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Reducing overdiagnosis by polygenic risk-stratified screening: findings from the Finnish section of the ERSPC.

https://arctichealth.org/en/permalink/ahliterature269042
Source
Br J Cancer. 2015 Sep 29;113(7):1086-93
Publication Type
Article
Date
Sep-29-2015
Author
Nora Pashayan
Paul Dp Pharoah
Johanna Schleutker
Kirsi Talala
Teuvo Lj Tammela
Liisa Määttänen
Patricia Harrington
Jonathan Tyrer
Rosalind Eeles
Stephen W Duffy
Anssi Auvinen
Source
Br J Cancer. 2015 Sep 29;113(7):1086-93
Date
Sep-29-2015
Language
English
Publication Type
Article
Keywords
Adult
Aged
Early Detection of Cancer - methods
Finland
Humans
Likelihood Functions
Male
Mass Screening - methods
Medical Overuse - prevention & control - statistics & numerical data
Middle Aged
Prostatic Neoplasms - diagnosis
Risk Assessment - methods
Abstract
We derived estimates of overdiagnosis by polygenic risk groups and examined whether polygenic risk-stratified screening for prostate cancer reduces overdiagnosis.
We calculated the polygenic risk score based on genotypes of 66 known prostate cancer loci for 4967 men from the Finnish section of the European Randomised Study of Screening for Prostate Cancer. We stratified the 72?072 men in the trial into those with polygenic risk below and above the median. Using a maximum likelihood method based on interval cancers, we estimated the mean sojourn time (MST) and episode sensitivity. For each polygenic risk group, we estimated the proportion of screen-detected cancers that are likely to be overdiagnosed from the difference between the observed and expected number of screen-detected cancers.
Of the prostate cancers, 74% occurred among men with polygenic risk above population median. The sensitivity was 0.55 (95% confidence interval (CI) 0.45-0.65) and MST 6.3 (95% CI 4.2-8.3) years. The overall overdiagnosis was 42% (95% CI 37-52) of the screen-detected cancers, with 58% (95% CI 54-65) in men with the lower and 37% (95% CI 31-47) in those with higher polygenic risk.
Targeting screening to men at higher polygenic risk could reduce the proportion of cancers overdiagnosed.
Notes
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PubMed ID
26291059 View in PubMed
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Low socioeconomic status of a patient's residential area is associated with worse prognosis after acute myocardial infarction in Sweden.

https://arctichealth.org/en/permalink/ahliterature269125
Source
Int J Cardiol. 2015 Mar 1;182:141-7
Publication Type
Article
Date
Mar-1-2015
Author
Göran Bergström
Björn Redfors
Oskar Angerås
Christian Dworeck
Yangzhen Shao
Inger Haraldsson
Petur Petursson
Davor Milicic
Hans Wedel
Per Albertsson
Truls Råmunddal
Annika Rosengren
Elmir Omerovic
Source
Int J Cardiol. 2015 Mar 1;182:141-7
Date
Mar-1-2015
Language
English
Publication Type
Article
Keywords
Aged
Disease Progression
Female
Healthcare Disparities
Hospitalization - trends
Humans
Male
Myocardial Infarction - economics - mortality
Registries
Retrospective Studies
Risk Assessment - methods
Risk factors
Socioeconomic Factors
Survival Rate - trends
Sweden - epidemiology
Abstract
Previous studies have established a relationship between socioeconomic status (SES) and survival in coronary heart disease. Acute cardiac care in Sweden is considered to be excellent and independent of SES. We studied the influence of area-level socioeconomic status on mortality after hospitalization for acute myocardial infarction (AMI) between 1995 and 2013 in the Gothenburg metropolitan area, which has little over 800,000 inhabitants and includes three city hospitals.
Data were obtained from the SWEDEHEART registry (Swedish Websystem for Enhancement of Evidence-Based Care in Heart Disease Evaluated According to Recommended Therapies) and the Swedish Central Bureau of Statistics for patients hospitalized for ST-elevation myocardial infarction (STEMI) and non-STEMI in the city of Gothenburg in Western Sweden. The groups were compared using Cox proportional hazards regression and logistic regression.
10,895 (36% female) patients were hospitalized due to AMI during the study period. Patients residing in areas with lower SES had higher rates of smoking and diabetes (P
PubMed ID
25577750 View in PubMed
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Sensitivity of regression calibration to non-perfect validation data with application to the Norwegian Women and Cancer Study.

