Jørgen Vestbo

University of Southern Denmark, Odense, South Denmark, Denmark

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Publications (409)2062.75 Total impact

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    ABSTRACT: Rationale: Radiographically-confirmed pneumonia risk has not been assessed with inhaled corticosteroid use in chronic obstructive pulmonary disease (COPD). Objectives: To determine the incidence of pneumonia, risk factors and clinical attributes with inhaled fluticasone furoate in COPD patients with an exacerbation history. Methods: Two replicate, 1-year, double-blind clinical trials enrolled COPD subjects with moderate to very severe airflow limitation and at least one exacerbation in the prior year. Subjects were randomized 1:1:1:1 to receive inhaled once-daily vilanterol 25 µg or vilanterol 25 µg combined with 50 µg, 100 µg, or 200 µg fluticasone furoate. Subjects were required to have a chest radiograph at screening and within 48 hours of any suspected pneumonia or exacerbation. Measurements and Main Results: Of 3255 randomized subjects, 205 pneumonia events occurred in 181 subjects. Chest imaging was available for 195 (95%) of these events. Chest radiographs were also obtained for 1793 (70%) of the 2545 moderate and severe exacerbations. For vilanterol alone and the combination with 50 µg, 100 µg, or 200 µg fluticasone furoate, reported pneumonia incidence was 3%, 6%, 6% and 7%, respectively. However, for events with compatible parenchymal infiltrates, respective incidences were 2%, 4%, 4% and 5%. Factors associated with at least a two-fold increase in the risk of pneumonia with FF/VI were being a current smoker, having prior pneumonia, BMI < 25kg/m2, and severe airflow limitation. Conclusions: Although the incidence of pneumonia is low, radiographically-confirmed pneumonia risk is increased with inhaled FF/VI, although lower than investigator-defined rates. Clinical trial registered with clinicaltrials.gov NCT01009463 (HZC102871); NCT01017952 (HZC102970).
    Annals of the American Thoracic Society. 12/2014;
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a multifaceted condition that cannot be fully described by the severity of airway obstruction. The limitations of spirometry and clinical history have prompted researchers to investigate a multitude of surrogate biomarkers of disease for the assessment of patients, prediction of risk, and guidance of treatment. The aim of this review is to provide a comprehensive summary of observations for a selection of recently investigated pulmonary inflammatory biomarkers (Surfactant protein D (SP-D), Club cell protein 16 (CC-16), and Pulmonary and activation-regulated chemokine (PARC/CCL-18)) and systemic inflammatory biomarkers (C-reactive protein (CRP) and fibrinogen) with COPD. The relevance of these biomarkers for COPD is discussed in terms of their biological plausibility, their independent association to disease, their hard clinical outcomes, their modification by interventions, and whether changes in clinical outcomes are reflected by changes in the biomarker.
    Respiratory research. 11/2014; 15(1):147.
  • Jørgen Vestbo, Bartolome Celli
    American Journal of Respiratory and Critical Care Medicine 11/2014; 190(9):968-70. · 11.04 Impact Factor
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    ABSTRACT: Objectives Oxygen-enhanced MRI (OE-MRI) biomarkers have potential value in assessment of COPD, but need further evaluation before treatment-induced changes can be interpreted. The objective was to evaluate how OE-MRI parameters of regional ventilation and oxygen uptake respond to standard pharmacological interventions in COPD, and how the response compares to that of gold standard pulmonary function tests. Materials and Methods COPD patients (n = 40), mean FEV1 58% predicted normal, received single-dose inhaled formoterol 9 μg, or placebo, followed by 8 weeks treatment bid with a combination of budesonide and formoterol Turbuhaler® 320/9 μg or formoterol Turbuhaler®. OE-MRI biomarkers were obtained, as well as X-ray computed tomography (CT) biomarkers and pulmonary function tests, in a two-center study. An ANCOVA statistical model was used to assess effect size of intervention measurable in OE-MRI parameters of lung function. Results OE-MRI data were successfully acquired at both study sites. 8-week treatment with budesonide/formoterol significantly decreased lung wash-out time by 31% (p < 0.01), decreased the change in lung oxygen level upon breathing pure oxygen by 13% (p < 0.05) and increased oxygen extraction from the lung by 58% (p < 0.01). Single-dose formoterol increased both lung wash-out time (+47%, p < 0.05) and lung oxygenation time (+47%, p < 0.05). FEV1 was improved by single-dose formoterol (+12%, p < 0.001) and 8 weeks of budesonide/formoterol (+ 18%, p < 0.001), consistent with published studies. Conclusions In COPD, OE-MRI parameters showed response to both single-dose bronchodilatory effects of a β2-agonist, formoterol, and 8-week treatment with an inhaled corticosteroid, budesonide, and the measurements are feasible in a small-scale multi-center trial setting.
