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1. The effect of COPD severity and study duration on exacerbation outcome in randomized controlled trials

Author: Eriksson G, Calverley PM, Jenkins CR, Anzueto AR, Make BJ, Lindberg M, Fagerås M, and Postma DS
Subjects: Chronic obstructive pulmonary disease, RCT, differential drop-out, exacerbation, study duration, disease severity, Diseases of the respiratory system, RC705-779
Abstract: Göran Eriksson,1 Peter M Calverley,2 Christine R Jenkins,3,4 Antonio R Anzueto,5 Barry J Make,6 Magnus Lindberg,7 Malin Fagerås,7 Dirkje S Postma8 1Department of Respiratory Medicine and Allergology, University Hospital, Lund, Sweden; 2Pulmonary and Rehabilitation Research Group, University Hospital Aintree, Liverpool, UK; 3Concord Clinical School, University of Sydney, 4The George Institute for Global Health, Sydney, Australia; 5Department of Pulmonary Medicine and Critical Care, University of Texas Health Sciences Center and South Texas Veterans’ Health Care System, San Antonio, Texas, 6Division of Pulmonary Sciences and Critical Care Medicine, National Jewish Health, University of Colorado, Denver, Colorado, USA; 7AstraZeneca R&D, Mölndal, Sweden; 8Department of Pulmonary Medicine and Tuberculosis, University Medical Center Groningen, GRIAC Research Institute, University of Groningen, Groningen, the Netherlands Background: When discontinuation in COPD randomized controlled trials (RCTs) is unevenly distributed between treatments (differential dropout), the capacity to demonstrate treatment effects may be reduced. We investigated the impact of the time of differential dropout on exacerbation outcomes in RCTs, in relation to study duration and COPD severity.Methods: A post hoc analysis of 2,345 patients from three RCTs of 6- and 12-month duration was performed to compare budesonide/formoterol and formoterol in moderate, severe, and very severe COPD. Outcomes were exacerbation rate, time-to-first exacerbation, or discontinuation; patients were stratified by disease severity. Outcomes were studied by censoring data monthly from 1 to 12 months.Results: In patients treated with budesonide/formoterol, annualized exacerbation rates (AERs) were comparable for each study duration (rate ratio [RR] =0.6). With formoterol, the AER decreased with study duration (RR =1.20 at 1 month to RR =0.86 at 12 months). There was a treatment-related difference in exacerbation rates of 45%–48% for shorter study durations (≤4 months) and 27% for 12-month duration. This treatment-related difference in exacerbation rates was comparable for the three disease severities in studies ≤4 months (range: 39%–51%), but this difference decreased with longer study durations, especially in more severe groups (22% and 29% at 12 months). There were fewer discontinuations with budesonide/formoterol; the treatment-related difference in time-to-first discontinuation decreased by study duration (35%, 30%, 26%, and 22% at 3, 6, 9, and 12 months, respectively). Numbers of differential dropouts increased with increasing disease severity, being greatest during second, third, and fourth months.Conclusions: COPD severity and study duration impact exacerbation as an outcome in double-blind RCTs. This effect is most obvious in patients with severe/very severe COPD and in studies that are longer than 4 months. Early differential dropout particularly impacts study outcome, producing a “healthy survivor effect,” which reduces estimations of treatment impact on exacerbations. Keywords: healthy survivor effect, exacerbation outcomes, early differential dropout, RCT, disease severity
Published: 2017

2. Control of moderate-to-severe asthma with randomized ciclesonide doses of 160, 320 and 640 μg/day

Author: Pedersen SE, Prasad N, Goehring UM, Andersson H, and Postma DS
Subjects: Asthma, ICS, ciclesonide, Immunologic diseases. Allergy, RC581-607
Abstract: Søren E Pedersen,1 Niyati Prasad,2 Udo-Michael Goehring,3 Henrik Andersson,4 Dirkje S Postma5 1Pediatric Research Unit, Kolding Hospital, University of Southern Denmark, Kolding, Denmark; 2Vertex, Phase IV & Global Strategy, London, UK; 3Vifor Pharma Ltd, Clinical Research & Biometrics, Glattbrugg, Switzerland; 4Swedish Social Insurance Agency, Government Offices of Sweden, Stockholm, Sweden; 5Department of Pulmonology, Griac Research Institute, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands Background: The inhaled corticosteroid (ICS) ciclesonide (Cic), controls asthma symptoms in the majority of patients at the recommended dose of 160 µg/day. However, the relationship between the level of asthma control and increasing doses of Cic is unknown. This study investigated whether long-term treatment with higher doses of Cic would further improve asthma symptoms in patients with uncontrolled asthma despite ICS use. Patients and methods: In a double-blind, randomized, parallel-group study, 367 patients were allocated to one of three treatment arms (Cic 160, 320 and 640 μg/day). After a single-blind, 3-week baseline period with Cic 160 µg/day, eligible patients were randomized to receive 52 weeks of treatment with Cic 160, 320 or 640 μg/day (double-blind period) during which forced expiratory volume in 1 second (FEV1), exacerbations and Asthma Control Questionnaire (ACQ) scores were measured. Results: Treatment with all the three doses was associated with significant improvements in ACQ scores, FEV1 and asthma symptoms (P
Published: 2017

3. Early efficacy of budesonide/formoterol in patients with moderate-to-very-severe COPD

Author: Calverley PM, Eriksson G, Jenkins CR, Anzueto AR, Make BJ, Persson A, Fagerås M, and Postma DS
Subjects: Bronchodilator agents, Clinical respiratory medicine, Clinical trials, COPD, Diseases of the respiratory system, RC705-779
Abstract: Peter M Calverley,1 Göran Eriksson,2 Christine R Jenkins,3 Antonio R Anzueto,4 Barry J Make,5 Anders Persson,6 Malin Fagerås,6 Dirkje S Postma7 1Pulmonary and Rehabilitation Research Group, University Hospital Aintree, Liverpool, UK; 2Department of Respiratory Medicine and Allergology, University Hospital, Lund, Sweden; 3George Institute for Global Health, The University of Sydney and Concord Clinical School, Sydney, Australia; 4Department of Pulmonary Medicine and Allergology, University of Texas Health Sciences Center and South Texas Veterans’ Health Care System, San Antonio, Texas, 5Division of Pulmonary Sciences and Critical Care Medicine, National Jewish Health, University of Colorado, Denver, Colorado, USA; 6AstraZeneca R&D, Gothenburg, Sweden; 7Department of Pulmonary Medicine and Tuberculosis, GRIAC Research Institute, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands Background and objective: Large clinical trials have confirmed the long-term efficacy of inhaled corticosteroid/long-acting β2-agonist combinations in patients with chronic obstructive pulmonary disease (COPD). It was hypothesized that significant treatment effects would already be present within 3 months after the initiation of treatment across a range of clinical outcomes, irrespective of COPD severity. Methods: Post hoc analysis of 3-month post-randomization outcomes, including exacerbation rates, dropouts, symptoms, reliever use, and lung function, from three studies with similar inclusion criteria of moderate-to-very-severe COPD. Patients (n=1,571) were treated with budesonide/formoterol (B/F) 320/9 µg or placebo, twice daily; in one study, tiotropium 18 µg once daily was also given. Results: Over the first 3 months of treatment, fewer patients randomized to B/F experienced exacerbations versus the placebo group (111 and 196 patients with ≥1 exacerbation, respectively). This was true in each COPD severity group. Compared with placebo, B/F treatment led to significantly lower 3-month exacerbation rates in the moderate and severe COPD severity groups (46% and 57% reduction, respectively), with a nonsignificant reduction (29%) in very severe COPD. Fewer dropouts occurred among patients treated with B/F versus placebo, this effect being greater with increasing COPD severity. B/F was associated with improved forced expiratory volume in 1 s, morning peak expiratory flow rate, total reliever use, and total symptom score versus placebo. Conclusion: Treatment with B/F decreased exacerbations in patients with moderate-to-very-severe COPD within 3 months of commencing treatment. This effect was paralleled by improved lung function, less reliever medication use, and fewer symptoms, irrespective of disease severity. Keywords: bronchodilator agents, clinical respiratory medicine, clinical trials, COPD
Published: 2016

4. Early response to inhaled bronchodilators and corticosteroids as a predictor of 12-month treatment responder status and COPD exacerbations

Author: Calverley PM, Postma DS, Anzueto AR, Make BJ, Eriksson G, Peterson S, and Jenkins CR
Subjects: anti-inflammatories, bronchodilator effect, chronic obstructive pulmonary disease, predictors, risk assessment, risk factors, Diseases of the respiratory system, RC705-779
Abstract: Peter M Calverley,1 Dirkje S Postma,2 Antonio R Anzueto,3,4 Barry J Make,5 Göran Eriksson,6 Stefan Peterson,7 Christine R Jenkins8 1Pulmonary and Rehabilitation Research Group, University Hospital Aintree, Liverpool, UK; 2Department of Pulmonary Medicine and Tuberculosis, Gronigen Research Institute for Asthma and COPD, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; 3Division of Pulmonary Diseases and Critical Care Medicine, University of Texas Health Sciences Center, School of Medicine, University of Texas, 4South Texas Veterans Health Care System, San Antonio, TX, 5Division of Pulmonary Sciences and Critical Care Medicine, National Jewish Health, University of Colorado, Denver, CO, USA; 6Department of Respiratory Medicine and Allergology, University Hospital, 7StatMind AB, Lund, Sweden; 8George Institute for Global Health, Concord Clincal School, The University of Sydney, Sydney, NSW, Australia Background: Early treatment response markers, for example, improvement in forced expiratory volume in 1 second (FEV1) and St George’s Respiratory Questionnaire (SGRQ) total score, may help clinicians to better manage patients with chronic obstructive pulmonary disease (COPD). We investigated the prevalence of clinically important improvements in FEV1 and SGRQ scores after 2-month budesonide/formoterol or formoterol treatment and whether such improvements predict subsequent improvements and exacerbation rates.Methods: This post hoc analysis is based on data from three double-blind, randomized studies in patients with moderate-to-very-severe COPD receiving twice-daily budesonide/formoterol or formoterol alone for 6 or 12 months. Prebronchodilator FEV1 and SGRQ total score were measured before treatment and at 2 and 12 months; COPD exacerbation rates were measured during months 2–12. Responders were defined by ≥100 mL improvement in prebronchodilator FEV1 and ≥4-point decrease in SGRQ total score.Results: Overall, 2,331 and 1,799 patients were included in the 0–2- and 0–12-month responder analyses, respectively, and 2,360 patients in the 2–12-month exacerbation rate analysis. At 2 months, 35.1% of patients were FEV1 responders and 44.3% were SGRQ responders. The probability of response was significantly greater with budesonide/formoterol than with formoterol or placebo for both parameters. Two-month responders had a greater chance of 12-month response than 2-month nonresponders for both FEV1 (odds ratio, 5.57; 95% confidence interval, 4.14–7.50) and SGRQ (odds ratio, 3.87; 95% confidence interval, 2.83–5.31). Two-month response in FEV1 (P
Published: 2016

5. A score to predict short-term risk of COPD exacerbations (SCOPEX)

Author: Make BJ, Eriksson G, Calverley PM, Jenkins CR, Postma DS, Peterson S, Östlund O, and Anzueto A
Subjects: Diseases of the respiratory system, RC705-779
Abstract: Barry J Make,1 Göran Eriksson,2 Peter M Calverley,3 Christine R Jenkins,4 Dirkje S Postma,5 Stefan Peterson,6 Ollie Östlund,7 Antonio Anzueto8 1Division of Pulmonary Sciences and Critical Care Medicine, National Jewish Health, University of Colorado Denver School of Medicine, Denver, CO, USA; 2Department of Respiratory Medicine and Allergology, University Hospital, Lund, Sweden; 3Pulmonary and Rehabilitation Research Group, University Hospital Aintree, Liverpool, UK; 4George Institute for Global Health, The University of Sydney and Concord Clinical School, Woolcock Institute of Medical Research, Sydney, NSW, Australia; 5Department of Pulmonology, University of Groningen and GRIAC Research Institute, University Medical Center Groningen, Groningen, The Netherlands; 6StatMind AB, Lund, Sweden; 7Department of Medical Sciences and Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden; 8Department of Pulmonary/Critical Care, University of Texas Health Sciences Center and South Texas Veterans Healthcare System, San Antonio, TX, USA Background: There is no clinically useful score to predict chronic obstructive pulmonary disease (COPD) exacerbations. We aimed to derive this by analyzing data from three existing COPD clinical trials of budesonide/formoterol, formoterol, or placebo in patients with moderate-to-very-severe COPD and a history of exacerbations in the previous year. Methods: Predictive variables were selected using Cox regression for time to first severe COPD exacerbation. We determined absolute risk estimates for an exacerbation by identifying variables in a binomial model, adjusting for observation time, study, and treatment. The model was further reduced to clinically useful variables and the final regression coefficients scaled to obtain risk scores of 0–100 to predict an exacerbation within 6 months. Receiver operating characteristic (ROC) curves and the corresponding C-index were used to investigate the discriminatory properties of predictive variables. Results: The best predictors of an exacerbation in the next 6 months were more COPD maintenance medications prior to the trial, higher mean daily reliever use, more exacerbations during the previous year, lower forced expiratory volume in 1 second/forced vital capacity ratio, and female sex. Using these risk variables, we developed a score to predict short-term (6-month) risk of COPD exacerbations (SCOPEX). Budesonide/formoterol reduced future exacerbation risk more than formoterol or as-needed short-acting ß2-agonist (salbutamol). Conclusion: SCOPEX incorporates easily identifiable patient characteristics and can be readily applied in clinical practice to target therapy to reduce COPD exacerbations in patients at the highest risk. Keywords: chronic obstructive pulmonary disease, exacerbation, model, predictor, inhaled corticosteroids, bronchodilators
Published: 2015