https://arctichealth.org/en/permalink/ahliterature269316
Source
Stat Med. 2015 Apr 15;34(8):1389-403
Publication Type
Article
Date
Apr-15-2015
Author
John P Buonaccorsi
Ingvild Dalen
Petter Laake
Anette Hjartåker
Dagrun Engeset
Magne Thoresen
Source
Stat Med. 2015 Apr 15;34(8):1389-403
Date
Apr-15-2015
Language
English
Publication Type
Article
Keywords
Bias (epidemiology)
Calibration
Colonic Neoplasms - epidemiology - etiology - prevention & control
Diet Records
Female
Humans
Linear Models
Logistic Models
Longitudinal Studies
Meat - statistics & numerical data
Norway - epidemiology
Odds Ratio
Reference Values
Registries
Regression Analysis
Risk Assessment - methods
Seafood - statistics & numerical data
Abstract
Measurement error occurs when we observe error-prone surrogates, rather than true values. It is common in observational studies and especially so in epidemiology, in nutritional epidemiology in particular. Correcting for measurement error has become common, and regression calibration is the most popular way to account for measurement error in continuous covariates. We consider its use in the context where there are validation data, which are used to calibrate the true values given the observed covariates. We allow for the case that the true value itself may not be observed in the validation data, but instead, a so-called reference measure is observed. The regression calibration method relies on certain assumptions.This paper examines possible biases in regression calibration estimators when some of these assumptions are violated. More specifically, we allow for the fact that (i) the reference measure may not necessarily be an 'alloyed gold standard' (i.e., unbiased) for the true value; (ii) there may be correlated random subject effects contributing to the surrogate and reference measures in the validation data; and (iii) the calibration model itself may not be the same in the validation study as in the main study; that is, it is not transportable. We expand on previous work to provide a general result, which characterizes potential bias in the regression calibration estimators as a result of any combination of the violations aforementioned. We then illustrate some of the general results with data from the Norwegian Women and Cancer Study.
PubMed ID
25627982 View in PubMed
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A new approach of nonparametric estimation of incidence and lifetime risk based on birth rates and incident events.

https://arctichealth.org/en/permalink/ahliterature87169
Source
BMC Med Res Methodol. 2007;7:53
Publication Type
Article
Date
2007
Author
Støvring Henrik
Wang Mei-Cheng
Author Affiliation
Research Unit for General Practice, University of Southern Denmark, J,B, Winsløwsvej 9A, 5000 Odense C, Denmark. hstovring@health.sdu.dk
Source
BMC Med Res Methodol. 2007;7:53
Date
2007
Language
English
Publication Type
Article
Keywords
Age of Onset
Birth rate
Denmark - epidemiology
Diabetes Mellitus - epidemiology
Female
Humans
Incidence
Male
Risk Assessment - methods
Statistics, nonparametric
Abstract
BACKGROUND: Incidence and lifetime risk of diabetes are important public health measures. Traditionally, nonparametric estimates are obtained from survey data by means of a Nelson-Aalen estimator which requires data information on both incident events and risk sets from the entire cohort. Such data information is rarely available in real studies. METHODS: We compare two different approaches for obtaining nonparametric estimates of age-specific incidence and lifetime risk with emphasis on required assumptions. The first and novel approach only considers incident cases occurring within a fixed time window-we have termed this cohort-of-cases data-which is linked explicitly to the birth process in the past. The second approach is the usual Nelson-Aalen estimate which requires knowledge on observed time at risk for the entire cohort and their incident events. Both approaches are used on data on anti-diabetic medications obtained from Odense Pharmacoepidemiological Database, which covers a population of approximately 470,000 over the period 1993-2003. For both methods we investigate if and how incidence rates can be projected. RESULTS: Both the new and standard method yield similar sigmoidal shaped estimates of the cumulative distribution function of age-specific incidence. The Nelson-Aalen estimator gives somewhat higher estimates of lifetime risk (15.65% (15.14%; 16.16%) for females, and 17.91% (17.38%; 18.44%) for males) than the estimate based on cohort-of-cases data (13.77% (13.74%; 13.81%) for females, 15.61% (15.58%; 15.65%) for males). Accordingly the projected incidence rates are higher based on the Nelson-Aalen estimate-also too high when compared to observed rates. In contrast, the cohort-of-cases approach gives projections that fit observed rates better. CONCLUSION: The developed methodology for analysis of cohort-of-cases data has potential to become a cost-effective alternative to a traditional survey based study of incidence. To allow more general use of the methodology, more research is needed on how to relax stationarity assumptions.
PubMed ID
18096045 View in PubMed
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Major gender difference in association of FTO gene variant among severely obese children with obesity and obesity related phenotypes.