    European Journal of Radiology 11/2014; · 2.51 Impact Factor
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    ABSTRACT: Background and objectiveWe tested the hypothesis that gastro-esophageal reflux disease is a risk factor for exacerbations in individuals with chronic obstructive pulmonary disease (COPD).Methods Among 9622 participants in the Copenhagen City Heart Study, we identified 1259 individuals with COPD and information on gastro-esophageal reflux disease and the regular use of acid inhibitory treatment. These individuals were followed for 5 years with regard to medically treated COPD exacerbations, which we defined as a short course treatment with oral corticosteroids alone or in combination with antibiotics. We applied a multivariable Cox regression analysis with adjustment for well-established risk factors associated with COPD exacerbations or gastro-esophageal reflux disease, including COPD severity, and symptoms.ResultsIndividuals with COPD and gastro-esophageal reflux disease had more chronic bronchitis (31 vs 21%, P = 0.004), more breathlessness (39 vs 22%, P < 0.001), and more of them had a history of respiratory infections (6.8 vs 1.4%, P < 0.001) than individuals with COPD but without gastro-esophageal reflux disease. Among individuals with COPD and gastro-esophageal reflux disease, those who did not use acid inhibitory treatment regularly had an increased risk of COPD exacerbations during follow-up, hazards ratio (HR): HR = 2.7 (1.3–5.4, P = 0.006). Individuals with gastro-esophageal reflux disease, using acid inhibitory treatment regularly did not have an increased risk of exacerbations, HR = 1.2 (0.6–2.7, P = 0.63).Conclusions Gastro-esophageal reflux disease was associated with an increased risk of medically treated exacerbations of COPD, but only in those individuals who did not use acid inhibitory treatment regularly.
    Respirology 11/2014; · 2.78 Impact Factor
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    ABSTRACT: We performed an audit on all admissions with chronic obstructive pulmonary disease (COPD) in ex-acerbation to the Department of Emergency Medicine, Odense University Hospital (DEM) in the second half of 2012 to evaluate if an organisational change had altered visitation, treatment, initiation of non-invasive ventilation (NIV) and monitoring. We chose not to include the entire year to avoid data influenced by organisational start-up difficulties. The hypothesis was that NIV was initiated according to guidelines to the same extent as prior to the implementation of DEM.
    Danish Medical Journal 11/2014; 61(11):A4958. · 0.76 Impact Factor
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    ABSTRACT: Background:Exacerbations of chronic obstructive pulmonary disease (COPD) requiring hospital admission have important clinical and societal implications. Objective:We sought to investigate the incidence, recurrence, risk factors, and mortality of COPD patients with exacerbations requiring hospital admission compared to those without hospital admission during 3-year follow-up in 2138 COPD patients from the ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints) observational cohort. Methods:Time to first event of hospital admission analysis using Kaplan-Meier curves and Cox proportional hazard regression adjusting for possible confounders. Results:670 (31%) patients reported a total of 1452 COPD exacerbations requiring hospital admission during the study period; 313 patients (15%) reported multiple (>1) events. A prior history of exacerbation of COPD requiring hospital admission was the factor associated with the highest risk of a new hospitalization for exacerbation (hazard ratio 2.71, 95% confidence interval: 2.24-3.29, P <.001). Other risk factors included more severe airflow limitation, poorer health status, older age, radiological evidence of emphysema, and higher white blood cell count. Having been hospitalized for exacerbation significantly increased the risk of mortality (P <.001). Conclusions:Exacerbations of COPD requiring hospital admission occur across all stages of airflow limitation and are a significant prognostic factor of reduced survival across all COPD stages. COPD patients at a high risk of hospitalization can be identified by their past history for similar events, and other factors, including the severity of airflow limitation, poor health status, age, presence of emphysema, and leukocytosis. Trial registration:clinicaltrials.gov/show/NCT00292552.
