Bruno H Ch Stricker

Erasmus MC, Rotterdam, South Holland, Netherlands

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Publications (380)1927.46 Total impact

  • Gut 10/2014; · 10.73 Impact Factor
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    ABSTRACT: Many longitudinal cohort studies have both genome-wide measures of genetic variation and repeated measures of phenotypes and environmental exposures. Genome-wide association study analyses have typically used only cross-sectional data to evaluate quantitative phenotypes and binary traits. Incorporation of repeated measures may increase power to detect associations, but also requires specialized analysis methods. Here, we discuss one such method—generalized estimating equations (GEE)—in the contexts of analysis of main effects of rare genetic variants and analysis of gene-environment interactions. We illustrate the potential for increased power using GEE analyses instead of cross-sectional analyses. We also address challenges that arise, such as the need for small-sample corrections when the minor allele frequency of a genetic variant and/or the prevalence of an environmental exposure is low. To illustrate methods for detection of gene-drug interactions on a genome-wide scale, using repeated measures data, we conduct single-study analyses and meta-analyses across studies in three large cohort studies participating in the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium—the Atherosclerosis Risk in Communities study, the Cardiovascular Health Study, and the Rotterdam Study. Copyright © 2014 John Wiley & Sons, Ltd.
    Statistics in Medicine 10/2014; · 2.04 Impact Factor
  • Bruno H C Stricker
    Drug safety : an international journal of medical toxicology and drug experience. 09/2014;
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    ABSTRACT: High levels of serum uric acid are associated with hypertension in observational studies. The aim of this study was to investigate the association of uric acid gene variants with blood pressure. We studied 5791 participants aged ≥55 years from the Rotterdam Study. Thirty gene variants identified for serum uric acid level were used to compile genetic risk score (GRS). We used linear regression models to investigate the association of the uric acid GRS with systolic and diastolic blood pressure in the whole study population and separately in participants with and without comorbidities and medication use. In the age- and sex-adjusted model, each SD increase in uric acid GRS was associated with 0.75 mm Hg lower systolic blood pressure (95% confidence interval, -1.31 to -0.19) and 0.42 mm Hg lower diastolic blood pressure (95% confidence interval, -0.72 to -0.13). The association did not attenuate after further adjustment for antihypertensive medication use and conventional cardiovascular risk factors. In subgroup analysis, the association of uric acid GRS with systolic blood pressure was significantly stronger in participants (n=885) on diuretic treatment (P for interaction, 0.007). In conclusion, we found that higher uric acid GRS is associated with lower systolic and diastolic blood pressure. Diuretics treatment may modify the association of uric acid genetic risk score and systolic blood pressure. Our study suggests that genome wide association study's findings can be associated with an intermediate factor or have a pleiotropic role and, therefore, should be applied for Mendelian Randomization with caution.
    Hypertension 09/2014; · 6.87 Impact Factor
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    ABSTRACT: B-type natriuretic peptide (BNP) and C-reactive protein (CRP) predict atrial fibrillation (AF) risk. However, their risk stratification abilities in the broad community remain uncertain. We sought to improve risk stratification for AF using biomarker information.
    07/2014;
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    ABSTRACT: Elevated homocysteine levels are a risk indicator for cardiovascular disease, fractures and cognitive decline. Previous studies indicated associations between homocysteine levels and medication use, including antihypertensive, lipid-lowering and antidiabetic medication. However, results were often contradictory and inconclusive. Our objective was to study the associations established previously in more detail by sub-classifying medication groups, and investigate the potential mediating role of vitamin B12 and folate status.