6. Comparing the effectiveness of small-particle versus large-particle inhaled corticosteroid in COPD

Author: Postma DS, Roche N, Colice G, Israel E, Martin RJ, van Aalderen WMC, Grigg J, Burden A, Hillyer EV, von Ziegenweidt J, Gopalan G, and Price D
Subjects: Diseases of the respiratory system, RC705-779
Abstract: Dirkje S Postma,1 Nicolas Roche,2 Gene Colice,3 Elliot Israel,4 Richard J Martin,5 Willem MC van Aalderen,6 Jonathan Grigg,7 Anne Burden,8 Elizabeth V Hillyer,8 Julie von Ziegenweidt,8 Gokul Gopalan,9 David Price8,10 1University of Groningen, Department of Pulmonary Medicine and Tuberculosis, University Medical Center Groningen, Groningen, the Netherlands; 2Respiratory and Intensive Care Medicine, Cochin Hospital Group, APHP, Paris-Descartes University (EA2511), Paris, France; 3Pulmonary, Critical Care and Respiratory Services, Washington Hospital Center and George Washington University School of Medicine, Washington DC, USA; 4Pulmonary and Critical Care Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; 5Department of Medicine, National Jewish Health, Denver, CO, USA; 6Dept of Pediatric Respiratory Medicine and Allergy, Emma Children's Hospital AMC, Amsterdam, the Netherlands; 7Blizard Institute, Queen Mary University London, London, UK; 8Research in Real Life, Ltd, Cambridge, UK; 9Respiratory, Global Scientific Affairs, Teva Pharmaceuticals, Frazer, PA, USA; 10Academic Primary Care, Division of Applied Health Sciences, University of Aberdeen, Aberdeen, UK Purpose: Small airway changes and dysfunction contribute importantly to airway obstruction in chronic obstructive pulmonary disease (COPD), which is currently treated with inhaled corticosteroids (ICS) and long-acting bronchodilators at Global initiative for Obstructive Lung Disease (GOLD) grades 2–4. This retrospective matched cohort analysis compared effectiveness of a representative small-particle ICS (extrafine beclomethasone) and larger-particle ICS (fluticasone) in primary care patients with COPD. Patients and methods: Smokers and ex-smokers with COPD ≥40 years old initiating or stepping-up their dose of extrafine beclomethasone or fluticasone were matched 1:1 for demographic characteristics, index prescription year, concomitant therapies, and disease severity during 1 baseline year. During 2 subsequent years, we evaluated treatment change and COPD exacerbations, defined as emergency care/hospitalization for COPD, acute oral corticosteroids, or antibiotics for lower respiratory tract infection. Results: Mean patient age was 67 years, 57%–60% being male. For both initiation (n=334:334) and step-up (n=189:189) patients, exacerbation rates were comparable between extrafine beclomethasone and fluticasone cohorts during the 2 year outcome period. Odds of treatment stability (no exacerbation or treatment change) were significantly greater for patients initiating extrafine beclomethasone compared with fluticasone (adjusted odds ratio 2.50; 95% confidence interval, 1.32–4.73). Median ICS dose exposure during 2 outcome years was significantly lower (P
Published: 2014

7. Bronchodilation improves endurance but not muscular efficiency in chronic obstructive pulmonary disease

Author: van der Vaart H, Postma DS, Grevink R, Roemer W, and ten Hacken NHT
Subjects: Diseases of the respiratory system, RC705-779
Abstract: Hester van der Vaart1, Dirkje S Postma1, René Grevink1, Willem Roemer2, Nick ten Hacken11University Medical Center, Groningen, The Netherlands; 2Boehringer Ingelheim bv, Alkmaar, The NetherlandsAbstract: We hypothesized that bronchodilator treatment not only improves hyperinflation and endurance capacity but also muscular efficiency in stable chronic obstructive pulmonary disease (COPD). We aimed to demonstrate that tiotropium and salmeterol improve muscular efficiency compared with placebo. Twenty-five COPD patients were studied, including 20 males of mean (standard deviation) age 62 years (7 years) with baseline forced expiratory volume in 1 second of 41% (10%) predicted, and maximal workload of 101 Watt (36 Watt). Subjects were randomized for 6-week treatment with tiotropium 18 µg once daily, salmeterol 50 µg twice daily, or placebo using a double-blind, crossover design. Muscular efficiency and endurance time were measured during cycling at 50% of maximal work load. Resting energy expenditure was measured using a ventilated hood. Muscular efficiency after tiotropium, salmeterol, and placebo treatment was 14.6%, 14.4%, and 14.4%, respectively (P > 0.05), and resting energy expenditure was 1485 kcal/24 hours, 1709 kcal/24 hours, and 1472 kcal/24 hours (P > 0.05), respectively. Endurance time after tiotropium treatment was significantly higher than that after placebo (27.0 minutes versus 19.3 minutes [P = 0.02]), whereas endurance time after salmeterol treatment was not higher than that after placebo (23.3 minutes [P = 0.22]). In this small study, we were not able to demonstrate that bronchodilator therapy improved muscular efficiency. Apparently, reduced costs of breathing relative to total energy expenditure were too small to be detected. Keywords: bronchodilation, chronic obstructive pulmonary disease, energy expenditure, muscle energetics, muscular exercise
Published: 2011

8. Genetic variation in TIMP1 but not MMPs predict excess FEV1 decline in two general population-based cohorts

Author: Blokstra A, Siedlinski M, Postma DS, van Diemen CC, Smit HA, and Boezen HM
Subjects: Diseases of the respiratory system, RC705-779
Abstract: Abstract Background An imbalance in Matrix MetalloProteases (MMPs) and Tissue Inhibitors of MMPs (TIMPs) contributes to Chronic Obstructive Pulmonary Disease (COPD) development. Longitudinal studies investigating Single Nucleotide Polymorphisms (SNPs) in MMPs and TIMPs with respect to COPD development and lung function decline in the general population are lacking. Methods We genotyped SNPs in MMP1 (G-1607GG), MMP2 (-1306 C/T), MMP9 (3 tagging SNPs), MMP12 (A-82G and Asn357Ser) and TIMP1 (Phe124Phe and Ile158Ile) in 1390 Caucasians with multiple FEV1 measurements from a prospective cohort study in the general population. FEV1 decline was analyzed using linear mixed effect models adjusted for confounders. Analyses of the X-chromosomal TIMP1 gene were stratified according to sex. All significant associations were repeated in an independent general population cohort (n = 1152). Results MMP2 -1306 TT genotype carriers had excess FEV1 decline (-4.0 ml/yr, p = 0.03) compared to wild type carriers. TIMP1 Ile158Ile predicted significant excess FEV1 decline in both males and females. TIMP1 Phe124Phe predicted significant excess FEV1 decline in males only, which was replicated (p = 0.10) in the second cohort. The MMP2 and TIMP1 Ile158Ile associations were not replicated. Although power was limited, we did not find associations with COPD development. Conclusions We for the first time show that TIMP1 Phe124Phe contributes to excess FEV1 decline in two independent prospective cohorts, albeit not quite reaching conventional statistical significance in the replication cohort. SNPs in MMPs evidently do not contribute to FEV1 decline in the general population.
Published: 2011
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9. ST13 polymorphisms and their effect on exacerbations in steroid‐treated asthmatic children and young adults

Author: Vijverberg, SJH, Koster, ES, Tavendale, R, Leusink, M, Koenderman, L, Raaijmakers, JAM, Postma, DS, Koppelman, GH, Turner, SW, Mukhopadhyay, S, Tse, SM, Tantisira, KG, Hawcutt, DB, Francis, B, Pirmohamed, M, Pino-Yanes, M, Eng, C, Burchard, EG, Palmer, CNA, and Maitland-van der Zee, AH
Subjects: Biomedical and Clinical Sciences, Immunology, Clinical Research, Lung, Pediatric, Asthma, Genetics, Aetiology, 2.1 Biological and endogenous factors, Respiratory, Adolescent, Adrenal Cortex Hormones, Anti-Asthmatic Agents, Carrier Proteins, Child, Child, Preschool, Cohort Studies, Disease Progression, Female, Humans, Male, Odds Ratio, Polymorphism, Single Nucleotide, Treatment Outcome, Tumor Suppressor Proteins, Young Adult, childhood asthma, corticosteroids, exacerbations, pharmacogenomics, ST13, Nutrition and Dietetics, Public Health and Health Services, Allergy
Abstract: BackgroundThe clinical response to inhaled corticosteroids (ICS) is associated with single nucleotide polymorphisms (SNPs) in various genes. This study aimed to relate variations in genes in the steroid pathway and asthma susceptibility genes to exacerbations in children and young adults treated with ICS.MethodsWe performed a meta-analysis of three cohort studies: Pharmacogenetics of Asthma Medication in Children: Medication with Anti-Inflammatory effects (n = 357, age: 4-12 years, the Netherlands), BREATHE (n = 820, age: 3-22 years, UK) and Paediatric Asthma Gene Environment Study (n = 391, age: 2-16 years, UK). Seventeen genes were selected based on a role in the glucocorticoid signalling pathway or a reported association with asthma. Two outcome parameters were used to reflect exacerbations: hospital visits and oral corticosteroid (OCS) use in the previous year. The most significant associations were tested in three independent validation cohorts; the Childhood Asthma Management Programme (clinical trial, n = 172, age: 5-12 years, USA), the Genes- environment and Mixture in Latino Americans II- study (n = 745, age: 8-21, USA) and the Pharmacogenetics of adrenal suppression cohort (n = 391, age: 5-18, UK) to test the robustness of the findings. Finally, all results were meta-analysed.ResultsTwo SNPs in ST13 (rs138335 and rs138337), but not in the other genes, were associated at a nominal level with an increased risk of exacerbations in asthmatics using ICS in the three cohorts studied. In a meta-analysis of all six studies, ST13 rs138335 remained associated with an increased risk of asthma-related hospital visits and OCS use in the previous year; OR = 1.22 (P = 0.013) and OR = 1.22 (P = 0.0017), respectively.Conclusion and clinical relevanceA novel susceptibility gene, ST13, coding for a cochaperone of the glucocorticoid receptor, is associated with exacerbations in asthmatic children and young adults despite their ICS use. Genetic variation in the glucocorticoid signalling pathway may contribute to the interindividual variability in clinical response to ICS treatment in children and young adults.
Published: 2015

10. Genome-wide association analysis identifies six new loci associated with forced vital capacity

Author: Loth, DW, Artigas, MS, Gharib, SA, Wain, LV, Franceschini, N, Koch, B, Pottinger, TD, Smith, AV, Duan, Q, Oldmeadow, C, Lee, MK, Strachan, DP, James, AL, Huffman, JE, Vitart, V, Ramasamy, A, Wareham, NJ, Kaprio, J, Wang, XQ, Trochet, H, Kähönen, M, Flexeder, C, Albrecht, E, Lopez, LM, De Jong, K, Thyagarajan, B, Alves, AC, Enroth, S, Omenaas, E, Joshi, PK, Fall, T, Viñuela, A, Launer, LJ, Loehr, LR, Fornage, M, Li, G, Wilk, JB, Tang, W, Manichaikul, A, Lahousse, L, Harris, TB, North, KE, Rudnicka, AR, Hui, J, Gu, X, Lumley, T, Wright, AF, Hastie, ND, Campbell, S, Kumar, R, Pin, I, Scott, RA, Pietiläinen, KH, Surakka, I, Liu, Y, Holliday, EG, Schulz, H, Heinrich, J, Davies, G, Vonk, JM, Wojczynski, M, Pouta, A, Johansson, A, Wild, SH, Ingelsson, E, Rivadeneira, F, Völzke, H, Hysi, PG, Eiriksdottir, G, Morrison, AC, Rotter, JI, Gao, W, Postma, DS, White, WB, Rich, SS, Hofman, A, Aspelund, T, Couper, D, Smith, LJ, Psaty, BM, Lohman, K, Burchard, EG, Uitterlinden, AG, Garcia, M, Joubert, BR, McArdle, WL, Musk, AB, Hansel, N, Heckbert, SR, Zgaga, L, Van Meurs, JBJ, Navarro, P, Rudan, I, Oh, YM, Redline, S, Jarvis, DL, Zhao, JH, Rantanen, T, O'Connor, GT, and Ripatti, S
Subjects: Developmental Biology, Medical and Health Sciences, Biological Sciences
Abstract: Forced vital capacity (FVC), a spirometric measure of pulmonary function, reflects lung volume and is used to diagnose and monitor lung diseases. We performed genome-wide association study meta-analysis of FVC in 52,253 individuals from 26 studies and followed up the top associations in 32,917 additional individuals of European ancestry. We found six new regions associated at genome-wide significance (P < 5 × 10-8) with FVC in or near EFEMP1, BMP6, MIR129-2-HSD17B12, PRDM11, WWOX and KCNJ2. Two loci previously associated with spirometric measures (GSTCD and PTCH1) were related to FVC. Newly implicated regions were followed up in samples from African-American, Korean, Chinese and Hispanic individuals. We detected transcripts for all six newly implicated genes in human lung tissue. The new loci may inform mechanisms involved in lung development and the pathogenesis of restrictive lung disease.© 2014 Nature America, Inc. All rights reserved.
Published: 2014

11. Risk factors for chronic mucus hypersecretion in individuals with and without COPD: influence of smoking and job exposure on CMH

Author: Dijkstra, Akkelies E, de Jong, Kim, Boezen, H Marike, Kromhout, Hans, Vermeulen, Roel, Groen, Harry J M, Postma, Dirkje S, Vonk, Judith M, Alizadeh, BZ, de Boer, RA, Boezen, H M, Bruinenberg, M, Franke, L, van der Harst, P, Hillege, HL, van der Klauw, MM, Navis, G, Ormel, J, Postma, DS, Rosmalen, JGM, Slaets, JP, Snieder, H, Stolk, RP, Wolffenbuttel, BHR, and Wijmenga, C
Published: 2014
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12. Pesticides and other occupational exposures are associated with airway obstruction: the LifeLines cohort study

Author: de Jong, K, Boezen, H M, Kromhout, H, Vermeulen, R, Postma, D S, Vonk, J M, Alizadeh, BZ, de Boer, RA, Boezen, H M, Bruinenberg, M, Franke, L, van der Harst, P, Hillege, HL, van der Klauw, MM, Navis, G, Ormel, J, Postma, DS, Rosmalen, JGM, Slaets, JP, Snieder, H, Stolk, RP, Wolffenbuttel, BHR, and Wijmenga, C
Published: 2014
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13. Identifying a nasal gene expression signature associated with hyperinflation and treatment response in severe COPD