    Chest 10/2014; · 7.13 Impact Factor
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    ABSTRACT: BACKGROUND: We tested the hypothesis that statin use in individuals with COPD is associated with a reduced risk of exacerbations. METHODS: We identified 5794 individuals with COPD and a measurement of C reactive protein (CRP) in the Copenhagen General Population Study (2003-2008). During 3 years of follow-up we recorded exacerbations with hospital admissions or oral corticosteroid treatment. In a nested case-control design, matching on age, gender, smoking, COPD severity and comorbidity, we estimated the association between statin use and exacerbations. In addition, we examined the association between statin use and high CRP (>3 mg/L), and the association between high CRP and exacerbations during follow-up. RESULTS: Statin use was associated with reduced odds of exacerbations in crude analysis, OR=0.68 (95% CI 0.51 to 0.91, p=0.01), as well as in multivariable conditional logistic regression analysis, OR=0.67 (0.48 to 0.92, p=0.01). However, in the subgroup with the most severe COPD and without cardiovascular comorbidity, we observed a null association between statin use and exacerbations, OR=1.1 (0.5 to 2.1, p=0.83). Furthermore, statin use was associated with reduced odds of a high CRP, OR=0.69 (0.56 to 0.85, p<0.001), and a high CRP was associated with an increased risk of exacerbations, HR=1.62 (1.35 to 1.94, p<0.001). We estimated the percentage of excess risk of the association of statin use with exacerbations possibly mediated through a reduction of CRP to be 14% (4-51%). CONCLUSIONS: Statin use was associated with reduced odds of exacerbations in individuals with COPD from the general population, although this was not apparent in those with the most severe COPD without cardiovascular comorbidity. Statins may thus only associate with reduced risk of exacerbations in patients with COPD with coexisting cardiovascular disease.
    Thorax 10/2014; · 8.38 Impact Factor
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    ABSTRACT: Background COPD patients with chronic bronchitis include a subgroup with persistent sputum production on most or every day. We hypothesized that COPD patients with persistent sputum production have a different profile of airway inflammation, and more severe clinical characteristics. Objective To compare the airway inflammation profile and clinical characteristics of COPD persistent and non-persistent sputum producers. Methods COPD persistent sputum producers (n = 26) and non-persistent sputum producers (n = 26) underwent sputum induction and pulmonary function tests. Exacerbation history was recorded; the St. George’s Respiratory Questionnaire, Modified Medical Research Council Dyspnoea scale and COPD Assessment Tool were completed. 33 COPD patients provided sputum for bacteriology. Results Persistent sputum producers had lower post-bronchodilator FEV1% predicted (p = 0.01), diffusion capacity (p = 0.04), 6 minute walk test distance (p = 0.05), and higher closing volume (p = 0.01), BODE index (p = 0.01), rate of bacterial colonization (p = 0.004) and exacerbations (p = 0.03) compared to non-persistent sputum producers. The mean SGRQ and CAT scores were higher in persistent sputum producers (p = 0.01 and 0.03 respectively). Sputum neutrophil and eosinophil total cell counts were higher in persistent sputum producers (p = 0.02 and 0.05 respectively). Sputum levels of eotaxin (p = 0.02), MCP-1 (p = 0.02), TNF-α (p = 0.03) and IL-6 (p = 0.05) were higher in persistent sputum producers. Conclusion COPD persistent sputum producers have more severe clinical characteristics and increased concentrations of some inflammatory mediators in the airways.