    Drugs & Aging 07/2014; · 2.50 Impact Factor
  • Epidemiology (Cambridge, Mass.) 05/2014; 25(3):470-1. · 5.51 Impact Factor
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    ABSTRACT: Context: Low bone mineral density (BMD) has been associated with increased all-cause mortality. Cause-specific mortality studies have been controversial. Objective: To investigate associations between BMD and all-cause mortality and in-depth cause-specific mortality. Design and setting: Two cohorts from the prospective Rotterdam Study (RS), initiated in 1990 (RS-I) and 2000 (RS-II) with average follow-up of 17.1 (RS-I) and 10.2 (RS-II) years until January 2011. Baseline femoral neck BMD was analyzed in standard deviations. Deaths were classified according to International Classification of Diseases into 7 groups: cardiovascular diseases, cancer, infections, external, dementia, chronic lung diseases and other causes. Gender-stratified Cox and competing-risks models were adjusted for age, body mass index and smoking. Participants: 5779 (RS-I); 2055 (RS-II) subjects. Main outcome measurements: all-cause; cause-specific mortality. Results: A significant inverse association between BMD and all-cause mortality was found in males (HR(95%CI) RS-I: 1.07 (1.01-1.13), p=0.020; RS-II: 1.31 (1.12-1.55), p=0.001) but not in females (RS-I: 1.05 (0.99-1.11), p=0.098; RS-II: 0.91 (0.74-1.12), p=0.362). An inverse association with chronic lung disease mortality was found in males (RS-I: 1.75 (1.34-2.29), p <0.001; RS-II: 2.15 (1.05-4.42), p=0.037) and in RS-I in females (1.72 (1.16-2.57), p=0.008) persisting after multiple adjustments and excluding prevalent chronic obstructive pulmonary disease. A positive association between BMD and cancer mortality was detected in females in RS-I (0.89 (0.80-0.99), p=0.043). No association was found with cardiovascular mortality. Conclusions: BMD is inversely associated with mortality. The strong association of BMD with chronic lung disease mortality is a novel finding that needs further analysis to clarify underlying mechanisms.
    The Journal of Clinical Endocrinology and Metabolism 02/2014; · 6.31 Impact Factor
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    ABSTRACT: Observational and intervention studies suggest that low dose aspirin use may prevent cancer. The objective of this study was to investigate the protective effect of long term low dose aspirin use (≤ 100 mg daily) on cancer in general and site-specific cancer among low dose aspirin users in the Dutch general population. We conducted a population-based cohort study with detailed information on aspirin exposure and cancer incidence. Only incident (new) low dose aspirin users, who were included in the linkage between PHARMO and the Eindhoven Cancer Registry (1998-2010) and free of cancer before the start of follow up were included. A Cox proportional hazard model with cumulative aspirin use as a time-varying determinant was used to obtain hazard ratios (HR). Duration of aspirin use amongst 109,276 incident low dose aspirin users was not associated with a decreased risk of any of the site-specific cancers or cancer in general (adjusted HR per year of aspirin use for all cancers: 1.02, 95% confidence interval [CI] 1.00-1.04, HR of >6 years aspirin use compared to <2 years: 1.17, 95% CI 1.02-1.34). After adjusting for current and past aspirin use, 2-6 years of low dose aspirin use was associated with a reduced colorectal cancer risk compared to less than two years of aspirin use (adjusted HR 0.75, 95% CI 0.59-0.96). However, a clear dose-response relationship was not observed (adjusted HR >6 years aspirin use 0.95, 95% CI 0.60-1.49). Our results do not support the primary prevention of cancer among long term aspirin users. © 2013 Wiley Periodicals, Inc.
    International Journal of Cancer 11/2013; · 6.20 Impact Factor
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    ABSTRACT: BACKGROUND: Several methods have been proposed to assess causality in drug-induced liver injury but none have been tested in the specific context of acute liver failure leading to transplantation (ALFT). OBJECTIVE: We took advantage of the Study of Acute Liver Transplant (SALT), a European case-population study of ALFT, to test different causality scales. METHODS: Causality was assessed by experts in SALT, a 7-country case-population study from 2005 to 2007 of adult otherwise unexplained ALFT, for all drugs found within 30 days prior to the date of initial symptoms of liver disease (index date), using information content, causality scales, and data circuit determined from a pilot study, Salome. RESULTS: The consensus points from Salome were to provide full data on drugs including international non-proprietary name (INN) and doses except for non-steroidal anti-inflammatory drugs (NSAIDs) and to use the World Health Organization (WHO) causality scale. In SALT, among the 9,479 identified patients, 600 (6.3 %) were cases of ALFT, of which 187 had been exposed to drugs within 30 days, without overdose. In 130 (69.5 %) of these the causality score was possible, probable, or highly probable. CONCLUSION: In ALFT cases, once other clinical causes have been excluded and drug exposure established within 30 days, the main discriminant characteristic for causality will be previous knowledge of possible hepatotoxicity.