https://arctichealth.org/en/permalink/ahliterature87240
Source
Biochem Biophys Res Commun. 2008 Apr 11;368(3):476-82
Publication Type
Article
Date
Apr-11-2008
Author
Jacobsson Josefin A
Danielsson Pernilla
Svensson Victoria
Klovins Janis
Gyllensten Ulf
Marcus Claude
Schiöth Helgi B
Fredriksson Robert
Author Affiliation
Department of Neuroscience, Functional Pharmacology, Uppsala University, Uppsala, Sweden.
Source
Biochem Biophys Res Commun. 2008 Apr 11;368(3):476-82
Date
Apr-11-2008
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Body mass index
Child
Genetic Predisposition to Disease - epidemiology - genetics
Humans
Insulin Resistance - genetics
Obesity - epidemiology - genetics
Phenotype
Polymorphism, Single Nucleotide - genetics
Prevalence
Proteins - genetics
Risk Assessment - methods
Risk factors
Sex Distribution
Sex Factors
Sweden - epidemiology
Variation (Genetics) - genetics
Abstract
Recent studies have shown that SNPs in the FTO gene predispose to childhood and adult obesity. In this study, we examined the association between variants in FTO and KIAA1005, a gene that maps closely to FTO, and obesity, as well as obesity related traits among 450 well characterised severely obese children and 512 normal weight controls. FTO showed significant association with several obesity related traits while SNPs in KIAA1005 did not. When stratified by gender, the FTO variant rs9939609 showed association with obesity and BMI among girls (P=0.006 and 0.004, respectively) but not among boys. Gender differences were also found in the associations of the FTO rs9939609 with obesity related traits such as insulin sensitivity and plasma glucose. This study suggests that FTO may have an important role for gender specific development of severe obesity and insulin resistance in children.
PubMed ID
18249188 View in PubMed
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Occurrence of ochratoxin A in sweet wines produced in Spain and other countries.

https://arctichealth.org/en/permalink/ahliterature87553
Source
Food Addit Contam. 2007 Sep;24(9):976-86
Publication Type
Article
Date
Sep-2007
Author
Burdaspal P.
Legarda T.
Author Affiliation
Centro Nacional de Alimentación, 28220 Majadahonda, Madrid, Spain. pburdas@isciii.es
Source
Food Addit Contam. 2007 Sep;24(9):976-86
Date
Sep-2007
Language
English
Publication Type
Article
Keywords
Carcinogens, Environmental - analysis
Chromatography, Affinity - methods
Chromatography, High Pressure Liquid - methods
Climate
Data Collection - methods
Drinking
Environmental Exposure - adverse effects
Food contamination - analysis
Mycotoxins - analysis
Ochratoxins - analysis
Risk Assessment - methods
Spain
Wine - analysis
Abstract
A survey for the presence of ochratoxin A (OTA) was undertaken from 2001 to 2005 in 188 samples of sweet wines produced in Spain and in 102 samples originating from other countries: France (n = 49), Austria (9), Chile (9), Portugal (9), Greece (6), Italy (5), Germany (3), Hungary (2), Slovenia (2), Switzerland (2), Canada (1), Japan (1), New Zealand (1), Ukraine (1), South Africa (1) and the USA (1). The analytical method was based on immunoaffinity chromatography clean-up and high-performance liquid chromatography (HPLC) with fluorescence detection. The limit of detection (defined as a signal-noise ratio = 3) was estimated to be 0.01 microg l(-1). The limit of quantification (0.02 microg l(-1)) was checked as being the lowest measurable concentration. OTA was detected in 281 out of 290 samples analysed (96.9% positive) at concentrations ranging from 0.01 to 4.63 microg l(-1). The overall mean and median levels were estimated to be 0.50 and 0.14 microg l(-1), respectively. In Spanish sweet wines OTA was found in 99% of the samples, with mean and median values of 0.65 and 0.19 microg l(-1), respectively. The mean value obtained in this study for OTA in the Spanish sweet wines would result in an intake of about 37.5 and 3.2 ng day(-1) of OTA for regular consumers and for the overall population, respectively. These figures represent a minor contribution to the provisional tolerable weekly intake (PTWI) or TWI established by the Joint Expert Committee on Food Additives (JECFA) and the European Food Safety Authority: 3.8 and 3.1% for regular consumers; and 0.4 and 0.3% for the whole adult population, respectively.
PubMed ID
17691011 View in PubMed
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[Model for estimation of cardiovascular risk in Norway]