Author: Faiz A, Imkamp K, van der Wiel E, Boudewijn IM, Koppelman GH, Brandsma C-A, Kerstjens HAM, Timens W, Vroegop S, Pasma HR, Boersma WG, Wielders P, van den Elshout F, Mansour K, Steiling K, Spira A, Lenburg ME, Heijink IH, Postma DS, and van den Berge M
Subjects: respiratory system, respiratory tract diseases
Abstract: Hyperinflation contributes to dyspnea intensity in COPD. Little is known about the molecular mechanisms underlying hyperinflation and how inhaled corticosteroids (ICS) affect this important aspect of COPD pathophysiology. To investigate the effect of ICS/long-acting β2-agonist (LABA) treatment on both lung function measures of hyperinflation, and the nasal epithelial gene-expression profile in severe COPD. 117 patients were screened and 60 COPD patients entered a 1-month run-in period on low-dose ICS/LABA budesonide/formoterol (BUD/F) 200/6 one inhalation b.i.d. Patients were then randomly assigned to 3-month treatment with either a high dose BDP/F 100/6 two inhalations b.i.d. (n = 31) or BUD/F 200/6 two inhalations b.i.d. (n = 29). Lung function measurements and nasal epithelial gene-expression were assessed before and after 3-month treatment and validated in independent datasets. After 3-month ICS/LABA treatment, residual volume (RV)/total lung capacity (TLC)% predicted was reduced compared to baseline (p
Published: 2020

14. Differential lung tissue gene expression in males and females: implications for the susceptibility to develop COPD

Author: van den Berge M, Brandsma C-A, Faiz A, de Vries M, Rathnayake SNH, Paré PD, Sin DD, Bossé Y, Laviolette M, Nickle DC, Hao K, Obeidat M, Dragani TA, Colombo F, Timens W, and Postma DS
Subjects: 11 Medical and Health Sciences, 1116 Medical Physiology, Respiratory System
Published: 2019

15. Genetic loci associated with chronic obstructive pulmonary disease overlap with loci for lung function and pulmonary fibrosis

Author: Hobbs, BD, de Jong, K, Lamontagne, M, Bossé, Y, Shrine, N, Artigas, MS, Wain, LV, Hall, IP, Jackson, VE, Wyss, AB, London, SJ, North, KE, Franceschini, N, Strachan, DP, Beaty, TH, Hokanson, JE, Crapo, JD, Castaldi, PJ, Chase, RP, Bartz, TM, Heckbert, SR, Psaty, BM, Gharib, SA, Zanen, P, Lammers, JW, Oudkerk, M, Groen, HJ, Locantore, N, Tal-Singer, R, Rennard, SI, Vestbo, J, Timens, W, Paré, PD, Latourelle, JC, Dupuis, J, O'Connor, GT, Wilk, JB, Kim, WJ, Lee, MK, Oh, Y-M, Vonk, JM, de Koning, HJ, Leng, S, Belinsky, SA, Tesfaigzi, Y, Manichaikul, A, Wang, X-Q, Rich, SS, Barr, RG, Sparrow, D, Litonjua, AA, Bakke, P, Gulsvik, A, Lahousse, L, Brusselle, GG, Stricker, BH, Uitterlinden, AG, Ampleford, EJ, Bleecker, ER, Woodruff, PG, Meyers, DA, Qiao, D, Lomas, DA, Yim, J-J, Kim, DK, Hawrylkiewicz, I, Sliwinski, P, Hardin, M, Fingerlin, TE, Schwartz, DA, Postma, DS, MacNee, W, Tobin, MD, Silverman, EK, Boezen, HM, Cho, MH, COPDGene Investigators, ECLIPSE Investigators, LifeLines Investigators, SPIROMICS Research Group, International COPD Genetics Network Investigators, UK BiLEVE Investigators, and International COPD Genetics Consortium
Subjects: respiratory tract diseases
Abstract: Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality worldwide. We performed a genetic association study in 15,256 cases and 47,936 controls, with replication of select top results (P < 5 × 10(-6)) in 9,498 cases and 9,748 controls. In the combined meta-analysis, we identified 22 loci associated at genome-wide significance, including 13 new associations with COPD. Nine of these 13 loci have been associated with lung function in general population samples, while 4 (EEFSEC, DSP, MTCL1, and SFTPD) are new. We noted two loci shared with pulmonary fibrosis (FAM13A and DSP) but that had opposite risk alleles for COPD. None of our loci overlapped with genome-wide associations for asthma, although one locus has been implicated in joint susceptibility to asthma and obesity. We also identified genetic correlation between COPD and asthma. Our findings highlight new loci associated with COPD, demonstrate the importance of specific loci associated with lung function to COPD, and identify potential regions of genetic overlap between COPD and other respiratory diseases.
Published: 2017

16. TRPA1 gene polymorphisms and childhood asthma

Author: Gallo, V, Dijk, FN, Holloway, JW, Ring, SM, Koppelman, GH, Postma, DS, Strachan, DP, Granell, R, Jongste, Johan, Jaddoe, Vincent, den Dekker, Martijn, Duijts, Liesbeth, Henderson, AJ, Shaheen, SO, Groningen Research Institute for Asthma and COPD (GRIAC), Pediatrics, Epidemiology, and Erasmus MC other
Subjects: Generation R, AIRWAY INFLAMMATION, paracetamol, genotype, HYPERREACTIVITY, PIAMA BIRTH COHORT, Avon Longitudinal Study of Parents and Children, birth cohort, prenatal exposure, ASSOCIATION, asthma, PREVENTION, DISEASE, gene-environment interaction, transient receptor potential ankyrin-1, RECEPTOR POTENTIAL ANKYRIN-1, RODENTS, gene–environment interaction, ACETAMINOPHEN, Prevention and Incidence of Asthma and Mite Allergy, NEUROGENIC INFLAMMATION
Abstract: BackgroundAnimal data have suggested that the transient receptor potential ankyrin-1 (TRPA1) ion channel plays a key role in promoting airway inflammation in asthma and may mediate effects of paracetamol on asthma, yet confirmatory human data are lacking. To study associations of TRPA1 gene variants with childhood asthma and total IgE concentration, and interactions between TRPA1 and prenatal paracetamol exposure on these outcomes.MethodsWe analysed associations between 31 TRPA1 single nucleotide polymorphisms (SNPs) and current doctor-diagnosed asthma and total IgE concentration at 7.5 years in the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort. We sought to confirm the most significant associations with comparable outcomes in the Prevention and Incidence of Asthma and Mite Allergy (PIAMA) and Generation R birth cohorts. In ALSPAC, we explored interactions with prenatal paracetamol exposure.ResultsIn ALSPAC, there was strong evidence for association between six SNPs and asthma: rs959974 and rs1384001 (per-allele odds ratio for both: 1.30 (95% CI: 1.15–1.47), p = 0.00001), rs7010969 (OR 1.28 (1.13–1.46), p = 0.00004), rs3735945 (OR 1.30 (1.09–1.55), p = 0.003), rs920829 (OR 1.30 (1.09–1.54), p = 0.004) and rs4738202 (OR 1.22 (1.07–1.39), p = 0.004). In a meta-analysis across the three cohorts, the pooled effect estimates confirmed that all six SNPs were significantly associated with asthma. In ALSPAC, TRPA1 associations with asthma were not modified by prenatal paracetamol, although associations with IgE concentration were.ConclusionThis study suggests that TRPA1 may play a role in the development of childhood asthma. (249 words)
Published: 2017
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17. PTTG1IP and MAML3, novel GWAS genes for severity of hyperresponsiveness in adult asthma

Author: Nieuwenhuis, MA, Vonk, JM, Himes, BE, Sarnowski, C, Minelli, C, Jarvis, D, Bouzigon, E, Nickle, DC, Laviolette, M, Sin, D, Weiss, ST, Van den Berge, M, Koppelman, GH, and Postma, DS
Subjects: Science & Technology, Allergy, RECEPTOR, Immunology, asthma, VARIANTS, AIRWAY HYPERRESPONSIVENESS, RESPONSIVENESS, LUNG-FUNCTION, 1107 Immunology, E-CADHERIN, BRONCHIAL HYPERRESPONSIVENESS, genetics, TUMOR-TRANSFORMING GENE, BINDING-FACTOR, Life Sciences & Biomedicine, POLYMORPHISMS
Abstract: BACKGROUND: The severity of bronchial hyperresponsiveness (BHR) is a fundamental feature of asthma. The severity of BHR varies between asthmatics and is associated with lack of asthma control. The mechanisms underlying this trait are still unclear. This study aims to identify genes associated with BHR severity, using a genome wide association study (GWAS) on the slope of BHR in adult asthmatics. METHODS: We performed a GWAS on BHR severity in adult asthmatics from the Dutch Asthma GWAS cohort (n=650), adjusting for smoking and inhaled corticosteroid use, and verified results in 3 other cohorts. Furthermore, we performed eQTL and co-expression analyses in lung tissue. RESULTS: In the discovery cohort, one genome wide significant hit located in phosphodiesterase 4D, cAMP-specif (PDE4D) and 26 SNPs with p-values
Published: 2016

18. Novel childhood asthma genes interact with in utero and early-life tobacco smoke exposure

Author: Scholtens, S, Postma, DS, Moffatt, MF, Panasevich, S, Granell, R, Henderson, AJ, Melén, E, Nyberg, F, Pershagen, G, Jarvis, D, Ramasamy, A, Wjst, M, Svanes, C, Bouzigon, E, Demenais, F, Kauffmann, F, Siroux, V, Von Mutius, E, Ege, MJ, Braun-Fahrländer, C, Genuneit, J, Brunekreef, B, Smit, HA, Wijga, AH, Kerkhof, M, Curjuric, I, Imboden, M, Thun, GA, Probst-Hensch, N, Freidin, MB, Bragina, EI, Deev, IA, Puzyrev, VP, Daley, D, Park, J, Becker, A, Chan-Yeung, M, Kozyrskyj, AL, Pare, P, Marenholz, I, Lau, S, Keil, T, Lee, YA, Kabesch, M, Wijmenga, C, Franke, L, Nolte, IM, Vonk, J, Kumar, A, Farrall, M, Cookson, WOCM, Strachan, DP, Koppelman, GH, Boezen, HM, Life Course Epidemiology (LCE), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Groningen Research Institute for Asthma and COPD (GRIAC), and Stem Cell Aging Leukemia and Lymphoma (SALL)
Subjects: Candidate gene, Passive smoking, Immunology, Single-nucleotide polymorphism, VARIANTS, medicine.disease_cause, Polymorphism, Single Nucleotide, PARKIN, Tobacco smoke, 03 medical and health sciences, 0302 clinical medicine, Missing heritability problem, Genetic predisposition, medicine, Humans, Immunology and Allergy, Letter to the Editor, 030304 developmental biology, Asthma, Genetics, 0303 health sciences, business.industry, Microfilament Proteins, medicine.disease, 3. Good health, 030228 respiratory system, Maternal Exposure, Cardiovascular and Metabolic Diseases, Motile cilium, Female, Gene-Environment Interaction, Tobacco Smoke Pollution, business
Abstract: To the Editor: Complex diseases, including asthma, have genetic and environmental origins. Genome-wide association studies have identified multiple genes for the development of asthma, yet they only explain a limited proportion of asthma heritability. Interactions between genetic predisposition and exposure to passive smoking might explain in part the hidden heritability of childhood asthma. However, to date, this approach has not been reported for the discovery of interactions between genes and tobacco smoke exposure. We performed a genome-wide interaction study (GWIS) on childhood asthma to identify genes that interact with 2 well-known environmental risk factors for childhood-onset asthma: in utero and childhood tobacco smoke exposure. We meta-analyzed interaction results from 9 studies participating in the GABRIEL consortium1 including more than 6,000 subjects of European descent. We replicated our findings in 4 independent studies including more than 13,000 subjects. Childhood-onset asthma was defined as asthma diagnosed by a doctor before the age of 16 years, which is consistent with the definition in the GABRIEL consortium.1 In utero tobacco smoke exposure was defined as “exposure to maternal tobacco smoking at any time during pregnancy.” Childhood tobacco smoke exposure was defined as “exposure to passive tobacco smoking at any time from birth until 16 years of age.” Details on the number of subjects, the design of the individual studies, and outcome and exposure definitions are provided in Tables E1 to E4 in this article's Online Repository at www.jacionline.org. The effects of in utero tobacco smoke exposure and childhood tobacco smoke exposure were analyzed separately. All individual studies were analyzed by using a logistic regression model containing the genetic effect, the effect of tobacco smoke exposure, and an interaction term indicating the interaction between the genetic effect and tobacco smoke exposure. Further methodological considerations on GWISs and details on the statistical analyses are described in this article's Online Repository at www.jacionline.org. For in utero tobacco smoke exposure, the discovery genome-wide meta-analysis consisted of 2,654 cases and 3,073 control subjects derived from 7 studies (see Table E1). Overall, in utero tobacco smoke exposure increased the risk of childhood-onset asthma (see Fig E1 in this article's Online Repository at www.jacionline.org). A total of 536,705 single nucleotide polymorphisms (SNPs) were included in the interaction meta-analysis. Fig E2 in this article's Online Repository at www.jacionline.org shows the Manhattan plot. We identified 27 SNPs in the discovery sample with a P value of less than 10−4 based on the fixed effect model (Table I and see Table E5 in this article's Online Repository at www.jacionline.org). Findings did not reach genome-wide significance but were consistent over all studies included, and no significant heterogeneity across studies was present (P value Q-statistic < .05). Four of these SNPs on chromosome 10 were in high linkage disequilibrium with each other in the discovery meta-analysis (r2 = 0.82-0.96). The most prominent marker was located on chromosome 18 near EPB41L3 (Forest plot, see Fig E3 in this article's Online Repository at www.jacionline.org). Table E6 in this article's Online Repository at www.jacionline.org shows the associations in exposed and nonexposed subjects. EPB41L3 belongs to the protein 4.1 family of membrane-associated proteins, is involved in cell-cell junctions,2 and might play a role in apoptosis.3 The literature shows that in utero tobacco smoke exposure affects the expression of genes involved in biological processes, such as cell proliferation and apoptosis, and influences lung development of the child in general.4 Our data suggest that this effect of in utero smoke exposure might potentially occur through mechanisms involving EPB41L3 (see the additional text in this article's Online Repository). Table I Results of the GWIS of in utero tobacco smoke exposure and childhood-onset asthma For childhood tobacco smoke exposure, the discovery genome-wide meta-analysis consisted of 3,048 cases and 3,509 control subjects derived from 9 studies (see Table E1). Overall, childhood tobacco smoke exposure increased the risk of childhood-onset asthma (see Fig E1). A total of 538,233 SNPs were included in the interaction meta-analysis. Fig E4 in this article's Online Repository at www.jacionline.org shows the Manhattan plot. We identified 35 SNPs in the discovery sample with a P value of less than 10−4 based on the fixed effect model. Four of these SNPs were excluded because they showed heterogeneity, and the P value of the random effect was greater than 10−4. Findings did not reach genome-wide significance. Table II and Table E7 (see this article's Online Repository at www.jacionline.org) the results for the top SNPs. Seven SNPs on chromosome 5 (except rs2312164) were in high linkage disequilibrium with each other in the discovery studies (r2 = 0.83-1.00). Table II Results of the GWIS on childhood tobacco smoke exposure and childhood-onset asthma The most prominent marker was located on chromosome 6 in PACRG (parkin coregulated gene; Forest plot, see Fig E5 in this article's Online Repository at www.jacionline.org). Table E8 in this article's Online Repository at www.jacionline.org shows the associations in exposed and nonexposed subjects. PACRG is located next to and has an overlapping promoter region with parkin 2 (PARK2).5 The gene has been associated with leprosy and parkinsonian diseases and has an important role in motile cilia function and cilia morphogenesis.2,6 PACRG is relatively highly expressed in the trachea and nasal mucosa. Ciliary dysfunction might impair mucus clearance from the airways and has been shown to affect asthma severity. Our data suggest that changes in ciliary function particularly affect the development of asthma in children exposed to passive tobacco smoke. The genes that have been reported previously to interact with tobacco smoke exposure with respect to asthma development (ie, TNF,7 GSTP1,7 and ADAM338) were not among our most significant hits. This can be explained by the fact that the genetic variants in these candidate gene studies have a strong main effect on asthma development. Bouzigon et al9 showed a more pronounced effect of the 17q21 region on the development of early-onset asthma in children with early-life tobacco smoke exposure than in those without. The genetic effect of these markers in our GWIS showed a similar direction, but the interaction was not significant. This study on childhood asthma is the first hypothesis-free GWIS specifically aiming to identify SNPs that interact with tobacco smoke exposure in disease development. We found suggestive evidence for an interaction between rs8094633 on chromosome 18 near EPB41L3 and in utero tobacco smoke exposure and an interaction between rs1575472 on chromosome 6 in PACRG and childhood tobacco smoke exposure. The SNPs found have not been identified previously in general genome-wide association studies on childhood asthma. Interestingly, the SNPs interacting with in utero and childhood tobacco smoke exposure were different and were not involved in the same pathway (see Fig E6 in this article's Online Repository at www.jacionline.org). Interactions between these SNPs and tobacco smoke exposure in utero and in childhood might explain part of the missing heritability of asthma. Future research needs to confirm these findings and further unravel the biological pathways.
Published: 2016

