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Träfflista för sökning "(AMNE:(MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin)) pers:(Nilsson Peter) srt2:(2015-2019)"

Sökning: (AMNE:(MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin)) pers:(Nilsson Peter) > (2015-2019)

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1.
  • Kalkan, Almina, et al. (författare)
  • Increased healthcare utilization costs following initiation of insulin treatment in type 2 diabetes : A long-term follow-up in clinical practice
  • 2017
  • Ingår i: Primary Care Diabetes. - : Elsevier. - 1751-9918 .- 1878-0210. ; 11:2, s. 184-192
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims: To compare long-term changes in healthcare utilization and costs for type 2 diabetes patients before and after insulin initiation, as well as healthcare costs after insulin versus non-insulin anti-diabetic (NIAD) initiation. Methods: Patients newly initiated on insulin (n = 2823) were identified in primary health care records from 84 Swedish primary care centers, between 1999 to 2009. First, healthcare costs per patient were evaluated for primary care, hospitalizations and secondary outpatient care, before and up to seven years after insulin initiation. Second, patients prescribed insulin in second line were matched to patients prescribed NIAD in second line, and the healthcare costs of the matched groups were compared. Results: The total mean annual healthcare cost increased from 1656 per patient 2 years before insulin initiation to 3814 seven years after insulin initiation. The total cumulative mean healthcare cost per patient at year 5 after second-line treatment was 13,823 in the insulin group compared to 9989 in the NIAD group. Conclusions: Initiation of insulin in type 2 diabetes patients was followed by increased healthcare costs. The increases in costs were larger than those seen in a matched patient population initiated on NIAD treatment in second-line. (C) 2016 The Author(s). Published by Elsevier Ltd on behalf of Primary Care Diabetes Europe. This is an open access article under the CC BY-NC-ND license.
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2.
  • Dybjer, Elin, et al. (författare)
  • Diabetes, kognition och demens
  • 2019. - 2
  • Ingår i: Diabetes och Metabola Syndromet. - 9789144133621 ; , s. 115-119
  • Bokkapitel (refereegranskat)
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3.
  • Fall, Tove, et al. (författare)
  • Age- and sex-specific causal effects of adiposity on cardiovascular risk factors
  • 2015
  • Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 64:5, s. 1841-1852
  • Tidskriftsartikel (refereegranskat)abstract
    • Observational studies have reported different effects of adiposity on cardiovascular risk factors across age and sex. Since cardiovascular risk factors are enriched in obese individuals, it has not been easy to dissect the effects of adiposity from those of other risk factors. We used a Mendelian randomization approach, applying a set of 32 genetic markers to estimate the causal effect of adiposity on blood pressure, glycemic indices, circulating lipid levels, and markers of inflammation and liver disease in up to 67,553 individuals. All analyses were stratified by age (cutoff 55 years of age) and sex. The genetic score was associated with BMI in both nonstratified analysis (P = 2.8 × 10(-107)) and stratified analyses (all P < 3.3 × 10(-30)). We found evidence of a causal effect of adiposity on blood pressure, fasting levels of insulin, C-reactive protein, interleukin-6, HDL cholesterol, and triglycerides in a nonstratified analysis and in the <55-year stratum. Further, we found evidence of a smaller causal effect on total cholesterol (P for difference = 0.015) in the ≥55-year stratum than in the <55-year stratum, a finding that could be explained by biology, survival bias, or differential medication. In conclusion, this study extends previous knowledge of the effects of adiposity by providing sex- and age-specific causal estimates on cardiovascular risk factors.
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4.
  • Frej, Fyhrquist, et al. (författare)
  • Telomere Biology and Vascular Aging
  • 2015
  • Ingår i: Early Vascular Aging (EVA) : New Directions in Cardiovascular Protection - New Directions in Cardiovascular Protection. - 9780128013878 - 9780128016763 ; , s. 201-211
  • Bokkapitel (refereegranskat)abstract
    • Telomeres form the end segment of the DNA helix and shorten with every cell division until getting so short that the cell stops dividing and will undergo programmed cell death (apoptosis). Research has supported the view that telomere length could be regarded as a marker of biological aging, even if methodological problems could interfere with the interpretation of telomere length in cross-sectional studies when causality cannot be proven. Ideally the telomere attrition rate should be calculated based on repeated measurements during follow-up. So far, epidemiological studies have supported the role of short telomeres being predictive of coronary heart disease (CHD) events but not stroke, based on meta-analysis. A genetic risk score based on several genetic markers of telomere biology is associated with CHD risk, which proves that a true causal and unconfounded relationship may exist. Future intervention studies will hopefully reveal whether telomere length is possible to influence by lifestyle improvements or drug therapy in randomized, controlled studies.
