289 research outputs found

    Value of Information: A Tool to Improve Research Prioritization and Reduce Waste

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    In a Guest Editorial, Cosetta Minelli and Gianluca Baio explain how VOI analysis can prioritize research projects by identifying uncertainty in existing knowledge and then estimating expected benefits from reducing that uncertainty

    Can the association of adult lung function with weight in early life be explained by early life factors?

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    IntroductionWeight in early life is known to be associated with forced vital capacity (FVC) in adulthood, but whether it is also associated with airflow obstruction (FEV1/FVC) in adulthood is unclear. The observed association between weight in early life and lung function could be confounded by maternal risk factors, such as maternal smoking. Therefore, we examine whether maternal factors might explain this association.MethodsUsing linear regression among 3,832 participants of the Northern Finland Birth Cohort 1966, we examined the association of adult lung function (FVC and FEV1/FVC) with weight in early life (birth weight and weight gain in the first year of life). We then tested whether this association could be explained by maternal factors (maternal weight, height, BMI, age, smoking, education, socio-economic status and parity) by adjusting for them.ResultsFVC was positively associated with birth weight and weight gain. FEV1/FVC was not associated with birth weight and was negatively associated with weight gain. Mean FVC in adulthood (95%CI) increased by 86mL (51,121) and 24mL (7.7, 40) for each kilogram increase in birth weight and weight gain, respectively. One kg increase in weight gain was associated with a reduction of 0.003 units (-0.004,-0.001) of FEV1/FVC. Although several maternal factors were associated with both adult lung function and weight in early life, adjusting for them did not substantially alter the results.ConclusionAdult lung function and weight in early life were both associated with several early life factors, but these did not explain the association between adult lung function and weight in early life.<br/

    Communication of personalised disease risk by general practitioners to motivate smoking cessation in England: a cost-effectiveness and research prioritisation study

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    Background and aims: Communication of personalised disease risk can motivate smoking cessation. We assessed whether routine implementation of this intervention by general practitioners (GPs) in England is cost-effective or whether we need further research to better establish its effectiveness. Design: Cost-effectiveness analysis (CEA) with value of information (VoI) analysis from the UK National Health Service perspective, using GP communication of personalised disease risk on smoking cessation versus usual care. Setting: GP practices in England. Study population: Healthy smokers aged 35-60 attending the GP practice. Measurements: Effectiveness of GP communication of personalised disease risk on smoking cessation was estimated through systematic review and meta-analysis. A Bayesian CEA was then performed using a lifetime Markov model on smokers aged 35-60 that measured lifetime costs and quality-adjusted life-years (QALYs) assigned to the four diseases contributing the most to smoking-related morbidity, mortality and costs: chronic obstructive pulmonary disease, lung cancer, myocardial infarction, and stroke. Costs and QALYs for each disease state were obtained from the literature. VoI analysis identified sources of uncertainty in the CEA and assessed how much would be worth investing in further research to reduce this uncertainty. Findings: The meta-analysis odds ratio for the effectiveness estimate of GP communication of personalised disease risk was 1.48 (95% credibility interval (CrI): 0.91-2.26), an absolute increase in smoking cessation rates of 3.84%. The probability of cost-effectiveness ranged from 89-94% depending on sex and age. VoI analysis indicated that: 1) uncertainty in the effectiveness of the intervention was the driver of the overall uncertainty in the CEA and 2) a research investment to reduce this uncertainty is justified if lower than £27.6million (£7 per smoker). Conclusions: Evidence to date shows that, in England, incorporating disease risk communication into general practitioners' practices to motivate smoking cessation is likely to be cost-effective compared with usual care

    Risk factors for post-operative eye pain in patients with non-painful eye disease undergoing pars plana vitrectomy: the VItrectomy Pain (VIP) study

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    BACKGROUND: Pars Plana Vitrectomy (PPV), a surgical procedure used to treat different ophthalmic pathologies, could be associated with moderate to severe eye pain The aim of the present study was to evaluate the incidence of postoperative eye pain and its risk factors following Pars Plana Vitrectomy (PPV) in a selected population of patients with non-painful eye disease, receiving regional anaesthesia and moderate sedation with benzodiazepines, without use of narcotics.METHODS: Single-center, prospective observational cohort study. We recorded the presence of pain at operating room discharge, at 6 and 24 hours, using the numeric rating scale (NRS). We recorded also age, sex, ethnic origin, American Society of Anaesthesia physical status (ASA PS) classification, Charlson Comorbidity Index, the aetiology of the vitreoretinal pathology, length of surgery, and type of surgical procedure performed.RESULTS: Eye pain (NRS > 3) was present in 3 patients (0.7%) at operating room discharge, 59 (13.2%) at 6 and 65 (14.6%) at 24 hours after surgery. LASSO logistic regression analysis identified age, ASA PS, race, along with tamponade as independent risk factors for eye pain at 6 hours. Scleral buckling was selected for eye pain at 24 hrs.CONCLUSIONS: A protocol for pain control after PPV should be considered, especially in younger, non-Caucasian people, and patients with high ASA PS grade. Moreover, attention must be paid when additional surgical procedures are requested, restricting them to selected patients, and using the appropriate agent for intraocular tamponade

    Ambient heat exposure and COPD hospitalisations in England: a nationwide case-crossover study during 2007-2018