    Drug Safety 06/2013; · 2.62 Impact Factor
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    ABSTRACT: Venous thromboembolism (VTE) is a common, heritable disease resulting in high rates of hospitalization and mortality. Yet few associations between VTE and genetic variants, all in the coagulation pathway, have been established. To identify additional genetic determinants of VTE, we conducted a two-stage genome-wide association study (GWAS) among individuals of European ancestry in the extended cohorts for heart and aging research in genomic epidemiology (CHARGE) VTE consortium. The discovery GWAS comprised 1,618 incident VTE cases out of 44,499 participants from six community-based studies. Genotypes for genome-wide single-nucleotide polymorphisms (SNPs) were imputed to approximately 2.5 million SNPs in HapMap and association with VTE assessed using study-design appropriate regression methods. Meta-analysis of these results identified two known loci, in F5 and ABO. Top 1,047 tag SNPs (P ≤ 0.0016) from the discovery GWAS were tested for association in an additional 3,231 cases and 3,536 controls from three case-control studies. In the combined data from these two stages, additional genome-wide significant associations were observed on 4q35 at F11 (top SNP rs4253399, intronic to F11) and on 4q28 at FGG (rs6536024, 9.7 kb from FGG; P < 5.0 × 10(-13) for both). The associations at the FGG locus were not completely explained by previously reported variants. Loci at or near SUSD1 and OTUD7A showed borderline yet novel associations (P < 5.0 × 10(-6) ) and constitute new candidate genes. In conclusion, this large GWAS replicated key genetic associations in F5 and ABO, and confirmed the importance of F11 and FGG loci for VTE. Future studies are warranted to better characterize the associations with F11 and FGG and to replicate the new candidate associations.
    Genetic Epidemiology 05/2013; · 4.02 Impact Factor
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    ABSTRACT: BACKGROUND: -An elevated resting heart rate is associated with re-hospitalization for heart failure and is a modifiable risk factor in heart failure patients. We aimed to examine the association between resting heart rate and incident heart failure in a population-based cohort study of healthy adults without pre-existing overt heart disease. METHODS AND RESULTS: -We studied 4,768 men and women aged 55 years or older from the population-based Rotterdam Study. We excluded participants with prevalent heart failure, coronary heart disease, pacemaker, atrial fibrillation, atrio-ventricular block, and those using beta-blockers or calcium channel blockers. We used extended Cox-models allowing for time-dependent variation of resting heart rate along follow-up. Over a median of 14.6 years of follow-up, 656 participants developed heart failure. The risk of heart failure was higher in men with higher resting heart rate. For each increment of 10 beats per minute, the multivariable adjusted hazard ratios in men were 1.16 (95% confidence interval [CI], 1.05-1.28, p=0.005) in the time-fixed heart rate model and 1.13 (95% CI 1.02-1.25, p=0.017) in the time-dependent heart rate model. The association could not be demonstrated in women (p for interaction = 0.004). Censoring participants for incident coronary heart disease, or using time-dependent models to account for the use of beta-blockers or calcium channel blockers during follow-up did not alter the results. CONCLUSIONS: -Baseline or persistent higher resting heart rate is an independent risk factor for the development of heart failure in healthy older men in the general population.
    Circulation Heart Failure 04/2013; · 6.68 Impact Factor
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    ABSTRACT: Tiotropium, a long-acting anticholinergic, is delivered via HandiHaler(®) or via Respimat(®). RCTs suggest that use of Tiotropium Respimat(®) increases the risk of dying. We compared the risk of mortality between tiotropium Respimat(®) vs. HandiHaler(®).Within the Integrated Primary Care Information database, we defined a source population of patients, ≥40 years, with at least 1 year of follow-up. Based on prescription data, we defined episodes of tiotropium use (Respimat(®) or Handihaler(®)). The risk of mortality, within these episodes, was calculated using a Cox proportional hazard regression analysis.From the source population, 11287 patients provided 24522 episodes of tiotropium use. 496 patients died while being exposed to Handihaler(®) or Respimat(®). Use of Respimat(®) was associated with almost 30% increased risk of dying (HRadj 1.27, 95% CI 1.03-1.57) with the highest risk for cardiovascular/cerebrovascular death (HRadj 1.56, 95% CI 1.08-2.25). The risk was higher in patients with co-existing cardiovascular disease (HRadj 1.36, 95% CI 1.07-1.73) than in patients without (HRadj 1.02, 95% CI 0.61-1.71).Use of tiotropium Respimat(®) was associated with an almost 30% increase of mortality compared to Handihaler(®) and the association was the strongest for cardiovascular/cerebrovascular death. It is unclear whether this association is causal or due to residual confounding by COPD severity.