19. Genome-wide association study on the FEV1/FVC ratio in never-smokers identifies HHIP and FAM13A

Author: van der Plaat, DA, de Jong, K, Lahousse, L, Faiz, A, Vonk, JM, van Diemen, CC, Nedeljkovic, I, Amin, N, Brusselle, GG, Hofman, A, Brandsma, C-A, Bossé, Y, Sin, DD, Nickle, DC, van Duijn, CM, Postma, DS, and Boezen, HM
Subjects: Adult, Male, Risk, Allergy, Adolescent, Genotype, Quantitative Trait Loci, Vital Capacity, Polymorphism, Single Nucleotide, Cohort Studies, Pulmonary Disease, Chronic Obstructive, Young Adult, Forced Expiratory Volume, Humans, Genetic Predisposition to Disease, Lung, Aged, Aged, 80 and over, Membrane Glycoproteins, GTPase-Activating Proteins, Smoking, Middle Aged, 1107 Immunology, Spirometry, Female, Carrier Proteins, Genome-Wide Association Study
Abstract: BACKGROUND: Although a striking proportion (25% to 45%) of patients with chronic obstructive pulmonary disease are never-smokers, most genetic susceptibility studies have not focused on this group exclusively. OBJECTIVE: The aim of this study was to identify common genetic variants associated with FEV1 and its ratio to forced vital capacity (FVC) in never-smokers. METHODS: Genome-wide association studies were performed in 5070 never-smokers of the identification cohort LifeLines, and results (P
Published: 2016

20. Multi-ancestry genome-wide association study of 21,000 cases and 95,000 controls identifies new risk loci for atopic dermatitis

Author: Paternoster, L, Standl, M, Waage, J, Baurecht, H, Hotze, M, Strachan, DP, Curtin, JA, Bonnelykke, K, Tian, C, Takahashi, A, Esparza-Gordillo, J, Alves, AC, Thyssen, JP, den Dekker, HT, Ferreira, MA, Altmaier, E, Sleiman, PMA, Xiao, FL, Gonzalez, JR, Marenholz, I, Kalb, B, Pino-Yanes, M, Xu, C-J, Carstensen, L, Groen-Blokhuis, MM, Venturini, C, Pennell, CE, Barton, SJ, Levin, AM, Curjuric, I, Bustamante, M, Kreiner-Moller, E, Lockett, GA, Bacelis, J, Bunyavanich, S, Myers, RA, Matanovic, A, Kumar, A, Tung, JY, Hirota, T, Kubo, M, McArdle, WL, Henderson, AJ, Kemp, JP, Zheng, J, Smith, GD, Rueschendorf, F, Bauerfeind, A, Lee-Kirsch, MA, Arnold, A, Homuth, G, Schmidt, CO, Mangold, E, Cichon, S, Keil, T, Rodriguez, E, Peters, A, Franke, A, Lieb, W, Novak, N, Foelster-Holst, R, Horikoshi, M, Pekkanen, J, Sebert, S, Husemoen, LL, Grarup, N, De Jongste, JC, Rivadeneira, F, Hofman, A, Jaddoe, VWV, Pasmans, SGMA, Elbert, NJ, Uitterlinden, AG, Marks, GB, Thompson, PJ, Matheson, MC, Robertson, CF, Ried, JS, Li, J, Zuo, XB, Zheng, XD, Yin, XY, Sun, LD, McAleer, MA, O'Regan, GM, Fahy, CMR, Campbell, LE, Macek, M, Kurek, M, Hu, D, Eng, C, Postma, DS, Feenstra, B, Geller, F, Hottenga, JJ, Middeldorp, CM, Hysi, P, Bataille, V, Spector, T, Tiesler, CMT, Thiering, E, Pahukasahasram, B, Yang, JJ, Imboden, M, Huntsman, S, Vilor-Tejedor, N, Relton, CL, Myhre, R, Nystad, W, Custovic, A, Weiss, ST, Meyers, DA, Soederhaell, C, Melen, E, Ober, C, Raby, BA, Simpson, A, Jacobsson, B, Holloway, JW, Bisgaard, H, Sunyer, J, Probst-Hensch, NM, Williams, LK, Godfrey, KM, Wang, CA, Boomsma, DI, Melbye, M, Koppelman, GH, Jarvis, D, McLean, WHI, Irvine, AD, Zhang, XJ, Hakonarson, H, Gieger-, C, Burchard, EG, Martin, NG, Duijts, L, Linneberg, A, Jarvelin, M-R, Noethen, MM, Lau, S, Huebner, N, Lee, Y-A, Tamari, M, Hinds, DA, Glass, D, Brown, SJ, Heinrich, J, Evans, DM, Weidinger, S, AAGC, AAGC, and Epidemio, EGL
Abstract: Genetic association studies have identified 21 loci associated with atopic dermatitis risk predominantly in populations of European ancestry. To identify further susceptibility loci for this common, complex skin disease, we performed a meta-analysis of >15 million genetic variants in 21,399 cases and 95,464 controls from populations of European, African, Japanese and Latino ancestry, followed by replication in 32,059 cases and 228,628 controls from 18 studies. We identified ten new risk loci, bringing the total number of known atopic dermatitis risk loci to 31 (with new secondary signals at four of these loci). Notably, the new loci include candidate genes with roles in the regulation of innate host defenses and T cell function, underscoring the important contribution of (auto)immune mechanisms to atopic dermatitis pathogenesis.
Published: 2015

21. A novel common variant in DCST2 is associated with length in early life and height in adulthood

Author: van der Valk RJ, Kreiner-Møller E, Kooijman MN, Guxens M, Stergiakouli E, Sääf A, Bradfield JP, Geller F, Hayes MG, Cousminer DL, Körner A, Thiering E, Curtin JA, Myhre R, Huikari V, Joro R, Kerkhof M, Warrington NM, Pitkänen N, Ntalla I, Horikoshi M, Veijola R, Freathy RM, Teo YY, Barton SJ, Evans DM, Kemp JP, St Pourcain B, Ring SM, Davey Smith G, Bergström A, Kull I, Hakonarson H, Mentch FD, Bisgaard H, Chawes B, Stokholm J, Waage J, Eriksen P, Sevelsted A, Melbye M, Early Genetics and Lifecourse Epidemiology (EAGLE) Consortium, van Duijn CM, Medina-Gomez C, Hofman A, de Jongste JC, Taal HR, Uitterlinden AG, Genetic Investigation of ANthropometric Traits (GIANT) Consortium, Armstrong LL, Eriksson J, Palotie A, Bustamante M, Estivill X, Gonzalez JR, Llop S, Kiess W, Mahajan A, Flexeder C, Tiesler CM, Murray CS, Simpson A, Magnus P, Sengpiel V, Hartikainen AL, Keinanen-Kiukaanniemi S, Lewin A, Da Silva Couto Alves A, Blakemore AI, Buxton JL, Kaakinen M, Rodriguez A, Sebert S, Vaarasmaki M, Lakka T, Lindi V, Gehring U, Postma DS, Ang W, Newnham JP, Lyytikäinen LP, Pahkala K, Raitakari OT, Panoutsopoulou K, Zeggini E, Boomsma DI, Groen-Blokhuis M, Ilonen J, Franke L, Hirschhorn JN, Pers TH, Liang L, Huang J, Hocher B, Knip M, Saw SM, Holloway JW, Melén E, Grant SF, Feenstra B, Lowe WL, Widén E, Sergeyev E, Grallert H, Custovic A, Jacobsson B, Jarvelin MR, Atalay M, Koppelman GH, Pennell CE, Niinikoski H, Dedoussis GV, Mccarthy MI, Frayling TM, Sunyer J, Timpson NJ, Rivadeneira F, Bønnelykke K, Jaddoe VW, and Early Growth Genetics (EGG) Consortium
Subjects: Genetic variants, DCST2, Single nucleotide polymorphisms (SNPs), Skeletal growth, Adult height, Early growth
Abstract: Common genetic variants have been identified for adult height, but not much is known about the genetics of skeletal growth in early life. To identify common genetic variants that influence fetal skeletal growth, we meta-analyzed 22 genome-wide association studies (Stage 1; N = 28 459). We identified seven independent top single nucleotide polymorphisms (SNPs) (P < 1 × 10(-6)) for birth length, of which three were novel and four were in or near loci known to be associated with adult height (LCORL, PTCH1, GPR126 and HMGA2). The three novel SNPs were followed-up in nine replication studies (Stage 2; N = 11 995), with rs905938 in DC-STAMP domain containing 2 (DCST2) genome-wide significantly associated with birth length in a joint analysis (Stages 1 + 2; β = 0.046, SE = 0.008, P = 2.46 × 10(-8), explained variance = 0.05%). Rs905938 was also associated with infant length (N = 28 228; P = 5.54 × 10(-4)) and adult height (N = 127 513; P = 1.45 × 10(-5)). DCST2 is a DC-STAMP-like protein family member and DC-STAMP is an osteoclast cell-fusion regulator. Polygenic scores based on 180 SNPs previously associated with human adult stature explained 0.13% of variance in birth length. The same SNPs explained 2.95% of the variance of infant length. Of the 180 known adult height loci, 11 were genome-wide significantly associated with infant length (SF3B4, LCORL, SPAG17, C6orf173, PTCH1, GDF5, ZNFX1, HHIP, ACAN, HLA locus and HMGA2). This study highlights that common variation in DCST2 influences variation in early growth and adult height. R.M.F. is supported by a Sir Henry Wellcome Postdoctoral Fellowship (Wellcome Trust grant 085541/Z/08/Z). T.H.P. is supported by The Danish Council for Independent Research Medical Sciences (FSS) The Alfred Benzon Foundation. B.F. is supported by an Oak Foundation fellowship. M.M. is a Wellcome Trust Senior Investigator (Wellcome Trust grant 090532) and a NIHR Senior Investigator. T.M.F. is supported by the European Research Council grant: SZ-245 50371- GLUCOSEGENES-FP7-IDEAS-ERC. F.R. (VIDI 016.136.367) and V.W.V.J. (VIDI 016.136.361) received grants from the Netherlands Organization for Health Research and Development.
Published: 2015