    Respiratory Medicine. 10/2014;
  • European Respiratory Society Annual Congress 2014; 10/2014
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    ABSTRACT: Background: The prevalence of obesity has increased during the last decades and varies from 10-20% in most European countries to approximately 32% in the United States. However, data on how obesity affects the presence of airflow limitation (AFL) defined as a reduced ratio between forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) are scarce. Methods: Data was derived from the third examination of the Copenhagen City Heart Study from 1991 until 1994 (n = 10,135). We examine the impact of different adiposity markers (weight, body mass index (BMI), waist circumference, waist-hip ratio, and abdominal height) on AFL. AFL was defined in four ways: FEV1/FVC ratio < 0.70, FEV1/FVC ratio < lower limit of normal (LLN), FEV1/FVC ratio <0.70 including at least one respiratory symptom, and FEV1/FVC ratio < LLN and FEV1% of predicted < LLN. Results: All adiposity markers were positively and significantly associated with FEV1/FVC independent of age, sex, height, smoking status, and cumulative tobacco consumption. Among all adiposity markers, BMI was the strongest predictor of FEV1/FVC. FEV1/FVC increased with 0.04 in men and 0.03 in women, as BMI increased with 10 units (kg · m-2). Consequently, diagnosis of AFL was significantly less likely in subjects with BMI ≥ 25 kg · m-2 with odds ratios 0.63 or less compared to subjects with BMI between 18.5–24.9 kg · m-2 when AFL was defined as FEV1/FVC < 0.70. Conclusion: High BMI reduces the probability of AFL. Ultimately, this may result in under-diagnosis and under-treatment of COPD among individuals with overweight and obesity.
    COPD Journal of Chronic Obstructive Pulmonary Disease 10/2014; · 2.73 Impact Factor
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    ABSTRACT: We tested the hypothesis that use of and adherence to maintenance medication is low among in-dividuals in the general population who have chronic obstructive pulmonary disease (COPD) , even in cases of severe and very severe COPD.
    Journal of General Internal Medicine 09/2014; · 3.28 Impact Factor
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    ABSTRACT: BackgroundCOPD patients have increased numbers of macrophages and neutrophils in the lungs. Interleukin-6 (IL-6) trans-signaling via its soluble receptor sIL-6R, governs the influx of innate immune cells to inflammatory foci through regulation of the chemokine CCL3. We hypothesized that there would be enhanced levels of IL-6, sIL-6R and CCL3 in COPD sputum.Methods59 COPD patients, 15 HNS and 15 S underwent sputum induction and processing with phosphate buffered saline to obtain supernatants for IL-6, sIL-6R and CCL3 analysis. Cytoslides were produced for differential cell counting and immunocytochemistry (COPD; n¿=¿3) to determine cell type surface expression of the CCL3 receptors CCR5 and CCR1.ResultsCOPD patients expressed higher levels (p¿<¿0.05) of sIL-6R and CCL3 compared to controls (sIL-6R medians pg/ml: COPD 166.4 vs S 101.1 vs HNS 96.4; CCL3 medians pg/ml: COPD 117.9 vs S 0 vs HNS 2.7). COPD sIL-6R levels were significantly correlated with sputum neutrophil (r¿=¿0.5, p¿<¿0.0001) and macrophage (r¿=¿0.3, p¿=¿0.01) counts. Immunocytochemical analysis revealed that CCR5 and CCR1 were exclusively expressed on airway macrophages.Conclusion Enhanced airway generation of sIL-6R may promote IL-6 trans-signaling in COPD. Associated upregulation of CCL3 may facilitate the recruitment of macrophages into the airways by ligation of CCR1 and CCR5.
    Respiratory research. 09/2014; 15(1):103.
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    ABSTRACT: COPD is today the third leading cause of death worldwide and its prevalence has steadily increased. Prevalence in Europe seems to be levelling, and in western and northern Europe, recent data even indicate a decrease. Beyond tobacco, other major risk factors have been identified, while objective possibilities for prevention exist. New medicines and treatment strategies can slow down disease progression. COPD heterogeneity is huge and restricts treatment options, and epidemiology can contribute to identifying clinically relevant phenotypes of COPD.
    Respiratory Epidemiology, Updated edition. edited by Isabella Annesi-Maesano, Bo Lundbäck, Giovanni Viegi, 09/2014: chapter 1: pages 1-17; European Respiratory Society Publications.., ISBN: 978-1-84984-052-1
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    ABSTRACT: Clinical studies have suggested that inhaled corticosteroid (ICS) increases the frequency of pneumonia in patients with chronic obstructive pulmonary disease (COPD). This article summarizes the risk of pneumonia by reviewing the largest clinical studies addressing pneumonia as an adverse effect of ICS treatment. The collected data show that treatment of COPD patients with ICS increases the rate of pneumonia compared with b2-agonists or placebo. Physicians are recommended to follow guidelines and solely treat COPD patients with ICS if the patients are at high risk of exacerbations.