    European Respiratory Journal 03/2013; · 6.36 Impact Factor
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    ABSTRACT: PURPOSE: Ultraviolet radiation exposure is the most important exogenous risk factor for cutaneous malignancies. It is possible that phototoxic drugs promote the development of cutaneous melanoma (CM) by intensifying the effect of ultraviolet light on the skin. We investigated the association between the use of common systemic phototoxic drugs and development of CM. METHODS: This study was a case-control study in a Dutch population-based cohort. The drug dispensing data was obtained from PHARMO, a Dutch drug dispensing and hospital admissions registry, and linked to PALGA, the nationwide pathology network of the Netherlands. The cases were patients diagnosed with pathologically confirmed primary CM between 1991 and 2004. Controls were sampled from the PHARMO population. Exposure to systemic phototoxic drugs was measured and included antimicrobial agents, diuretics, antipsychotic drugs, antidiabetic drugs, cardiac drugs, antimalarials and nonsteroidal anti-inflammatory drugs (NSAIDs). A multivariate conditional logistic regression analysis was performed to study the association between exposure to phototoxic drugs and CM. RESULTS: The study population included 1,318 cases and 6,786 controls. Any phototoxic drug during the study period was dispensed for 46 % of the cases and 43 % of the controls (p = 0.012). The use of quinolones [odds ratio (OR) 1.33, 95 % confidence interval (CI) 1.01-1.76] and propionic acid derivative NSAIDs (OR 1.33, 95 % CI 1.14-1.54) had a positive association with CM. CONCLUSIONS: Our study shows that the use of phototoxic drugs is associated with an increased risk of developing CM. Even a short-term use of phototoxic quinolones and propionic acid derivative NSAIDs may increase the risk for CM. Patient education to promote sun-protective behaviour is essential to avoid immediate adverse effects and possible long-term effects of phototoxic drugs.
    European Journal of Clinical Pharmacology 03/2013; · 2.74 Impact Factor
  • Maarten J G Leening, Jaap W Deckers, Bruno H Ch Stricker
    European Journal of Heart Failure 02/2013; · 5.25 Impact Factor
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    ABSTRACT: Tools for the prediction of atrial fibrillation (AF) may identify high-risk individuals more likely to benefit from preventive interventions and serve as a benchmark to test novel putative risk factors. Individual-level data from 3 large cohorts in the United States (Atherosclerosis Risk in Communities [ARIC] study, the Cardiovascular Health Study [CHS], and the Framingham Heart Study [FHS]), including 18 556 men and women aged 46 to 94 years (19% African Americans, 81% whites) were pooled to derive predictive models for AF using clinical variables. Validation of the derived models was performed in 7672 participants from the Age, Gene and Environment-Reykjavik study (AGES) and the Rotterdam Study (RS). The analysis included 1186 incident AF cases in the derivation cohorts and 585 in the validation cohorts. A simple 5-year predictive model including the variables age, race, height, weight, systolic and diastolic blood pressure, current smoking, use of antihypertensive medication, diabetes, and history of myocardial infarction and heart failure had good discrimination (C-statistic, 0.765; 95% CI, 0.748 to 0.781). Addition of variables from the electrocardiogram did not improve the overall model discrimination (C-statistic, 0.767; 95% CI, 0.750 to 0.783; categorical net reclassification improvement, -0.0032; 95% CI, -0.0178 to 0.0113). In the validation cohorts, discrimination was acceptable (AGES C-statistic, 0.664; 95% CI, 0.632 to 0.697 and RS C-statistic, 0.705; 95% CI, 0.664 to 0.747) and calibration was adequate. A risk model including variables readily available in primary care settings adequately predicted AF in diverse populations from the United States and Europe.
    Journal of the American Heart Association. 01/2013; 2(2):e000102.