22. Susceptibility to Chronic Mucus Hypersecretion, a Genome Wide Association Study

Author: Dijkstra, Akkelies E., Smolonska, J, Van Den Berge, M, Wijmenga, C, Zanen, P, Luinge, MA, Platteel, M, Lammers, JW, Dahlback, M, Tosh, K, Hiemstra, PS, Sterk, PJ, Spira, A, Vestbo, J, Nordestgaard, BG, Benn, M, Nielsen, SF, Dahl, M, Verschuren, WM, Picavet, HSJ, Smit, HA, Owsijewitsch, M, Kauczor, HU, De Koning, HJ, Nizankowska-Mogilnicka, E, Mejza, F, Nastalek, P, Van Diemen, CC, Cho, MH, Silverman, EK, Crapo, JD, Beaty, TH, Lomas, DA, Bakke, Per, Gulsvik, Amund, Bosse, Y, Obeidat, MA, Loth, DW, Lahousse, L, Rivadeneira, F, Uitterlinden, AG, Hofman, A, Stricker, BH, Brusselle, GG, Van Duijn, CM, Brouwer, U, Koppelman, GH, Vonk, JM, Nawijn, MC, Groen, HJM, Timens, W, Boezen, HM, Postma, DS, Alizadeh, BZ, De Boer, RA, Bruinenberg, M, Franke, L, Van Der Harst, P, Hillege, HL, Van Der Klauw, MM, Navis, G, Ormel, J, Rosmalen, J, Slaets, JP, Snieder, H, Stolk, RP, Wolffenbuttel, B, Amsterdam institute for Infection and Immunity, Pulmonology, Clinical Chemistry, Public Health, Otorhinolaryngology and Head and Neck Surgery, Epidemiology, Internal Medicine, Groningen Research Institute for Asthma and COPD (GRIAC), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Life Course Epidemiology (LCE), Damage and Repair in Cancer Development and Cancer Treatment (DARE), and Guided Treatment in Optimal Selected Cancer Patients (GUTS)
Subjects: CHROMATIN, Male, Chronic bronchitis, Pulmonology, Epidemiology, OBSTRUCTIVE PULMONARY-DISEASE CHRONIC-BRONCHITIS GENETIC EPIDEMIOLOGY GENERAL-POPULATION BINDING-PROTEIN RISK-FACTORS COPD CHROMATIN SATB1 EXPRESSION, lcsh:Medicine, Genome-wide association study, Lung/metabolism, Mucus/metabolism, Drug Addiction, Matrix Attachment Region Binding Proteins/genetics, Recreational Drug Addiction, Cohort Studies, Pulmonary Disease, Chronic Obstructive, Medicine and Health Sciences, Psychology, Clinical Epidemiology, lcsh:Science, Lung, Cells, Cultured, GENETIC EPIDEMIOLOGY, GENERAL-POPULATION, Aged, 80 and over, education.field_of_study, Multidisciplinary, Medical sciences: 700::Basic medical, dental and veterinary sciences: 710::Medical genetics: 714 [VDP], Genomics, respiratory system, Middle Aged, 3. Good health, Functional Genomics, BINDING-PROTEIN, medicine.anatomical_structure, CHRONIC-BRONCHITIS, Genetic Epidemiology, Medical sciences: 700::Clinical medical sciences: 750::Lung diseases: 777 [VDP], Epidemiological Methods and Statistics, Female, medicine.symptom, Transcriptome Analysis, Medisinske fag: 700::Klinisk medisinske fag: 750::Lungesykdommer: 777 [VDP], Research Article, EXPRESSION, Adult, Chronic Obstructive Pulmonary Disease, Population, Addiction, Single-nucleotide polymorphism, Biology, Environmental and Occupational Lung Diseases, OBSTRUCTIVE PULMONARY-DISEASE, Polymorphism, Single Nucleotide, Environmental Epidemiology, SATB1, SDG 3 - Good Health and Well-being, medicine, Genome-Wide Association Studies, Genetics, SNP, COPD, Humans, education, Lifecourse Epidemiology, Aged, lcsh:R, Biology and Life Sciences, Computational Biology, Correction, Matrix Attachment Region Binding Proteins, Genome Analysis, Pulmonary Disease, Chronic Obstructive/genetics, Medisinske fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710::Medisinsk genetikk: 714 [VDP], Mucus, Genetic epidemiology, Immunology, Respiratory Infections, Chronic Disease, RISK-FACTORS, Sputum, lcsh:Q, Genome Expression Analysis, Genome-Wide Association Study
Abstract: Background: Chronic mucus hypersecretion (CMH) is associated with an increased frequency of respiratory infections, excess lung function decline, and increased hospitalisation and mortality rates in the general population. It is associated with smoking, but it is unknown why only a minority of smokers develops CMH. A plausible explanation for this phenomenon is a predisposing genetic constitution. Therefore, we performed a genome wide association (GWA) study of CMH in Caucasian populations. Methods: GWA analysis was performed in the NELSON-study using the Illumina 610 array, followed by replication and metaanalysis in 11 additional cohorts. In total 2,704 subjects with, and 7,624 subjects without CMH were included, all current or former heavy smokers (>= 20 pack-years). Additional studies were performed to test the functional relevance of the most significant single nucleotide polymorphism (SNP). Results: A strong association with CMH, consistent across all cohorts, was observed with rs6577641 (p = 4.25610(-6), OR = 1.17), located in intron 9 of the special AT-rich sequence-binding protein 1 locus (SATB1) on chromosome 3. The risk allele (G) was associated with higher mRNA expression of SATB1 (4.3610 29) in lung tissue. Presence of CMH was associated with increased SATB1 mRNA expression in bronchial biopsies from COPD patients. SATB1 expression was induced during differentiation of primary human bronchial epithelial cells in culture. Conclusions: Our findings, that SNP rs6577641 is associated with CMH in multiple cohorts and is a cis-eQTL for SATB1, together with our additional observation that SATB1 expression increases during epithelial differentiation provide suggestive evidence that SATB1 is a gene that affects CMH. Background: Chronic mucus hypersecretion (CMH) is associated with an increased frequency of respiratory infections, excess lung function decline, and increased hospitalisation and mortality rates in the general population. It is associated with smoking, but it is unknown why only a minority of smokers develops CMH. A plausible explanation for this phenomenon is a predisposing genetic constitution. Therefore, we performed a genome wide association (GWA) study of CMH in Caucasian populations. Methods: GWA analysis was performed in the NELSON-study using the Illumina 610 array, followed by replication and meta-analysis in 11 additional cohorts. In total 2,704 subjects with, and 7,624 subjects without CMH were included, all current or former heavy smokers (≥20 pack-years). Additional studies were performed to test the functional relevance of the most significant single nucleotide polymorphism (SNP). Results: A strong association with CMH, consistent across all cohorts, was observed with rs6577641 (p = 4.25x10 -6, OR = 1.17), located in intron 9 of the special AT-rich sequence-binding protein 1 locus (SATB1) on chromosome 3. The risk allele (G) was associated with higher mRNA expression of SATB1 (4.3x10 -9) in lung tissue. Presence of CMH was associated with increased SATB1 mRNA expression in bronchial biopsies from COPD patients. SATB1 expression was induced during differentiation of primary human bronchial epithelial cells in culture. Conclusions: Our findings, that SNP rs6577641 is associated with CMH in multiple cohorts and is a cis-eQTL for SATB1, together with our additional observation that SATB1 expression increases during epithelial differentiation provide suggestive evidence that SATB1 is a gene that affects CMH.
Published: 2013

23. Early growth genetics C. New loci associated with birgh weight identify genetic links between intrauterine growth and adult height and metabolism

Author: Horikoshi, M, Yaghootkar, H, Mook, Dennis, Sovio, U, Taal, Rob, Hennig, BJ, Bradfield, JP, St Pourcain, B, Evans, DM, Charoen, P, Kaakinen, M, Cousminer, DL, Lehtimaki, T, Kreiner-Moller, E, Warrington, NM, Bustamante, M, Feenstra, B, Berry, DJ, Thiering, E, Pfab, T, Barton, SJ, Shields, BM, Kerkhof, M, Leeuwen, Elisa, Fulford, AJ, Kutalik, Z, Zhao, JH, den Hoed, M, Mahajan, A, Lindi, V, Goh, LK, Hottenga, JJ (Jouke Jan), Wu, Fenny, Raitakari, OT, Harder, M, Meirhaeghe, A, Ntalla, I, Salem, RM, Jameson, KA, Zhou, K, Monies, D, Lagou, V, Kirin, M, Heikkinen, J, Adair, LS, Alkuraya, FS, Al-Odaib, A, Amouyel, P, Andersson, EAS, Bennett, AJ, Blakemore, AIF, Buxton, JL, Dallongeville, J, Das, Suman, de Geus, EJC, Estivill, X, Flexeder, C, Froguel, P, Geller, F, Godfrey, KM, Gottrand, F, Groves, CJ, Hansen, T, Hirschhorn, JN, Hofman, Bert, Hollegaard, MV, Hougaard, DM, Hypponen, E, Inskip, H, Isaacs, Aaron, Jorgensen, T, Kanaka-Gentenbein, C, Kemp, JP, Kiess, W, Kipelainen, TO, Klopp, N, Knight, BA, Kuzawa, CW, McMahon, G, Newnham, JP, Niinikoski, H, Oostra, Ben, Pedersen, L, Postma, DS, Ring, SM, Rivadeneira, Fernando, Robertson, NR, Sebert, S, Simell, O, Slowinski, T, Tiesler, CMT, Tonjes, A, Vaag, A, Viikari, JS, Vink, JM, Vissing, NH, Wareham, NJ, Willemsen, G, Witte, DR, Zhang, H, Zhao, J, Wilson, JF, Stumvoll, M, Prentice, AM, Meyer, BF, Pearson, ER, Boreham, CA, Cooper, C, Gilman, MW, Dedoussis, GV, Moreno, LA, Pedersen, O, Saarinen, M, Mohlke, KL, Boomsma, DI, Saw, SM, Lakka, TA, Korner, A, Loos, RJ, Ong, KK, Vollenweider, P, Duijn, Cornelia, Koppelman, GH, Hattersley, AT, Holloway, JW, Hocher, B, Heinrich, J, Power, C, Melbye, M, Guxens Junyent, Monica, Pennell, CE, Bonnelykke, K, Bisgaard, H, Eriksson, JG, Widen, E, Hakonarson, H, Uitterlinden, André, Pouta, A, Lawlor, DA, Smith, GD, Frayling, TM, McCarthy, M, Grant, SFA, Jaddoe, Vincent, Jarvelin, MR, Timpson, NJ, Prokopenko, I, Freathy, RM, Erasmus MC other, Epidemiology, Medical Microbiology & Infectious Diseases, Clinical Genetics, Internal Medicine, and Hematology
Published: 2013

24. Allergic Rhinitis and its Impact on Asthma (ARIA): Achievements in 10 years and future needs

Author: Bousquet J, Schünemann HJ, Samolinski B, Demoly P, Baena-Cagnani CE, Bachert C, Bonini S, Boulet LP, Bousquet PJ, Brozek JL, Canonica GW, Casale TB, Cruz AA, Fokkens WJ, Fonseca JA, van Wijk RG, Grouse L, Haahtela T, Khaltaev N, Kuna P, Lockey RF, Lodrup Carlsen KC, Mullol J, Naclerio R, O'Hehir RE, Ohta K, Palkonen S, Papadopoulos NG, Passalacqua G, Pawankar R, Price D, Ryan D, Simons FE, Togias A, Williams D, Yorgancioglu A, Yusuf OM, Aberer W, Adachi M, Agache I, Aït-Khaled N, Akdis CA, Andrianarisoa A, Annesi-Maesano I, Ansotegui IJ, Baiardini I, Bateman ED, Bedbrook A, Beghé B, Beji M, Bel EH, Ben Kheder A, Bennoor KS, Bergmann KC, Berrissoul F, Bieber T, Bindslev Jensen C, Blaiss MS, Boner AL, Bouchard J, Braido F, Brightling CE, Bush A, Caballero F, Calderon MA, Calvo MA, Camargos PA, Caraballo LR, Carlsen KH, Carr W, Cepeda AM, Cesario A, Chavannes NH, Chen YZ, Chiriac AM, Chivato Pérez T, Chkhartishvili E, Ciprandi G, Costa DJ, Cox L, Custovic A, Dahl R, Darsow U, De Blay F, Deleanu D, Denburg JA, Devillier P, Didi T, Dokic D, Dolen WK, Douagui H, Dubakiene R, Durham SR, Dykewicz MS, El-Gamal Y, El-Meziane A, Emuzyte R, Fiocchi A, Fletcher M, Fukuda T, Gamkrelidze A, Gereda JE, González Diaz S, Gotua M, Guzmán MA, Hellings PW, Hellquist-Dahl B, Horak F, Hourihane JO, Howarth P, Humbert M, Ivancevich JC, Jackson C, Just J, Kalayci O, Kaliner MA, Kalyoncu AF, Keil T, Keith PK, Khayat G, Kim YY, Koffi N'goran B, Koppelman GH, Kowalski ML, Kull I, Kvedariene V, Larenas-Linnemann D, Le LT, Lemière C, Li J, Lieberman P, Lipworth B, Mahboub B, Makela MJ, Martin F, Marshall GD, Martinez FD, Masjedi MR, Maurer M, Mavale-Manuel S, Mazon A, Melen E, Meltzer EO, Mendez NH, Merk H, Mihaltan F, Mohammad Y, Morais-Almeida M, Muraro A, Nafti S, Namazova-Baranova L, Nekam K, Neou A, Niggemann B, Nizankowska-Mogilnicka E, Nyembue TD, Okamoto Y, Okubo K, Orru MP, Ouedraogo S, Ozdemir C, Panzner P, Pali-Schöll I, Park HS, Pigearias B, Pohl W, Popov TA, Postma DS, Potter P, Rabe KF, Ratomaharo J, Reitamo S, Ring J, Roberts R, Rogala B, Romano A, Roman Rodriguez M, Rosado-Pinto J, Rosenwasser L, Rottem M, Sanchez-Borges M, Scadding GK, Schmid-Grendelmeier P, Sheikh A, Sisul JC, Solé D, Sooronbaev T, Spicak V, Spranger O, Stein RT, Stoloff SW, Sunyer J, Szczeklik A, Todo-Bom A, Toskala E, Tremblay Y, Valenta R, Valero AL, Valeyre D, Valiulis A, Valovirta E, Van Cauwenberge P, Vandenplas O, van Weel C, Vichyanond P, Viegi G, Wang DY, Wickman M, Wöhrl S, Wright J, Yawn BP, Yiallouros PK, Zar HJ, Zernotti ME, Zhong N, Zidarn M, Zuberbier T, World Health Organization Collaborating Center for Asthma, and Rhinitis.
Published: 2012