https://arctichealth.org/en/permalink/ahliterature87657
Source
Tidsskr Nor Laegeforen. 2008 Jan 31;128(3):286-90
Publication Type
Article
Date
Jan-31-2008
Author
Selmer Randi
Lindman Anja Schou
Tverdal Aage
Pedersen Jan I
Njølstad Inger
Veierød Marit B
Author Affiliation
Divisjon for epidemiologi, Nasjonalt folkehelseinstitutt, Postboks 4404 Nydalen, 0403 Oslo. randi.selmer@fhi.no
Source
Tidsskr Nor Laegeforen. 2008 Jan 31;128(3):286-90
Date
Jan-31-2008
Language
Norwegian
Publication Type
Article
Keywords
Adult
Cardiovascular Diseases - etiology - mortality
Female
Humans
Male
Middle Aged
Models, Cardiovascular
Norway - epidemiology
Proportional Hazards Models
Risk Assessment - methods
Risk factors
Survival Analysis
Survival Rate
Abstract
BACKGROUND: Guidelines for prevention of cardiovascular disease (CVD) include calculation of total risk. A new risk model based on updated Norwegian data is needed, as the European SCORE function overestimates the risk of fatal CVD in Norway. NORRISK for 10-year CVD mortality is presented. It includes gender, age and smoking and levels of systolic blood pressure and serumtotal cholesterol. MATERIAL AND METHODS: NORRISK is based on national age- and sex specific mortality rates from Statistics Norway (1999-2003), mean levels of risk factors from Norwegian Health Surveys (2000-03) and relative risks from mortality follow-up of Norwegian Cardiovascular Screenings (1985-2002). The model is adjusted to the mortality level in the period 1999-2003 and is compared with the SCORE model. RESULTS: 10-year risk estimates calculated from NORRISK fall between SCORE high- and low-risk estimates and increase strongly with age. Very few persons below 50 years of age have a 10-year risk above 5% (European limit for high risk). More than half of men aged 60 years have estimated risks above this limit, while only 7% of 60-year-old women exceed the limit. Even if the risk limit is reduced to 1% for younger age groups, very few women below 50 years of age have risks above the limit. INTERPRETATION: NORRISK is more adapted to the current situation in Norway than the SCORE model and may be a useful and relevant tool in Norwegian clinical practice.
PubMed ID
18264151 View in PubMed
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Ongoing outbreak of hepatitis A in Nis, Serbia: a preliminary report.

https://arctichealth.org/en/permalink/ahliterature87727
Source
Euro Surveill. 2007 Dec;12(12):E071220.4
Publication Type
Article
Date
Dec-2007

The impact of nonlinear exposure-risk relationships on seasonal time-series data: modelling Danish neonatal birth anthropometric data.