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    Background: There is emerging evidence suggesting a link between ambient heat exposure and chronic obstructive pulmonary disease (COPD) hospitalisations. Individual and contextual characteristics can affect population vulnerabilities to COPD hospitalisation due to heat exposure. This study quantifies the effect of ambient heat on COPD hospitalisations and examines population vulnerabilities by age, sex and contextual characteristics. Methods: Individual data on COPD hospitalisation at high geographical resolution (postcodes) during 2007–2018 in England was retrieved from the small area health statistics unit. Maximum temperature at 1 km ×1 km resolution was available from the UK Met Office. We employed a case-crossover study design and fitted Bayesian conditional Poisson regression models. We adjusted for relative humidity and national holidays, and examined effect modification by age, sex, green space, average temperature, deprivation and urbanicity. Results: After accounting for confounding, we found 1.47% (95% Credible Interval (CrI) 1.19% to 1.73%) increase in the hospitalisation risk for every 1°C increase in temperatures above 23.2°C (lags 0–2 days). We reported weak evidence of an effect modification by sex and age. We found a strong spatial determinant of the COPD hospitalisation risk due to heat exposure, which was alleviated when we accounted for contextual characteristics. 1851 (95% CrI 1 576 to 2 079) COPD hospitalisations were associated with temperatures above 23.2°C annually. Conclusion: Our study suggests that resources should be allocated to support the public health systems, for instance, through developing or expanding heat-health alerts, to challenge the increasing future heat-related COPD hospitalisation burden

    Effects of BMI, fat mass, and lean mass on asthma in childhood : a Mendelian Randomization Study

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    Background Observational studies have reported associations between body mass index (BMI) and asthma, but confounding and reverse causality remain plausible explanations. We aim to investigate evidence for a causal effect of BMI on asthma using a Mendelian randomization approach. Methods and Findings We used Mendelian randomization to investigate causal effects of BMI, fat mass, and lean mass on current asthma at age 7½ y in the Avon Longitudinal Study of Parents and Children (ALSPAC). A weighted allele score based on 32 independent BMI-related single nucleotide polymorphisms (SNPs) was derived from external data, and associations with BMI, fat mass, lean mass, and asthma were estimated. We derived instrumental variable (IV) estimates of causal risk ratios (RRs). 4,835 children had available data on BMI-associated SNPs, asthma, and BMI. The weighted allele score was strongly associated with BMI, fat mass, and lean mass (all p-values<0.001) and with childhood asthma (RR 2.56, 95% CI 1.38–4.76 per unit score, p = 0.003). The estimated causal RR for the effect of BMI on asthma was 1.55 (95% CI 1.16–2.07) per kg/m2, p = 0.003. This effect appeared stronger for non-atopic (1.90, 95% CI 1.19–3.03) than for atopic asthma (1.37, 95% CI 0.89–2.11) though there was little evidence of heterogeneity (p = 0.31). The estimated causal RRs for the effects of fat mass and lean mass on asthma were 1.41 (95% CI 1.11–1.79) per 0.5 kg and 2.25 (95% CI 1.23–4.11) per kg, respectively. The possibility of genetic pleiotropy could not be discounted completely; however, additional IV analyses using FTO variant rs1558902 and the other BMI-related SNPs separately provided similar causal effects with wider confidence intervals. Loss of follow-up was unlikely to bias the estimated effects. Conclusions Higher BMI increases the risk of asthma in mid-childhood. Higher BMI may have contributed to the increase in asthma risk toward the end of the 20th century

    The application of bayesian and frequentist regularization and variable selection methods for the prediction of asthma in later childhood

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    Asthma is a global health problem and among the most common chronic conditions in childhood. Several models were proposed to predict asthma in children, but their reproducibility in external populations was limited and none was developed to predict asthma in adolescence. I conducted a systematic review of asthma predictive models validated in external populations; validation studies showed poorer predictive performances than development studies. I developed predictive models for asthma between 15 and 20 years, using data from the Study Team for Early Life Asthma Research (STELAR) consortium of five UK asthma cohorts. For one of these cohorts, the Ashford study, I developed an questionnaire to collect follow-up information when study subjects were age 20 years. I harmonised 41 variables across the STELAR cohorts, 39 of which were used as candidate predictors to develop predictive models, while the others were used to define asthma at 15–20 years. Asthma at that age was defined as positive responses to ‘current wheezing’ and ‘asthma medications in the last year’.Two of the five STELAR cohorts (development data) were combined to develop predictive models using stepwise regression and frequentist, Bayesian and empirical Bayes regularization models. The remaining cohorts (validation data) were used to assess predictive performance using discrimination and accuracy measures. Analyses were performed in two populations - all children and a subgroup with reported wheezing between two and five years (high-risk population). Sex, eczema, sensitization to house dust mite and doctor’s diagnosis of asthma in early childhood (4-7 years) were identified as asthma predictors at 15-20 years in both populations. Additional predictors in the general population included early wheezing symptoms and parental allergies, while in the high-risk population maternal allergies and pet in the house at one year were important for asthma prediction in adolescence. Sensitivity was higher in the general population, whereas positive predictive value was higher in the high-risk population. Although accuracy was good in both populations, the predictive ability of the models developed was limited.Open Acces
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