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    ABSTRACT: Genome-wide association studies have identified numerous genetic loci for spirometic measures of pulmonary function, forced expiratory volume in one second (FEV(1)), and its ratio to forced vital capacity (FEV(1)/FVC). Given that cigarette smoking adversely affects pulmonary function, we conducted genome-wide joint meta-analyses (JMA) of single nucleotide polymorphism (SNP) and SNP-by-smoking (ever-smoking or pack-years) associations on FEV(1) and FEV(1)/FVC across 19 studies (total N = 50,047). We identified three novel loci not previously associated with pulmonary function. SNPs in or near DNER (smallest P(JMA = )5.00×10(-11)), HLA-DQB1 and HLA-DQA2 (smallest P(JMA = )4.35×10(-9)), and KCNJ2 and SOX9 (smallest P(JMA = )1.28×10(-8)) were associated with FEV(1)/FVC or FEV(1) in meta-analysis models including SNP main effects, smoking main effects, and SNP-by-smoking (ever-smoking or pack-years) interaction. The HLA region has been widely implicated for autoimmune and lung phenotypes, unlike the other novel loci, which have not been widely implicated. We evaluated DNER, KCNJ2, and SOX9 and found them to be expressed in human lung tissue. DNER and SOX9 further showed evidence of differential expression in human airway epithelium in smokers compared to non-smokers. Our findings demonstrated that joint testing of SNP and SNP-by-environment interaction identified novel loci associated with complex traits that are missed when considering only the genetic main effects.
    PLoS Genetics 12/2012; 8(12):e1003098. · 8.52 Impact Factor
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    ABSTRACT: Background: High plasma dehydroepiandrosterone sulfate (DHEAS) levels have been associated with a reduced risk of cardiovascular disease and atherosclerosis. To our knowledge, no previous follow-up study has investigated the association between DHEAS and the development of atrial fibrillation. Our objective was to investigate the association between DHEAS levels and incident atrial fibrillation.Methods and results: The study was based on a random sample within the prospective population-based Rotterdam Study. The study population comprised 1180 participants without atrial fibrillation at baseline for whom baseline levels of DHEAS were measured in plasma. Atrial fibrillation was ascertained from centre visit electrocardiogram (ECG) assessments as well as medical records. During a mean follow-up period of 12.3 years, 129 participants developed atrial fibrillation. DHEAS levels were inversely associated with the risk of atrial fibrillation (hazard ratio (HR) per standard deviation (SD): 0.74, 95% confidence interval (CI): 0.58-0.94). Subjects in the highest DHEAS quartile had an almost three times lower risk of atrial fibrillation during follow-up, compared to those in the lowest DHEAS quartile (HR: 0.34, 95% CI: 0.18-0.64) adjusted for age, sex and cardiovascular risk factors.Conclusion: DHEAS can be regarded as an important indicator of future atrial fibrillation in both men and women, independent of known cardiovascular risk factors.
    European journal of preventive cardiology. 11/2012;
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    ABSTRACT: BACKGROUND: It is largely unknown if corticosteroid-induced open-angle glaucoma (OAG) is an entity that is limited to a few susceptible individuals or whether it contributes significantly to the overall population burden of OAG. OBJECTIVE: The aim of this study was to determine whether there is an association between corticosteroid use and the incidence of OAG in the general elderly population. METHODS: A prospective population-based cohort study was conducted in a general community setting. 3,939 participants of the Rotterdam Study aged 55 years and older for whom data from ophthalmic examinations at baseline and follow-up were available and who did not have glaucoma at baseline were included (baseline examination from 1991 to 1993; follow-up examinations from 1997 to 1999 and from 2002 to 2006). Ophthalmic examinations, including measurement of the intraocular pressure, assessment of the optic nerve head and perimetry, were performed at baseline and follow-up. The use of corticosteroids was monitored continuously during follow-up. Corticosteroids were stratified into five groups: ophthalmic steroids, inhaled steroids, nasal steroids, oral steroids and steroid ointments. Associations between the use of corticosteroids and incident OAG were assessed using logistic regression models. The study outcome measures were the odds ratios (ORs) of associations between the use of corticosteroids and incident OAG. RESULTS: During a mean follow-up of 9.8 years, 108 participants (2.8 %) developed OAG. The median number of steroid prescriptions during follow-up was 2 for ophthalmic, 7 for inhaled, 2 for nasal and 2 for oral steroids, and 3 for steroid ointments. The OR of the use of ophthalmic steroids was 1.04 [95 % confidence interval (CI) 0.66, 1.65; p = 0.86], inhaled steroids 0.79 (95 % CI 0.42, 1.48; p = 0.46), nasal steroids 1.26 (95 % CI 0.74, 2.13; p = 0.40), oral steroids 1.03 (95 % CI 0.65, 1.64; p = 0.89) and steroid ointments 0.70 (95 % CI 0.47, 1.05; p = 0.086). These analyses were adjusted for age, sex, high myopia and family history of glaucoma. The small median numbers of prescriptions made it difficult to evaluate dose-response relationships. CONCLUSION: None of the classes of steroids were associated with the incidence of OAG in this elderly population.