https://arctichealth.org/en/permalink/ahliterature87751
Source
BMC Med Res Methodol. 2007;7:45
Publication Type
Article
Date
2007
Author
McGrath John
Barnett Adrian
Eyles Darryl
Burne Thomas
Pedersen Carsten B
Mortensen Preben Bo
Author Affiliation
Queensland Centre for Mental Health Research, The Park Centre for Mental Health, Wacol, Q4076, Australia. john_mcgrath@qcmhr.uq.edu.au
Source
BMC Med Res Methodol. 2007;7:45
Date
2007
Language
English
Publication Type
Article
Keywords
Anthropometry
Birth weight
Body Height
Denmark
Female
Humans
Infant, Newborn
Male
Maternal Exposure - adverse effects - statistics & numerical data
Nonlinear Dynamics
Periodicity
Poisson Distribution
Pregnancy
Registries
Risk Assessment - methods - statistics & numerical data
Seasons
Temperature
Vitamin D deficiency
Abstract
BACKGROUND: Birth weight and length have seasonal fluctuations. Previous analyses of birth weight by latitude effects identified seemingly contradictory results, showing both 6 and 12 monthly periodicities in weight. The aims of this paper are twofold: (a) to explore seasonal patterns in a large, Danish Medical Birth Register, and (b) to explore models based on seasonal exposures and a non-linear exposure-risk relationship. METHODS: Birth weight and birth lengths on over 1.5 million Danish singleton, live births were examined for seasonality. We modelled seasonal patterns based on linear, U- and J-shaped exposure-risk relationships. We then added an extra layer of complexity by modelling weighted population-based exposure patterns. RESULTS: The Danish data showed clear seasonal fluctuations for both birth weight and birth length. A bimodal model best fits the data, however the amplitude of the 6 and 12 month peaks changed over time. In the modelling exercises, U- and J-shaped exposure-risk relationships generate time series with both 6 and 12 month periodicities. Changing the weightings of the population exposure risks result in unexpected properties. A J-shaped exposure-risk relationship with a diminishing population exposure over time fitted the observed seasonal pattern in the Danish birth weight data. CONCLUSION: In keeping with many other studies, Danish birth anthropometric data show complex and shifting seasonal patterns. We speculate that annual periodicities with non-linear exposure-risk models may underlie these findings. Understanding the nature of seasonal fluctuations can help generate candidate exposures.
PubMed ID
17937794 View in PubMed
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Short and long-term survival after primary percutaneous coronary intervention in young patients with ST-elevation myocardial infarction.

https://arctichealth.org/en/permalink/ahliterature276605
Source
Int J Cardiol. 2016 Jan 15;203:697-701
Publication Type
Article
Date
Jan-15-2016
Author
Homa Waziri
Erik Jørgensen
Henning Kelbæk
Martin Stagmo
Frants Pedersen
Bo Lagerqvist
Stefan James
Lars Køber
Kristian Wachtell
Source
Int J Cardiol. 2016 Jan 15;203:697-701
Date
Jan-15-2016
Language
English
Publication Type
Article
Keywords
Adult
Cause of Death - trends
Coronary Angiography
Denmark - epidemiology
Electrocardiography
Female
Follow-Up Studies
Humans
Male
Middle Aged
Myocardial Infarction - diagnosis - mortality - surgery
Percutaneous Coronary Intervention - mortality
Registries
Retrospective Studies
Risk Assessment - methods
Survival Rate - trends
Sweden - epidemiology
Time Factors
Abstract
The long-term prognosis of patients with ST-elevation myocardial infarction (STEMI) aged 45 years or younger and differences according to gender have not been well characterized.
We included 16,685 consecutive STEMI patients from 2003 to 2012 (67,992 patient-years follow-up) from the Eastern Danish Heart Registry and the Swedish Coronary Angiography and Angioplasty Registry who were treated with primary percutaneous coronary intervention (PCI).
We identified 1026 (6.2%) patients up to 45 years of age (mean age: 40.7 vs. 66.3 years, P
Notes
Comment In: Int J Cardiol. 2016 Jan 1;202:95326549565
Comment In: Int J Cardiol. 2016 May 1;210:54-526925922
PubMed ID
26583845 View in PubMed
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1343 records – page 1 of 135.