25. Blood pressure in 12-year-old children is associated with fatty acid composition of human milk

Author: van Rossem, Lenie, Wijga, AH, Jongste, Johan, Koppelman, GH, Oldenwening, M, Postma, DS, Abrahamse-Berkeveld, M, v.d. Heijning, B, Brunekreef, B, Smit, HA, Public Health, and Pediatrics
Published: 2012

26. Severe Chronic Allergic (and related) Diseases: a uniform approach- a MeDALL- GA(2)LEN-ARIA Position Paper

Author: WHO Collaborating Center for Asthma, Rhinitis, Bousquet, J, Anto, Jm, Demoly, P, Schünemann, Hj, Togias, A, Akdis, M, Auffray, C, Bachert, C, Bieber, T, Bousquet, Pj, Carlsen, Kh, Casale, Tb, Cruz, Aa, Keil, T, Lodrup Carlsen KC, Maurer, M, Ohta, K, Papadopoulos, Ng, Roman Rodriguez, M, Samolinski, B, Agache, I, Andrianarisoa, A, Ang, Cs, Annesi Maesano, I, Ballester, F, Baena Cagnani CE, Basagaña, X, Bateman, Ed, Bel, Eh, Bedbrook, A, Beghe', Bianca, Beji, M, Ben Kheder, A, Benet, M, Bennoor, Ks, Bergmann, Kc, Berrissoul, F, Bindslev Jensen, C, Bleecker, Er, Bonini, S, Boner, Al, Boulet, Lp, Brightling, Ce, Brozek, Jl, Bush, A, Busse, Ww, Camargos, Pa, Canonica, Gw, Carr, W, Cesario, A, Chen, Yz, Chiriac, Am, Costa, Dj, Cox, L, Custovic, A, Dahl, R, Darsow, U, Didi, T, Dolen, Wk, Douagui, H, Dubakiene, R, El Meziane, A, Fonseca, Ja, Fokkens, Wj, Fthenou, E, Gamkrelidze, A, Garcia Aymerich, J, Gerth van Wijk, R, Gimeno Santos, E, Guerra, S, Haahtela, T, Haddad, H, Hellings, Pw, Hellquist Dahl, B, Hohmann, C, Howarth, P, Hourihane, Jo, Humbert, M, Jacquemin, B, Just, J, Kalayci, O, Kaliner, Ma, Kauffmann, F, Kerkhof, M, Khayat, G, Koffi N'Goran, B, Kogevinas, M, Koppelman, Gh, Kowalski, Ml, Kull, I, Kuna, P, Larenas, D, Lavi, I, Le, Lt, Lieberman, P, Lipworth, B, Mahboub, B, Makela, Mj, Martin, F, Martinez, Fd, Marshall, Gd, Mazon, A, Melen, E, Meltzer, Eo, Mihaltan, F, Mohammad, Y, Mohammadi, A, Momas, I, Morais Almeida, M, Mullol, J, Muraro, A, Naclerio, R, Nafti, S, Namazova Baranova, L, Nawijn, Mc, Nyembue, Td, Oddie, S, O'Hehir, Re, Okamoto, Y, Orru, Mp, Ozdemir, C, Ouedraogo, Gs, Palkonen, S, Panzner, P, Passalacqua, G, Pawankar, R, Pigearias, B, Pin, I, Pinart, M, Pison, C, Popov, Ta, Porta, D, Postma, Ds, Price, D, Rabe, Kf, Ratomaharo, J, Reitamo, S, Rezagui, D, Ring, J, Roberts, R, Roca, J, Rogala, B, Romano, A, Rosado Pinto, J, Ryan, D, Sanchez Borges, M, Scadding, Gk, Sheikh, A, Simons, Fe, Siroux, V, Schmid Grendelmeier PD, Smit, Ha, Sooronbaev, T, Stein, Rt, Sterk, Pj, Sunyer, J, Terreehorst, I, Toskala, E, Tremblay, Y, Valenta, R, Valeyre, D, Vandenplas, O, van Weel, C, Vassilaki, M, Varraso, R, Viegi, G, Wang, Dy, Wickman, M, Williams, D, Wöhrl, S, Wright, J, Yorgancioglu, A, Yusuf, Om, Zar, Hj, Zernotti, Me, Zidarn, M, Zhong, N, Zuberbier, T., Beghe', B., Fthenou, E., Boudier, Anne, Hôpital Arnaud de Villeneuve [CHRU Montpellier], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM), IMIM-Hospital del Mar, Generalitat de Catalunya, Center for Research in Environmental Epidemiology (CREAL), Universitat Pompeu Fabra [Barcelona] (UPF)-Catalunya ministerio de salud, CIBER Epidemiologia y Salud Publica, CIBER de Epidemiología y Salud Pública (CIBERESP), Universitat Pompeu Fabra [Barcelona] (UPF), WHO Collaborating Center for Asthma and Rhinitis, Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Pharmacoepidemiologie et évaluation de l'impact des produits de santé sur les populations, Université Bordeaux Segalen - Bordeaux 2-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Clinical Epidemiology and Biostatistics and Medicine, McMaster University [Hamilton, Ontario], National Institute of Allergy and Infectious Diseases [Bethesda] (NIAID-NIH), National Institutes of Health [Bethesda] (NIH), Swiss Institute of Allergy and Asthma Research (SIAF), Universität Zürich [Zürich] = University of Zurich (UZH), Génomique fonctionnelle et biologie systémique pour la santé, Institut des Sciences Biologiques du CNRS, Upper Airway Research Laboratory (URL), Ghent University Hospital, Department of Dermatology and Allergy, VU University Medical Center [Amsterdam], Department of Paediatrics, University of Oslo (UiO)-Oslo University Hospital [Oslo], Division of Allergy and Immunology, Department of Medicine, Creighton University, ProAR - FMB, Federal University of Bahia School of Medicine, Epidemiology and Health Economics, Instittute of Social Health-Charité - UniversitätsMedizin = Charité - University Hospital [Berlin], Department of Dermatology, Medical School-Charité - UniversitätsMedizin = Charité - University Hospital [Berlin], Division of Respiratory Medicine and Allergology, Teikyo University School of Medicine, Allergy Department, 2nd Pediatric Clinic, Son Pisa Primary Care Centre, IB-Salut Balearic Health Service, Department of Prevention of Environmental Hazards and Allergology, Medical University of Warsaw - Poland-Faculté de Pharmacie de Paris, Department of Allergy and Clinical Immunology, Faculty of Medicine-Transylvania University, Public Hospital Medical Service, Ministry of Health [Mozambique], Epidémiologie des maladies infectieuses et modélisation (ESIM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Center for Public Health Research (CSISP), University of Valencia, Respiratory Medicine, Università degli studi di Genova = University of Genoa (UniGe)-School of Specialization, Faculty of Medicine, Catholic University, Health Sciences Faculty, University of Cape Town, Department of Pulmonology, University of Amsterdam [Amsterdam] (UvA)-Academic Medical Centre, Divisions of Human Genetics Infection, Inflammation and Repair, University of Southampton-School of Medicine, Service de Pneumologie Allergologie, Hôpital La Rabta [Tunis], Service de Pneumologie, Hôpital Abderrahmen Mami, National Asthma Centre, National Institute of Diseases of the Chest and Hospital (NIDCH), Pneumologie / Anesthésie - réanimation / Oxygénothérapie, Hôpital AKS Phnom Penh-Hôpital Provincial de Siemreap, Department of Dermatology and Allergy Center, Odense University Hospital, Center for Genomics and Personalized Medicine, Wake Forest University, Institute of Neurobiology and Molecular Medicine, CNR, Rome, Italy and Department of Medicine-University of Naples Federico II = Università degli studi di Napoli Federico II, Università degli studi di Verona = University of Verona (UNIVR), Institut de cardiologie et de pneumologie, Université Laval [Québec] (ULaval)-Centre Hospitalier de Laval (CH Laval), Department of Respiratory Medicine and Thoracic Surgery, University of Leicester-Institute for Lung Health, Department of Paediatric Respiratory Medicine, Imperial College London-Royal Brompton Hospital-National Heart and Lung Institute [UK], Department of Medicine, University of Wisconsin School of Medicine and Public Health, Department of Pediatrics, Universidade Federal de Minas Gerais [Belo Horizonte] (UFMG)-Medical School, Allergy & Respiratory Diseases, Università degli studi di Genova = University of Genoa (UniGe)-Department of Internal Medicine (DIMI), Allergy & Asthma Associates, University of California [Irvine] (UC Irvine), University of California (UC)-University of California (UC), Deputy Scientific Director, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Raffaele Pisana, Department of Thoracic Surgery, Università cattolica del Sacro Cuore = Catholic University of the Sacred Heart [Roma] (Unicatt), National Cooperative Group of Pediatric Research on Asthma, Asthma Clinic and Education Center of the Capital Institute of Pediatrics, Service des Premiers Soins, Université Montpellier 1 (UM1), Osteopathic College of Medicine, Nova Southeastern University (NSU), Respiratory Research Group, University of Manchester [Manchester]-School of Translational Medicine, Department of Respiratory Diseases, Aarhus University Hospital, Department of Dermatology and Allergy Biederstein, Technische Universität Munchen - Université Technique de Munich [Munich, Allemagne] (TUM), Service de pneumologie, Centre hospitalier de la région d'Annecy, Service de pneumo-allergologie, Centre Hospitalo-Universitaire de Béni-Messous, Allergy Centre, Vilnius University Antakalnis Hospital, Société Marocaine des Maladies Respiratoires, Centre of Respiratory Diseases and Allergy-Centre commercial Nadia, Allergy Division, Hospital S. João-Centre for Research in Health Technologies and Information Systems (CINTESIS)-Biostatistics and Medical Informatics Department-Porto University Medical School, Department of Otorhinolaryngology, Academic Medical Center - Academisch Medisch Centrum [Amsterdam] (AMC), University of Amsterdam [Amsterdam] (UvA)-University of Amsterdam [Amsterdam] (UvA), Department of Social Medicine, University of Crete [Heraklion] (UOC)-Faculty of Medicine, Health Care, Minister Of Labour-Ministry of Labor, Health and Social Affairs, Section of Allergology, Erasmus Medical Centre, Epidemiology and Biostatistics Division, University of Arizona-Associate Research Scientist, Respiratory Sciences-Arizona Respiratory Center, Helsinki University Hospital-Skin and Allergy Hospital, Centre Hospitalier de Bigorre [Tarbes]-Association Franco-Libanaise de Pneumologie (AFLP), Department of Otorhinolaryngology, Head, and Neck Surgery, University Hospital Leuven, Engineering and the Environment, University of Southampton, Paediatrics and Child Health, University College Cork (UCC), Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Antoine Béclère [Clamart], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre de l'Asthme et des Allergies [CHU Trousseau], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Pediatric Allergy and Asthma Unit, Ihsan Dogramaci Children's Hospital-Hacettepe University School of Medicine, Institute for Asthma and Allergy, George Washington University Medical School, Department of Epidemiology, University of Groningen [Groningen]-University Medical Center Groningen [Groningen] (UMCG)-Groningen Research Institute for Asthma and COPD (GRIAC), Université Saint-Joseph de Beyrouth (USJ)-Faculté de Médecine-Hôtel-Dieu de France, Service des Maladies Respiratoires, CHU de Cocody-UFR des Sciences Médicales, Pediatric Pulmonology, Allergology & Epidemiology, University of Groningen [Groningen]-University Medical Center Groningen [Groningen] (UMCG)-Beatrix Children's Hospital-Groningen Research Institute for Asthma and COPD, Department of Clinical Immunology and Allergy, Medical University of Łódź (MUL)-Faculty ot Medicine, Centre for Allergy Research, Karolinska Institutet [Stockholm], Department of Clinical Science and Education, Division of Internal Medicine, Asthma and Allergy, Medical University of Łódź (MUL)-Barlicki University Hospital, Hospital Medica Sur, Physiology Department, University of Medicine and Pharmacy, Division of Allergy Immunology, Department of Medicine-The University of Tennessee Health Science Center [Memphis] (UTHSC), university of dundee asthma - allergic rhinitis - COPD - beta-2-adrenoceptor, University of Dundee, Pulmonary and allergy unit, American University of Sharjah-Rashid Hospital-Dubai Health Authority (DHA), Association Franco-Vietnamienne de Pneumologie (AFVP), Centre Hospitalier de Compiègne (CHC), Arizona Respiratory Center, Department of Medicine, Clinical Immunology and Allergy, University of Mississippi Medical Center (UMMC), Institute of Environmental Medicine, Karolinska Institutet [Stockholm]-Karolinska University Hospital [Stockholm]-Astrid Lindgren Children's Hospital, Allergy & Asthma Medical Group & Research Center, University of California [San Diego] (UC San Diego), Pneumology Department, Marius Nasta Institute of Pneumology, Department of Internal Medicine, Tishreen University School of Medicine, Association Franco-Marocaine de Pathologie Thoracique (AFMAPATH), Collège National des Pneumologues Marocains, Epidémiologie Environnementale : Impact Sanitaire des Pollutions (EA 4064), Université Paris Descartes - Paris 5 (UPD5), Immunoallergy Department, Hospital CUF Descobertas, Rhinology Unit & Smell Clinic, Universitat de Barcelona (UB)-Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-Department of Medicine-Hospital Clinic-ENT Department, Allergy Unit, Università degli Studi di Padova = University of Padua (Unipd)-Department of Paediatrics, Section of Otolaryngology-Head & Neck Surgery (OHNS), University of Chicago, Clinique des maladies respiratoires, centre hospitalo-universitaire Mustapha Pacha d'Alger (CHUMA), Scientific Center for Children's Health, Russian Academy of Medical Sciences (RAMS), Laboratory of Allergology and Pulmonary Diseases, University of Groningen [Groningen]-University Medical Center Groningen [Groningen] (UMCG)-Department of Pathology and Medical Biology-GRIAC Research Institute, ENT Department, University of Kinshasa (UNIKIN), Bradford Neonatology, Bradford Teaching Hospitals NHS Foundation Trust-Bradford Institute for Health Research, Department of Allergy, Immunology and Respiratory Medicine, Alfred Hospital-Monash University Building, AMREP, Chiba University Hospital, Asthme Rhinite allergique, Pharmacie, Division of Pediatric Allergy and Immunology, marmara university, Pédiatrie, Centre Hospitalier National Pédiatrique Charles de Gaulle (CHNP-CDG), European Federation of Allergy (EFA), Airways Diseases Patients' Associations, Department of Allergology and Clinical Immunology, Charles University [Prague] (CU)-Medical Faculty in Pilsen, Immunopharmacology, Nippon Medical School-Medical Research Council Clinical, Laboratoire du Sommeil et de l'Effort, Société de Pneumologie de Langue Française (SPLF)-Clinique St George, Institut d'oncologie/développement Albert Bonniot de Grenoble (INSERM U823), Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de bioénergétique fondamentale et appliquée (LBFA), Université Joseph Fourier - Grenoble 1 (UJF)-Institut National de la Santé et de la Recherche Médicale (INSERM), Clinic of Allergy and Asthma, Medical University Sofia-Alexander's University Hospital, Regional Health Service - Lazio, Primary Care Respiratory Medicine, University of Aberdeen-Department of General Practice and Primary Care-General Practice Airways Group (GPIAG), Department of Pulmonary Medicine, Leiden University Medical Center (LUMC), Pneumalgia, Centre Hospitalier Regional-Espace Francophone de Pneumologie (EFP)-Société de Pneumologie de l'Océan Indien (SPOI), Association Franco-Algérienne de Pneumologie (AFAP), Espace Francophone de pneumologie de la SPLF, Department of Pneumology, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-Hospital Clínic de Barcelona-Institut Clínic del Tórax (ICT)-CIBER de Enfermedades Respiratorias (CIBERES)-University of Barcelona, Allergology and Clinical Immunology, Medical University of Silesia (SUM)-Chair and Clinical Department of Internal Diseases, UCSC-Allergy Unit, Complesso Integrato Columbus-Department of Internal Medicine and Geriatrics, Hospital da Luz, Medical Centre, Woodbrook Medical Centre, Research Fellow, University of Aberdeen-Department of General Practice, Centro Médico Docente La Trinidad, Department of Pharmacology, University College of London [London] (UCL)-The Royal National Throat, Nose and Ear Hospital, Primary Care Research & Development, University of Edinburgh-Centre for Population Health Sciences, Section of Allergy & Clinical Immunology, University of Manitoba [Winnipeg]-Department of Pediatrics & Child Health, Allergy Unit - Department of Dermatology, Julius Center for Health Sciences and Primary Care, University Medical Center [Utrecht], National Centre of Cardiology and Internal Medicine, Ministry of Health Kyrgyz Republic, School of Medicine, Pontifícia Universidade Católica, Department of ENT and Pediatrics, Finnish Institute of Occupational Health, Department of Obstetrics and Gynaecology, Université Laval [Québec] (ULaval)-Faculty of Medicine, Christian Doppler Laboratory for Allergy Research, Medizinische Universität Wien = Medical University of Vienna-Division of Immunopathology-Department of Pathophysiology and Allergy Research-Center for Pathophysiology, Infectiology and Immunology, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Avicenne [AP-HP], Department of Chest Medicine, Mont-Godinne Hospital-Catholic University of Louvain de Mont-Godinne, Department of Primary and Community Care, Radboud University Medical Center [Nijmegen], Epidemiology Unit, National Research Council (CNR)-Institute of Biomedicine and Molecular Immunology (IBIM), Pulmonary Environmental Epidemiology Unit, CNR Institute of Clinical Physiology, Department of Otolaryngology, National University of Singapore (NUS)-Yong Loo Lin School of Medicine, Karolinska Institutet [Stockholm]-Sachs' Children's Hospital, GLP Analytical Facility, School of Pharmacy, Department of Dermatology Division of Immunology, Allergy and Infectious Diseases (DIAID), Medical University of Vienna (MUW), Celal Bayar University School of Medicine, Allergy and Asthma Clinics, The Allergy and Asthma Institute, Department of Paediatrics and Child Health, Respiratory and Allergic Diseases, University Clinic of Respiratory and Allergic Diseases Golnik, State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases-Guangzhou Medical College, Secretary General of the Global Allergy and Asthma European Network (GA2LEN), Charité - UniversitätsMedizin = Charité - University Hospital [Berlin], In collaboration with the WHO Collaborating Center for Asthma and Rhinitis, University of Genoa (UNIGE)-School of Specialization, CNR, Rome, Italy and Department of Medicine-University of Naples Federico II, University of Verona (UNIVR), Medical School-Federal University of Minas Gerais, University of Genoa (UNIGE)-Department of Internal Medicine (DIMI), University of California [Irvine] (UCI), University of California-University of California, Catholic University Rome, University of Amsterdam [Amsterdam] (UvA)-Academic Medical Center - Academisch Medisch Centrum [Amsterdam] (AMC), University of Amsterdam [Amsterdam] (UvA), Centre Hospitalier de Bigorre (Tarbes)-Association Franco-Libanaise de Pneumologie (AFLP), CUF-Descobertas Hospital, Universita degli Studi di Padova-Department of Paediatrics, Medical Faculty in Pilsen-Charles University in Prague - the First Faculty of Medicine, Centro Medico-Docente La Trinidad, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Charité - UniversitätsMedizin = Charité - University Hospital [Berlin]-Instittute of Social Health, Department of Internal Medicine (DIMI)-University of Genoa (UNIGE), Medical University of Silesia-Chair and Clinical Department of Internal Diseases, Dermatology, Internal Medicine, Immunology, Hôpital Arnaud de Villeneuve, Centre Hospitalier Régional Universitaire [Montpellier] ( CHRU Montpellier ), Centre de recherche en épidémiologie et santé des populations ( CESP ), Université de Versailles Saint-Quentin-en-Yvelines ( UVSQ ) -Université Paris-Sud - Paris 11 ( UP11 ) -Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Center for Research in Environmental Epidemiology ( CREAL ), Universitat Pompeu Fabra [Barcelona]-Catalunya ministerio de salud, Universitat Pompeu Fabra [Barcelona], WHO(OMS), Université Bordeaux Segalen - Bordeaux 2-Université de Rouen Normandie ( UNIROUEN ), Normandie Université ( NU ) -Normandie Université ( NU ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), National Institute of Allergy and Infectious Diseases [Bethesda], National Institutes of Health ( NIH ), Swiss Institute of Allergy and Asthma Research ( SIAF ), University of Zürich [Zürich] ( UZH ), Upper Airway Research Laboratory ( URL ), University Medical Center, University of Oslo ( UiO ) -Oslo University Hospital, Charite-Universitatsmedizin Berlin [Berlin]-Instittute of Social Health, Medical School-Charité - University Medicine Berlin, Medical University of Warsaw-Faculté de Pharmacie de Paris, Ministry of Health, Epidémiologie des maladies infectieuses et modélisation ( ESIM ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Center for Public Health Research ( CSISP ), University of Genoa ( UNIGE ) -School of Specialization, University of Amsterdam [Amsterdam] ( UvA ) -Academic Medical Centre, University of Southampton [Southampton]-School of Medicine, Hôpital La Rabta [Tunis), Wake Forest University Health Sciences, CNR, Rome, Italy and Department of Medicine-Second University of Naples, Università degli Studi di Verona, Université Laval-l'Hôpital Laval, Imperial College London-Royal Brompton Hospital-National Heart and Lung Institute, University of Genoa ( UNIGE ) -Department of Internal Medicine (DIMI), Southern California Research, Université Montpellier 1 ( UM1 ), Nova Southeastern University, Technische Universität München [München] ( TUM ), Academic Medical Center [Amsterdam] ( AMC ), University of Amsterdam [Amsterdam] ( UvA ) -University of Amsterdam [Amsterdam] ( UvA ), University of Crete ( UOC ) -Faculty of Medicine, University of Southampton [Southampton], UUniversity College Cork - National University of Ireland, Cork (UCC), Université Paris-Sud - Paris 11 ( UP11 ) -Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Antoine Béclère, Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Trousseau [APHP], University of Groningen [Groningen]-University Medical Center Groningen-Groningen Research Institute for Asthma and COPD (GRIAC), Université Saint-Joseph de Beyrouth ( USJ ) -Faculté de Médecine-Hôtel-Dieu de France, University of Groningen [Groningen]-University Medical Center Groningen-Beatrix Children's Hospital-Groningen Research Institute for Asthma and COPD, Medical University of Łódź ( MUL ) -Faculty ot Medicine, Medical University of Łódź ( MUL ) -Barlicki University Hospital, Department of Medicine-University of Tennessee College for Medicine, Association Franco-Vietnamienne de Pneumologie ( AFVP ), University of Mississippi Medical Center, University of California [San Diego] ( UC San Diego ), Association Franco-Marocaine de Pathologie Thoracique ( AFMAPATH ), Epidémiologie Environnementale : Impact Sanitaire des Pollutions ( EA 4064 ), Université Paris Descartes - Paris 5 ( UPD5 ), Universitat de Barcelona ( UB ) -Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-Department of Medicine-Hospital Clinic-ENT Department, Section of Otolaryngology-Head & Neck Surgery ( OHNS ), University of Groningen [Groningen]-University Medical Center Groningen-Department of Pathology and Medical Biology-GRIAC Research Institute, University Hospital of Kinshasa, European Federation of Allergy ( EFA ), Institut d'oncologie/développement Albert Bonniot de Grenoble ( INSERM U823 ), Université Joseph Fourier - Grenoble 1 ( UJF ) -CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Bioenergétique fondamentale et appliquée ( LBFA ), Université Joseph Fourier - Grenoble 1 ( UJF ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Department of General Practice and Primary Care-General Practice Airways Group (GPIAG)-University of Aberdeen, Association Franco-Algérienne de Pneumologie ( AFAP ), Department of General Practice-University of Aberdeen, University College of London [London] ( UCL ) -The Royal National Throat, Nose and Ear Hospital, University Medical Center Utrecht, Faculty of Medicine-Laval University [Québec], Medical University of Vienna-Division of Immunopathology-Department of Pathophysiology and Allergy Research-Center for Pathophysiology, Infectiology and Immunology, Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Avicenne, National University of Singapore ( NUS ) -Yong Loo Lin School of Medicine, Department of Dermatology Division of Immunology, Allergy and Infectious Diseases ( DIAID ), Secretary General of the Global Allergy and Asthma European Network ( GA2LEN ), Network of Excellence, Charité - Universitätsmedizin Berlin, CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK (BIHR), Universiteit Leiden-Universiteit Leiden, and Medizinische Universität Wien = Medical University of Vienna
Subjects: MESH: Asthma, severity, MESH: Comorbidity, Comorbidity, Severity of Illness Index, urticaria, MESH : Chronic Disease, MESH: Practice Guidelines as Topic, MESH : Dermatitis, Atopic, MESH: Urticaria, risk, 216-31 [Rhinitis, atopy, allergen Int Arch Allergy Immunol. 2012,158(3)], atopic dermatitis, MESH : Rhinitis, MESH: Rhinitis, [ SDV.SPEE ] Life Sciences [q-bio]/Santé publique et épidémiologie, Effective primary care and public health [NCEBP 7], Immunoglobulin E - Asthma - Rhinitis - Rhinosinusitis - Urticaria - Atopic dermatitis, MESH : Practice Guidelines as Topic, Practice Guidelines as Topic, MESH : Comorbidity, MESH : Severity of Illness Index, IgE, MESH: Sinusitis, MESH : Urticaria, MESH: Hypersensitivity, macromolecular substances, MESH : Asthma, Dermatitis, Atopic, rhinitis, SDG 3 - Good Health and Well-being, MESH: Dermatitis, Atopic, MESH: Severity of Illness Index, Hypersensitivity, Humans, Sinusitis, rhinosinusitis, MESH : Hypersensitivity, MESH: Humans, MESH: Chronic Disease, MESH : Humans, Asthma, Atopic dermatitis, Immunoglobulin E, Rhinitis, Rhinosinusitis, Urticaria, asthma, allergy, MESH : Sinusitis, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, Chronic Disease, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, control
Abstract: Concepts of disease severity, activity, control and responsiveness to treatment are linked but different. Severity refers to the loss of function of the organs induced by the disease process or to the occurrence of severe acute exacerbations. Severity may vary over time and needs regular follow-up. Control is the degree to which therapy goals are currently met. These concepts have evolved over time for asthma in guidelines, task forces or consensus meetings. The aim of this paper is to generalize the approach of the uniform definition of severe asthma presented to WHO for chronic allergic and associated diseases (rhinitis, chronic rhinosinusitis, chronic urticaria and atopic dermatitis) in order to have a uniform definition of severity, control and risk, usable in most situations. It is based on the appropriate diagnosis, availability and accessibility of treatments, treatment responsiveness and associated factors such as comorbidities and risk factors. This uniform definition will allow a better definition of the phenotypes of severe allergic (and related) diseases for clinical practice, research (including epidemiology), public health purposes, education and the discovery of novel therapies. Copyright (C) 2012 S. Karger AG, Basel
Published: 2012