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5.
  • Nilsson, Peter M., et al. (författare)
  • Early Vascular Aging in the Young : Influence of Birth Weight and Prematurity
  • 2015
  • Ingår i: Early Vascular Aging (EVA) : New Directions in Cardiovascular Protection - New Directions in Cardiovascular Protection. - 9780128013878 - 9780128016763 ; , s. 129-136
  • Bokkapitel (refereegranskat)abstract
    • Longitudinal data from cohort studies show that early life factors such as low birth weight are associated with the development of hypertension, coronary heart disease, and type 2 diabetes in adulthood. Moreover, the majority of published studies concur that blood pressure is higher in adolescents and young adults with a history of low birth weight. Although the precise mechanisms linking early life factors with increased future cardiovascular risk are unclear, the architecture of the vascular system is programmed in utero and the majority of elastin, the major structural component underlying arterial wall elasticity, is synthesized and deposited during this time. Therefore, the arterial system has been a major focus of investigations aimed toward improving our understanding of the natural history of hypertension and future cardiovascular risk. A number of studies have now described properties relating to arterial structure and function in children, adolescents, and young adults, with a history of low birth weight, due to being either small for gestational age or premature. While the combination of prematurity and intrauterine growth retardation resulting in a small for gestational age phenotype appears to be associated with the most marked impairments in vascular structure and function, the small for gestational age phenotype, followed by a rapid "catch-up" growth also appears harmful. Further studies are needed to understand the long-term consequences of cardiovascular health of being born under adverse conditions, especially when post-natal growth trajectories are taken into account.
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6.
  • Nilsson, Peter M., et al. (författare)
  • Preface
  • 2015
  • Ingår i: Early Vascular Aging (EVA) : New Directions in Cardiovascular Protection - New Directions in Cardiovascular Protection. - 9780128013878 - 9780128016763
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)
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7.
  • Nilsson, Peter M., et al. (författare)
  • Preface
  • 2015
  • Ingår i: Early Vascular Aging (EVA) : New Directions in Cardiovascular Protection - New Directions in Cardiovascular Protection. - 9780128013878 - 9780128016763
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)
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8.
  • Pennells, Lisa, et al. (författare)
  • Equalization of four cardiovascular risk algorithms after systematic recalibration : individual-participant meta-analysis of 86 prospective studies
  • 2019
  • Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 40:7, s. 621-
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims: There is debate about the optimum algorithm for cardiovascular disease (CVD) risk estimation. We conducted head-to-head comparisons of four algorithms recommended by primary prevention guidelines, before and after ‘recalibration’, a method that adapts risk algorithms to take account of differences in the risk characteristics of the populations being studied.Methods and results: Using individual-participant data on 360 737 participants without CVD at baseline in 86 prospective studies from 22 countries, we compared the Framingham risk score (FRS), Systematic COronary Risk Evaluation (SCORE), pooled cohort equations (PCE), and Reynolds risk score (RRS). We calculated measures of risk discrimination and calibration, and modelled clinical implications of initiating statin therapy in people judged to be at ‘high’ 10 year CVD risk. Original risk algorithms were recalibrated using the risk factor profile and CVD incidence of target populations. The four algorithms had similar risk discrimination. Before recalibration, FRS, SCORE, and PCE over-predicted CVD risk on average by 10%, 52%, and 41%, respectively, whereas RRS under-predicted by 10%. Original versions of algorithms classified 29–39% of individuals aged ≥40 years as high risk. By contrast, recalibration reduced this proportion to 22–24% for every algorithm. We estimated that to prevent one CVD event, it would be necessary to initiate statin therapy in 44–51 such individuals using original algorithms, in contrast to 37–39 individuals with recalibrated algorithms.Conclusion: Before recalibration, the clinical performance of four widely used CVD risk algorithms varied substantially. By contrast, simple recalibration nearly equalized their performance and improved modelled targeting of preventive action to clinical need.
