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Träfflista för sökning "WFRF:(Dahlqwist E) "

Search: WFRF:(Dahlqwist E)

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  • Dahlqwist, E, et al. (author)
  • Regression standardization and attributable fraction estimation with between-within frailty models for clustered survival data
  • 2019
  • In: Statistical methods in medical research. - : SAGE Publications. - 1477-0334 .- 0962-2802. ; 28:2, s. 462-485
  • Journal article (peer-reviewed)abstract
    • The between-within frailty model has been proposed as a viable analysis tool for clustered survival time outcomes. Previous research has shown that this model gives consistent estimates of the exposure–outcome hazard ratio in the presence of unmeasured cluster-constant confounding, which the ordinary frailty model does not, and that estimates obtained from the between-within frailty model are often more efficient than estimates obtained from the stratified Cox proportional hazards model. In this paper, we derive novel estimation techniques for regression standardization with between-within frailty models. We also show how between-within frailty models can be used to estimate the attributable fraction function, which is a generalization of the attributable fraction for survival time outcomes. We illustrate the proposed methods by analyzing a large cohort on preterm birth and attention deficit hyperactivity disorder. To facilitate use of the proposed methods, we provide R code for all analyses.
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  • Dahlqwist, E, et al. (author)
  • Using instrumental variables to estimate the attributable fraction
  • 2020
  • In: Statistical methods in medical research. - : SAGE Publications. - 1477-0334 .- 0962-2802. ; 29:8, s. 2063-2073
  • Journal article (peer-reviewed)abstract
    • In order to design efficient interventions aimed to improve public health, policy makers need to be provided with reliable information of the health burden of different risk factors. For this purpose, we are interested in the proportion of cases that could be prevented had some harmful exposure been eliminated from the population, i.e. the attributable fraction. The attributable fraction is a causal measure; thus, to estimate the attributable fraction from observational data, we have to make appropriate adjustment for confounding. However, some confounders may be unobserved, or even unknown to the investigator. A possible solution to this problem is to use instrumental variable analysis. In this work, we present how the attributable fraction can be estimated with instrumental variable methods based on the two-stage estimator or the G-estimator. One situation when the problem of unmeasuredconfounding may be particularly severe is when assessing the effect of low educational qualifications on coronary heart disease. By using Mendelian randomization, a special case of instrumental variable analysis, it has been claimed that low educational qualifications is a causal risk factor for coronary heart disease. We use Mendelian randomization to estimate the causal risk ratio and causal odds ratio of low educational qualifications as a risk factor for coronary heart disease with data from the UK Biobank. We compare the two-stage and G-estimator as well as the attributable fraction based on the two estimators. The plausibility of drawing causal conclusion in this analysis is thoroughly discussed and alternative genetic instrumental variables are tested.
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  • Ueda, P., et al. (author)
  • The comparative cardiovascular and renal effectiveness of sodium-glucose co-transporter-2 inhibitors and glucagon-like peptide-1 receptor agonists: A Scandinavian cohort study
  • 2022
  • In: Diabetes Obesity & Metabolism. - : Wiley. - 1462-8902 .- 1463-1326. ; 24:3, s. 473-485
  • Journal article (peer-reviewed)abstract
    • Aim To assess the comparative cardiovascular and renal effectiveness of sodium-glucose co-transporter-2 (SGLT2) inhibitors versus glucagon-like peptide-1 (GLP-1) receptor agonists in routine clinical practice. Materials and Methods A cohort study of nationwide registers from Sweden, Denmark, and Norway, including 87 525 new users of SGLT2 inhibitors and 63 921 new users of GLP-1 receptor agonists, was conducted using data from 2013-2018. Co-primary outcomes, analysed using an intention-to-treat exposure definition, were major adverse cardiovascular events (MACE; myocardial infarction, stroke, and cardiovascular death), heart failure (hospitalization or death because of heart failure), and serious renal events (renal replacement therapy, hospitalization for renal events, and death from renal causes). Results Use of SGLT2 inhibitors versus GLP-1 receptor agonists was associated with a higher risk of MACE (adjusted incidence rate: 15.2 vs. 14.4 events per 1000 person-years; HR 1.07 [95% CI 1.01-1.15]), a similar risk of heart failure (6.0 vs. 6.0 events per 1000 person-years; HR 1.02 [0.92-1.12]), and a lower risk of serious renal events (2.9 vs. 4.0 events per 1000 person-years; HR 0.76 [0.66-0.87]). In as-treated analyses, the HR (95% CI) was 1.11 (1.00-1.24) for MACE, 0.88 (0.74-1.04) for heart failure, and 0.60 (0.47-0.77) for serious renal events. In secondary outcome analyses, use of SGLT2 inhibitors versus GLP-1 receptor agonists was not associated with statistically significant differences for the risk of myocardial infarction (HR 1.09 [95% CI 1.00-1.19]), cardiovascular death (HR 0.97 [95% CI 0.84-1.12]), death from renal causes (HR 0.75 [95% CI 0.41-1.35]), or any cause death (HR 1.01 [95% CI 0.94-1.09]), while the risk of stroke was higher (HR 1.14 [95% CI 1.03-1.26]), and the risk of renal replacement therapy (HR 0.74 [95% CI 0.56-0.97]) and hospitalization for renal events (HR 0.75 [95% CI 0.65-0.88]) were lower among users of SGLT2 inhibitors. Conclusions Use of SGLT2 inhibitors versus GLP-1 receptor agonists was associated with a similar risk of heart failure and a lower risk of serious renal events, while use of GLP-1 receptor agonists versus SGLT2 inhibitors was associated with a slightly lower risk of MACE. In as-treated analyses, the associations with MACE and serious renal events increased in magnitude, and the HR for heart failure tended towards a protective association for SGLT2 inhibitors.
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