27. Метаанализ геномных ассоциаций выявил новые локусы, ассоциированные с ожирением у детей

Author: Bradfield, Jp, Taal, Hr, Timpson, Nj, Scherag, A., Lecoeur, C., Warrington, Nm, Hypponen, E., Holst, C., Valcarcel, B., Thiering, E., Salem, Rm, Schumacher, Fr, Cousminer, Dl, Sleiman, Pm, Zhao, J., Berkowitz, Ri, Vimaleswaran, Ks, Jarick, I., Pennell, Ce, Evans, Dm, St, Pourcain, Berry, Dj, Mook-kanamori, Do, Hofman, A., Rivadeneira, F., Uitterlinden, Ag, Van, Duijn, VAN DER VALK RJ, De, Jongste, Postma, Ds, Boomsma, Di, Gauderman, Wj, Hassanein, Mt, Lindgren, Cm, Mägi, R., Boreham, Ca, Neville, Ce, Moreno, La, Elliott, P., Pouta, A., Hartikainen, Al, Li, M., Raitakari, O., Lehtimäki, T., Eriksson, Jg, Palotie, A., Dallongeville, J., Das, S., Deloukas, P., Mcmahon, G., Ring, Sm, Kemp, Jp, Buxton, Jl, Blakemore, Ai, Bustamante, M., Guxens, M., Hirschhorn, Jn, Gillman, Mw, Kreiner-møller, E., Bisgaard, H., Gilliland, Fd, Heinrich, J., Wheeler, E., Barroso, I., O'rahilly, S., Meirhaeghe, A., Sørensen, Ti, Power, C., Palmer, Lj, Hinney, A., Widen, E., Farooqi, Is, Mccarthy, Mi, Froguel, P., Meyre, D., Hebebrand, J., Jarvelin, Mr, Jaddoe, Vw, Smith, Gd, Hakonarson, H., and Grant, Sf
Published: 2012