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9.
  • Grundvold, Irene, et al. (författare)
  • Body weight and risk of atrial fibrillation in 7,169 patients with newly diagnosed type 2 diabetes; an observational study
  • 2015
  • Ingår i: Cardiovascular Diabetology. - : Springer Science and Business Media LLC. - 1475-2840. ; 14
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Obesity, type 2 diabetes and atrial fibrillation (AF) are closely associated, but the underlying mechanisms are not fully understood. We aimed to explore associations between body mass index (BMI) or weight change with risk of AF in patients with type 2 diabetes. Methods: A total of 7,169 participations with newly diagnosed type 2 diabetes were stratified according to baseline BMI, and after a second BMI measurement within 18 months, further grouped according to relative weight change as "weight gain" (> 1 BMI unit), " stable weight" (+/- 1 BMI unit) and " weight loss" (< 1 BMI unit). The mean follow-up period was 4.6 years, and the risk of AF was estimated using adjusted Cox regression models. Results: Average age at diabetes diagnosis was 60 years and the patients were slightly obese (mean BMI 30.2 kg/m(2)). During follow-up, 287 patients developed incident AF, and those with overweight or obesity at baseline had 1.9 fold and 2.9-fold higher risk of AF, respectively, than those with normal BMI. The 14% of the patients with subsequent weight gain had 1.5-fold risk of AF compared with those with stable weight or weight loss. Conclusions: In patients with newly diagnosed type 2 diabetes, baseline overweight and obesity, as well as modest weight increase during the first 18 months after diagnosis, were associated with a substantially increased risk of incident AF. Patients with type 2 diabetes may benefit from efforts to prevent weight gain in order to reduce the risk of incident AF.
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10.
  • Brand, J. S., et al. (författare)
  • Diabetes and onset of natural menopause : results from the European Prospective Investigation into Cancer and Nutrition
  • 2015
  • Ingår i: Human Reproduction. - : Oxford University Press. - 0268-1161 .- 1460-2350. ; 30:6, s. 1491-1498
  • Tidskriftsartikel (refereegranskat)abstract
    • STUDY QUESTION: Do women who have diabetes before menopause have their menopause at an earlier age compared with women without diabetes? SUMMARY ANSWER: Although there was no overall association between diabetes and age at menopause, our study suggests that early-onset diabetes may accelerate menopause. WHAT IS KNOWN ALREADY: Today, more women of childbearing age are being diagnosed with diabetes, but little is known about the impact of diabetes on reproductive health. STUDY DESIGN, SIZE, DURATION: We investigated the impact of diabetes on age at natural menopause (ANM) in 258 898 women from the European Prospective Investigation into Cancer and Nutrition (EPIC), enrolled between 1992 and 2000. PARTICIPANTS/MATERIALS, SETTING, METHODS: Determinant and outcome information was obtained through questionnaires. Time-dependent Cox regression analyses were used to estimate the associations of diabetes and age at diabetes diagnosis with ANM, stratified by center and adjusted for age, smoking, reproductive and diabetes risk factors and with age from birth to menopause or censoring as the underlying time scale. MAIN RESULTS AND THE ROLE OF CHANCE: Overall, no association between diabetes and ANM was found (hazard ratio (HR) = 0.94; 95% confidence interval (CI) 0.89-1.01). However, women with diabetes before the age of 20 years had an earlier menopause (10-20 years: HR = 1.43; 95% CI 1.02-2.01, <10 years: HR = 1.59; 95% CI 1.03-2.43) compared with non-diabetic women, whereas women with diabetes at age 50 years and older had a later menopause (HR = 0.81; 95% CI 0.70-0.95). None of the other age groups were associated with ANM. LIMITATIONS, REASONS FOR CAUTION: Strengths of the study include the large sample size and the broad set of potential confounders measured. However, results may have been underestimated due to survival bias. We cannot be sure about the sequence of the events in women with a late age at diabetes, as both events then occur in a short period. We could not distinguish between type 1 and type 2 diabetes. WIDER IMPLICATIONS OF THE FINDINGS: Based on the literature, an accelerating effect of early-onset diabetes on ANM might be plausible. A delaying effect of late-onset diabetes on ANM has not been reported before, and is not in agreement with recent studies suggesting the opposite association.
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