    Drugs & Aging 11/2012; · 2.50 Impact Factor
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    ABSTRACT: The purpose of this study was to determine the association of coronary artery calcification (CAC) with incident heart failure in the elderly and examine its independence of overt coronary heart disease (CHD). Heart failure is often observed as a first manifestation of coronary atherosclerosis rather than a sequela of overt CHD. Although numerous studies have shown that CAC, an established measure of coronary atherosclerosis, is a strong predictor of CHD, the association between CAC and future heart failure has not been studied prospectively. In the Rotterdam Study, a population-based cohort, 1,897 asymptomatic participants (mean age, 69.9 years; 58% women) underwent CAC scoring and were followed for the occurrence of heart failure and CHD. During a median follow-up of 6.8 years, there were 78 cases of heart failure and 76 cases of nonfatal CHD. After adjustment for cardiovascular risk factors, increasing CAC scores were associated with heart failure (p for trend = 0.001), with a hazard ratio of 4.1 (95% confidence interval [CI]: 1.7 to 10.1) for CAC scores >400 compared with CAC scores of 0 to 10. After censoring participants for incident nonfatal CHD, increasing extent of CAC remained associated with heart failure (p for trend = 0.046), with a hazard ratio of 2.9 (95% CI: 1.1 to 7.4) for CAC scores >400. Moreover, adding CAC to cardiovascular risk factors resulted in an optimism-corrected increase in the c-statistic by 0.030 (95% CI: 0.001 to 0.050) to 0.734 (95% CI: 0.698 to 0.770) and substantially improved the risk classification of subjects (continuous net reclassification index = 34.0%). CAC has a clear association with the risk of heart failure, independent of overt CHD. Because heart failure is highly prevalent in the elderly, it might be worthwhile to include heart failure as an outcome in future risk assessment programs incorporating CAC.
    JACC. Cardiovascular imaging 09/2012; 5(9):874-80. · 14.29 Impact Factor

Publication Stats

9k Citations
1,927.46 Total Impact Points

Institutions

  • 2001–2014
    • Erasmus MC
      • • Department of Epidemiology
      • • Department of Dermatology
      • • Department of Internal Medicine
      • • Department of Medical Informatics
      Rotterdam, South Holland, Netherlands
  • 2013
    • Pharmo Institute for Drug Outcomes Research
      Utrecht, Utrecht, Netherlands
  • 1994–2012
    • University of Groningen
      • Department of Ophthalmology
      Groningen, Province of Groningen, Netherlands
    • Universitair Ziekenhuis Leuven
      Louvain, Flanders, Belgium
  • 1993–2012
    • Erasmus Universiteit Rotterdam
      • • Department of Medical Informatics
      • • Department of Epidemiology
      • • Department of Internal Medicine
      Rotterdam, South Holland, Netherlands
  • 2002–2011
    • Universiteit Utrecht
      • Division of Pharmacoepidemiology and Pharmacotherapy
      Utrecht, Provincie Utrecht, Netherlands
  • 2010
    • Medicines Evaluation Board, Netherlands
      Utrecht, Utrecht, Netherlands
  • 2009
    • National Heart, Lung, and Blood Institute
      • Division of Cardiovascular Sciences (DCVS)
      Maryland, United States
    • Universitair Ziekenhuis Ghent
      Gand, Flanders, Belgium
    • Massachusetts General Hospital
      • Center for Human Genetic Research
      Boston, MA, United States
  • 2007
    • Canadian Society for Epidemiology and Biostatistics 
      Canada
    • Università degli Studi di Messina
      • Dipartimento di Medicina Clinica e Sperimentale
      Messina, Sicily, Italy
  • 2005–2007
    • National Institute for Public Health and the Environment (RIVM)
      Utrecht, Utrecht, Netherlands
  • 2006
    • St. Elisabeth Ziekenhuis Tilburg
      Tilburg, North Brabant, Netherlands
  • 2004
    • Netherlands Institute for Space Research, Utrecht
      Utrecht, Utrecht, Netherlands
  • 1986
    • Leiden University Medical Centre
      • Department of Gastroenterology and Hepatology
      Leiden, South Holland, Netherlands