    Ugeskrift for laeger 09/2014; 176(36).
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    ABSTRACT: Depression is highly prevalent among patients with Chronic Obstructive Pulmonary Disease (COPD). The relationship of depression with systemic inflammation in COPD remains unknown. The objective of this observational study was to compare depression scores at baseline and after 36 months follow-up between COPD patients with persistent systemic inflammation (PSI) and never inflamed patients (NI) in the ECLIPSE cohort.
    Respiratory medicine. 08/2014;
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    ABSTRACT: Little is known about changes in physical activity in subjects with chronic obstructive pulmonary disease (COPD) and its impact on mortality. Therefore, we aimed to study changes in physical activity in subjects with and without COPD and the impact of physical activity on mortality risk. Subjects from the Copenhagen City Heart Study with at least two consecutive examinations were selected. Each examination included a self-administered questionnaire and clinical examination. 1270 COPD subjects and 8734 subjects without COPD (forced expiratory volume in 1 s 67±18 and 91±15% predicted, respectively) were included. COPD subjects with moderate or high baseline physical activity who reported low physical activity level at follow-up had the highest hazard ratios of mortality (1.73 and 2.35, respectively; both p<0.001). In COPD subjects with low baseline physical activity, no differences were found in survival between unchanged or increased physical activity at follow-up. In addition, subjects without COPD with low physical activity at follow-up had the highest hazard ratio of mortality, irrespective of baseline physical activity level (p≤0.05). A decline to low physical activity at follow-up was associated with an increased mortality risk in subjects with and without COPD. These observational data suggest that it is important to assess and encourage physical activity in the earliest stages of COPD in order to maintain a physical activity level that is as high as possible, as this is associated with better prognosis.
    European Respiratory Journal 07/2014; · 6.36 Impact Factor
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    European Respiratory Journal 06/2014; · 6.36 Impact Factor
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    European Respiratory Journal 06/2014; · 6.36 Impact Factor
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    ABSTRACT: Hypoxemia is a major complication of Chronic Obstructive Pulmonary Disease (COPD) that correlates with disease prognosis. Identifying genetic variants associated with oxygenation may provide clues for deciphering the heterogeneity in prognosis among COPD patients. However, previous genetic studies have been restricted to investigating COPD candidate genes for association with hypoxemia. To report results from the first genome-wide association study (GWAS) of resting oxygen saturation in COPD cases, we performed a GWAS of pulse oximetry (SpO2) in two large, well-characterized COPD populations: COPDGene, including both the Non-Hispanic White and African American groups, and ECLIPSE. We identified several suggestive loci (P<1x10-5) associated with SpO2 in COPDGene in the Non-Hispanic White (N=2810) and ECLIPSE (N=1758) and two loci on chromosome 14 and 15 in the African American (N=820) from COPDGene achieving a level of genome-wide significance (P<5x10-8). The chromosome 14 SNP rs6576132, located in an intergenic region, was nominally replicated (P<0.05) in the Non-Hispanic White from COPDGene. The chromosome 15 SNPs were rare in subjects of European ancestry, so the results could not be replicated. The chromosome 15 region contains several genes including TICRR and KIF7 and is proximal to RHCG, Rh family C glyocoprotein gene. We have identified two loci associated with resting oxygen saturation in African Americans with COPD and several suggestive regions in COPD cases of European descent. Our study highlights the importance of investigating the genetics of complex traits in different racial groups.
