment.
Types of participants: women of reproductive age with anovulation due to PCOS with or without co-existing infertility factors.
Types of interventions: metformin administered before and during IVF or ICSI treatment.
Types of outcome measures: live birth rate, clinical pregnancy rate, miscarriage rate, incidence of ovarian hyperstimulation syndrome , incidence of participant-reported side effects, serum oestradiol level on the day of trigger, serum androgen level, and fasting insulin and glucose levels.
Data collection and analysis
Two review authors independently selected the studies, extracted the data according to the protocol and assessed study quality. The overall quality of the evidence was assessed using GRADE methods.
Main results
We included nine randomised controlled trials involving a total of 816 women with PCOS. When metformin was compared with placebo there was no clear evidence of a difference between the groups in live birth rates (OR 1.39, 95% CI 0.81 to 2.40, five RCTs, 551 women, I2 = 52%, low-quality evidence). Our findings suggest that for a woman with a 32 % chance of achieving a live birth using placebo, the corresponding chance using metformin treatment would be between 28% and 53%.
When metformin was compared with placebo or no treatment, clinical pregnancy rates were higher in the metformin group (OR 1.52; 95% CI 1.07 to 2.15; eight RCTs, 775 women, I2 = 18%, moderate-quality evidence). This suggests that for a woman with a 31% chance of achieving a clinical pregnancy using placebo or no treatment, the corresponding chance using metformin treatment would be between 32% and 49%.
The risk of ovarian hyperstimulation syndrome was lower in the metformin group (OR 0.29; 95% CI 0.18 to 0.49, eight RCTs, 798 women, I2 = 11%, moderate-quality evidence). This suggests that for a woman with a 27% risk of having OHSS without metformin the corresponding chance using metformin treatment would be between 6% and 15%.
Side effects (mostly gastrointestinal) were more common in the metformin group (OR 4.49, 95% CI 1.88 to 10.72, for RCTs, 431 women, I2=57%, low quality evidence)
The overall quality of the evidence was moderate for the outcomes of clinical pregnancy, OHSS and miscarriage, and low for other outcomes. The main limitations in the evidence were imprecision and inconsistency.
Authors' conclusions
This review found no conclusive evidence that metformin treatment before or during ART cycles improved live birth rates in women with PCOS. However, the use of this insulin-sensitising agent increased clinical pregnancy rates and decreased the risk of OHSS.
213 citations
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TL;DR: This overview summarises the evidence from systematic reviews of health systems arrangements and implementation strategies, with a particular focus on evidence relevant to primary health care in low-income and middle-income countries.
211 citations
Authors
Showing all 2000 results
Name | H-index | Papers | Citations |
---|---|---|---|
Douglas G. Altman | 253 | 1001 | 680344 |
John P. A. Ioannidis | 185 | 1311 | 193612 |
Jasvinder A. Singh | 176 | 2382 | 223370 |
George A. Wells | 149 | 941 | 114256 |
Shah Ebrahim | 146 | 733 | 96807 |
Holger J. Schünemann | 141 | 810 | 113169 |
Paul G. Shekelle | 132 | 601 | 101639 |
Peter Tugwell | 129 | 948 | 125480 |
Jeremy M. Grimshaw | 123 | 691 | 115126 |
Peter Jüni | 121 | 593 | 99254 |
John J. McGrath | 120 | 791 | 124804 |
Arne Astrup | 114 | 866 | 68877 |
Mike Clarke | 113 | 1037 | 164328 |
Rachelle Buchbinder | 112 | 613 | 94973 |
Ian Roberts | 112 | 714 | 51933 |