    American Journal of Respiratory Cell and Molecular Biology 05/2014; · 4.15 Impact Factor

Publication Stats

12k Citations
2,062.75 Total Impact Points


  • 2008–2014
    • University of Southern Denmark
      • • Institute of Clinical Research
      • • Institute of Public Health
      Odense, South Denmark, Denmark
    • University Hospitals Birmingham NHS Foundation Trust
      • Department of Medicine
      Birmingham, ENG, United Kingdom
    • Region Hovedstaden
      Hillerød, Capital Region, Denmark
  • 2006–2014
    • Odense University Hospital
      • Department of Respiratory Medicine - J
      Odense, South Denmark, Denmark
    • University of Nebraska Medical Center
      • Department of Internal Medicine
      Omaha, NE, United States
    • St. Paul's Hospital
      Saskatoon, Saskatchewan, Canada
    • University of Kentucky
      Lexington, Kentucky, United States
  • 2004–2014
    • University Hospital Of South Manchester NHS Foundation Trust
      Manchester, England, United Kingdom
    • The University of Manchester
      • • Respiratory Medicine Research Group
      • • School of Translational Medicine
      Manchester, England, United Kingdom
  • 2013
    • The Bracton Centre, Oxleas NHS Trust
      Дартфорде, England, United Kingdom
  • 2010–2013
    • Herlev Hospital
      Herlev, Capital Region, Denmark
    • Southern Medical Clinic
      San Fernando, City of San Fernando, Trinidad and Tobago
    • Haukeland University Hospital
      • Department of Thoracic Medicine
      Bergen, Hordaland Fylke, Norway
    • University of Groningen
      Groningen, Groningen, Netherlands
    • Harvard University
      Cambridge, Massachusetts, United States
  • 2002–2013
    • University of Nebraska at Omaha
      • • Division of Pulmonary, Critical Care, Sleep and Allergy
      • • Department of Internal Medicine
      Omaha, NE, United States
  • 2012
    • Royal Society of Medicine
      Londinium, England, United Kingdom
    • University of Barcelona
      Barcino, Catalonia, Spain
    • Brigham and Women's Hospital
      • Division of Pulmonary and Critical Care Medicine
      Boston, MA, United States
    • University College London
      • Centre for the History of Medicine
      London, ENG, United Kingdom
  • 2010–2012
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 1998–2012
    • IT University of Copenhagen
      København, Capital Region, Denmark
  • 1991–2012
    • University of Copenhagen
      • • Department of Public Health
      • • Department of Clinical Microbiology
      • • Department of International Health, Immunology and Microbiology
      Copenhagen, Capital Region, Denmark
    • Copenhagen University Hospital Hvidovre
      • • Department of Cardiology
      • • Department of Infectious Diseases
      Hvidovre, Capital Region, Denmark
  • 1988–2012
    • Bispebjerg Hospital, Copenhagen University
      • • Department of Cardiology
      • • Department of Pulmonary Medicine
      København, Capital Region, Denmark
  • 2011
    • CIRO
      • Program Development Centre
      Roermond, Provincie Limburg, Netherlands
    • Manchester Metropolitan University
      • Department of Health Professions
      Manchester, ENG, United Kingdom
  • 2007–2010
    • Aintree University Hospital NHS Foundation Trust
      Liverpool, England, United Kingdom
    • Virginia Commonwealth University
      • Virginia Institute for Psychiatric and Behavioral Genetics
      Richmond, VA, United States
    • Fundación Caubet-Cimera Centro Internacional de Medicina Respiratoria Avanzada
      Bunyola, Balearic Islands, Spain
  • 2009
    • University of Glasgow
      Glasgow, Scotland, United Kingdom
    • University of British Columbia - Vancouver
      • Division of Respiratory Medicine
      Vancouver, British Columbia, Canada
  • 2008–2009
    • The Nebraska Medical Center
      Omaha, Nebraska, United States
  • 2005–2009
    • GlaxoSmithKline plc.
      • Worldwide Epidemiology
      Londinium, England, United Kingdom
    • Glostrup Hospital
      • Research Centre for Prevention and Health
      Glostrup, Capital Region, Denmark
  • 1998–2008
    • Institut for Sygdomsforebyggelse
      København, Capital Region, Denmark
  • 2002–2007
    • University of Copenhagen Herlev Hospital
      Herlev, Capital Region, Denmark
  • 1997–2003
    • Copenhagen University Hospital
      København, Capital Region, Denmark
    • Danish Cancer Society
      København, Capital Region, Denmark
  • 1996
    • Rigshospitalet
      København, Capital Region, Denmark
    • København Zoo
      København, Capital Region, Denmark
    • Copenhagen Trial Unit
      København, Capital Region, Denmark
  • 1992
    • Sundhedsstyrelsen
      København, Capital Region, Denmark