28. Prevalence of asthma in young children Reply

Author: Wijga, A, Tabak, C, Postma, DS, Kerkhof, Marjon, Wieringa, Marjan, Hoekstra, MO, Brunekreef, B, Jongste, Johan, Smit, HA, Groningen Research Institute for Asthma and COPD (GRIAC), Gastroenterology & Hepatology, Otorhinolaryngology and Head and Neck Surgery, and Pediatrics
Published: 2011

29. Reply

Author: Wijga, A, Tabak, C, Postma, DS, Kerkhof, M, Wieringa, Marjan, Hoekstra, MO, Jongste, Johan, Smit, HA, Otorhinolaryngology and Head and Neck Surgery, and Pediatrics
Published: 2011

30. Toll-like receptor 2 and 4 genes influence susceptibility to adverse effects of traffic-related air polution on childhood asthma

Author: Kerkhof, M, Postma, DS, Brunekreef, B, Reijmerink, NE, Wijga, AH, Jongste, Johan, Gehring, U, Koppelman, GH, and Pediatrics
Published: 2010

31. Smoking cessation: a critical investigative tool in COPID

Author: Willemse, BWM, ten Hacken, NHT, Postma, DS, Timens, W, Lifestyle Medicine (LM), Groningen Research Institute for Asthma and COPD (GRIAC), and Guided Treatment in Optimal Selected Cancer Patients (GUTS)
Published: 2006

32. Detrimental effects of beta-blockers in COPD - A concern for nonselective beta-blockers

Author: van der Woude, HJ, Zaagsma, J, Postma, DS, Winter, TH, van Hulst, M, Aalbers, R, Groningen Research Institute of Pharmacy, and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: airway hyperresponsiveness, respiratory system, EUROPEAN RESPIRATORY SOCIETY, OBSTRUCTIVE PULMONARY-DISEASE, respiratory tract diseases, SEVERE BRONCHOCONSTRICTION, OFFICIAL STATEMENT, RESPONSIVENESS, AIR-FLOW OBSTRUCTION, LUNG-FUNCTION, beta-blockers, CHRONIC-BRONCHITIS, METHACHOLINE, COPD, WORKING PARTY STANDARDIZATION, circulatory and respiratory physiology
Abstract: Introduction: beta-Blockers are known to worsen FEV1 and airway hyperresponsiveness (AHR) in patients with asthma. Both characteristics determine the outcome of COPD, a disease with frequent cardiac comorbidity requiring beta-blocker treatment. Design: A double-blind, placebo-controlled, randomized, cross-over study. Setting: An ambulatory, hospital outpatient clinic of pulmonary diseases. Patients: Patients with mild-to-moderate irreversible COPD and AHR. Intervention: Fifteen patients received propranolol (80 mg), metoprolol (100 mg), celiprolol (200 mg), or placebo for 4 days, followed by a washout period >= 3 days. On day 4 of treatment, FEV1 and PC20 were assessed. Immediately hereafter, formoterol (12 mu g) was administered and FEV1 was measured for up to 30 min. Results: PC20 was significantly lower (p
Published: 2005

33. The influence of intravenous hydrocortisone on cytokine levels in children with asthma

Author: Landstra, AM, Kauffman, HF, Boezen, HM, van Aalderen, WMC, Zonderland, J, Postma, DS, Amsterdam institute for Infection and Immunity, Paediatric Pulmonology, Life Course Epidemiology (LCE), and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: IL-5, IL-8, INTERFERON-GAMMA, IL-4, cortisol, asthma, PERIPHERAL-BLOOD, IFN gamma, BLOOD MONONUCLEAR-CELLS, BRONCHOALVEOLAR LAVAGE, NOCTURNAL ASTHMA, ATOPIC ASTHMA, children, IL-5 MESSENGER-RNA, T-LYMPHOCYTES, ALLERGEN CHALLENGE, hydrocortisone, INDUCED SPUTUM
Abstract: Nocturnal airway obstruction occurs frequently in childhood asthma and results from increased airway inflammation. Lymphocytes are believed to be key effector cells of airway wall inflammation, releasing pro-inflammatory mediators and cytokines. A previous study showed that hydrocortisone infusion, an effective anti-inflammatory treatment, improves nocturnal and daytime FEV1 values. This study in 16 children with moderate asthma was designed to assess whether there exists day and night differences in IL-4, IL-5, IL-8, and IFN-γ production of concanavaline A stimulated peripheral blood mononuclear cells. Furthermore, we investigated whether substitution of low serum cortisol levels with intravenous hydrocortisone would affect those parameters. Saline (as a placebo) or hydrocortisone (30 μ g/m(2) body surface area/24 h) was intravenously administered in a randomized, double blind, cross-over design. Measurements under saline or hydrocortisone infusions were separated by 1 wk. At 04:00 and 16:00 hours 10 ml blood was taken for determination of peripheral blood mononuclear cell isolation and stimulation, and an eosinophil count. Hydrocortisone infusion significantly reduced the nocturnal fall in FEV1. Median values of IFNγ, IL-4, IL-5, and IL-8 produced by peripheral blood mononuclear cells did not significantly differ at 04:00 and 16:00 hours, both with saline and hydrocortisone infusion. Our results suggest that FEV1 improvement is not due to suppression of circulating peripheral blood mononuclear cell activation. We hypothesize that it is rather due to its effect on local lung tissue epithelial and/or fibroblasts thereby reducing airway inflammation and vascular leakage.
Published: 2005

34. Haem oxygenase-1 expression is diminished in alveolar macrophages of patients with COPD

Author: Slebos, DJ, Kerstjens, HAM, Rutgers, [No Value], Kauffman, HF, Choi, AMK, Postma, DS, and Groningen Research Institute for Asthma and COPD (GRIAC)
Published: 2004

35. Provocation with adenosine 5 '-monophosphate, but not methacholine, induces sputum eosinophilia

Author: van den Berge, M, Kerstjens, HAM, de Reus, DM, Koeter, GH, Kauffman, HF, Postma, DS, and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: AIRWAY INFLAMMATION, CYTOKINES, sputum, IN-VITRO, respiratory system, adenosine 5 '-monophosphate, ENDOTHELIAL-CELLS, respiratory tract diseases, ASTHMATIC SUBJECTS, INHALED LEUKOTRIENE D-4, hyper-responsiveness, adenosine, inflammation, DEPENDENT HISTAMINE-RELEASE, HUMAN MAST-CELL, CHALLENGE, MEDIATED MECHANISM
Abstract: Introduction Bronchial hyper-responsiveness is usually measured with direct stimuli such as methacholine (MCh) or histamine. Adenosine 5'-monophosphate (AMP), which acts indirectly via the secondary release of mediators, is another stimulus to measure bronchial hyper-responsiveness. Aim To investigate whether provocation with inhaled AMP itself initiates an inflammatory response resulting in an influx of eosinophils into the airway lumen. Methods We have included 21 non-smoking atopic asthmatic subjects (mean FEV1 101% predicted, mean age 34 years). Each subject performed three sputum inductions on different days, at least seven days apart: one without previous provocation, one hour after PC20 methacholine, and one hour after PC20 AMP. Results After provocation with AMP, but not methacholine, the percentage of sputum eosinophils increased significantly (from 1.9+/-0.5% to 4.5+/-1% (P Conclusion A provocation test with AMP leads to an increased percentage of sputum eosinophils. This observation cannot be explained by a non-specific response of the airways to a vigorous bronchoconstriction, since methacholine had no effect on inflammatory cells.
Published: 2004

36. ADAM33 gene: confirming a gene without linkage

Author: Postma, DS, Howard, T, and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: BRONCHIAL HYPERRESPONSIVENESS, ASTHMA, POPULATIONS, ASSOCIATION, DISINTEGRIN
Published: 2004

37. Association of a disintegrin and metalloprotease 33 (ADAM33) gene with asthma in ethnically diverse populations

Author: Howard, TD, Postma, DS, Jongepier, H, Moore, WC, Koppelman, GH, Zheng, SQL, Bleecker, ER, Meyers, DA, and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: haplotype, SUSCEPTIBILITY LOCI, IDENTIFICATION, ATOPY, ADAM33, association, IGE, asthma, MOUSE, respiratory tract diseases, FAMILY
Abstract: Background: Asthma is a complex genetic disease characterized by reversible intermittent airway obstruction and respiratory symptoms primarily caused by acute and chronic bronchial inflammation. Recently, a gene potentially involved in airway remodeling, a disintegrin and metalloprotease 33 (ADAM33), was implicated in asthma susceptibility. Objective: We sought to determine whether polymorphisms in ADAM33 are associated with asthma or closely related phenotypes in 4 different asthma populations. Methods: Eight single nucleotide polymorphisms (SNPs) were evaluated in the 3' portion of ADAM33 in 4 unique asthma populations (African American, US white, US Hispanic, and Dutch white). These SNPs were previously reported to be associated with asthma in white populations from the United States and United Kingdom. Results: Significant associations were observed with at least one SNP and asthma in each population (P = .0009-.04). Related phenotypes that included total serum IgE levels and skin test responsiveness were also associated (P = .003-.05). However, no single SNP was associated across all populations. Additionally, haplotype analysis revealed that no single haplotype accounted for asthma susceptibility risk, although potential risk haplotypes existed within some of the populations. Conclusion: Replication of the original ADAM33 findings in these 4 additional asthma populations suggests that this gene (and perhaps others that interact with it) is important in the development and pathogenesis of asthma.
Published: 2003

38. Effect of SCH55700, a humanized anti-human interleukin-5 antibody, in severe persistent asthma - A pilot study 164/rccm.200206-5250C

Author: Kips, JC, O'Connor, BJ, Langley, SJ, Woodcock, A, Kerstjens, HAM, Postma, DS, Danzig, M, Cuss, F, Pauwels, RA, Faculteit Medische Wetenschappen/UMCG, and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: EXPRESSION, EOSINOPHILIA, anti-human interleukin-5 antibody, MONOCLONAL-ANTIBODY, BRONCHIAL-MUCOSA, BONE-MARROW, glucocorticosteroids, asthma, IL-5 RECEPTOR, AIRWAY HYPERRESPONSIVENESS, T-CELLS, MAST-CELLS, eosinophil, interleukin-5, MESSENGER-RNA
Abstract: Antagonizing the effect of interleukin (IL)-5 is a potential new treatment strategy in allergic disorders. We evaluated the safety, biological activity, and pharmacokinetics of SCH55700, a humanized anti-human IL-5 antibody, in subjects with severe persistent asthma treated with oral or high doses of inhaled steroids. In a double-blind, randomized, multicenter trial, a rising single dose of SCH55700 (0.03 mg/kg [n = 2], 0.1 mg/kg [n = 4], 0.3 mg/kg [n = 6], or 1.0 mg/kg [n = 12]) or placebo (n = 8) was administered intravenously. SCH55700 dose dependently reduced circulating eosinophil counts. At a dose of 1.0 mg/kg, the decrease remained significant up to Day 30 [(0.07 +/- 0.01) X 10(9)/L versus (0.23 +/- 0.04) x 10(9)/L at baseline] (mean +/- SEM) (p = 0.05). After administration of SCH55700 at 0.3 and 1.0 mg/kg, a trend toward improvement in baseline FEV1 was observed, which reached significance 24 hours after the 0.3-mg/kg dose (p = 0.019 versus placebo). No significant changes occurred in other clinical indices of disease activity. Adverse events were not different between active treatment and placebo. We conclude that SCH55700 is a biologically active anti-human IL-5 antibody that can be safely used in severe steroid-treated asthma. Its therapeutic potential needs to be addressed in specifically designed efficacy trials.
Published: 2003

39. Bronchial responsiveness to adenosine-5-monophosphate and methacholine as predictors for nasal symptoms due to newly introduced allergens . A fellow-up study among laboratory animal workers and bakery apprentices

Author: de Meer, G, Postma, DS, Heederik, D, Universiteit Utrecht, Faculteit Diergeneeskunde, and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: bronchial hyper-responsiveness, follow‐up study, Coronacrisis-Taverne, RISK FACTOR, RHINITIS, occupational allergy, follow-up study, respiratory system, AIRWAY HYPERRESPONSIVENESS, respiratory tract diseases, SENSITIZATION, RESPIRATORY SYMPTOMS, INFLAMMATION, adenosine, methacholine, ADOLESCENTS, ASTHMA, COHORT, bronchial hyper‐responsiveness, ADENOSINE 5'-MONOPHOSPHATE
Abstract: Background In asthma patients, bronchial hyper‐responsiveness (BHR) to adenosine‐5′‐monophosphate (AMP) reflects bronchial inflammation more closely than BHR to methacholine. In this follow‐up study we studied bronchial responsiveness to both stimuli as predictors of new‐onset airway symptoms. Methods We included 118 laboratory animal workers and bakery apprentices with a work experience of maximally 1 year. The baseline survey comprised a questionnaire, skin prick tests (SPTs) to common and work allergens, blood eosinophil counting, and bronchial challenge with methacholine and AMP. At follow‐up, questionnaire and SPTs to work allergens were repeated. Airway symptoms to common allergens and work allergens were defined as nasal symptoms, chest tightness or asthma attack during or after contact with either common or work allergen. Bronchial challenge tests were analysed by BHR at a 15% fall in forced expiratory volume of 1 s (FEV1), and by dose–response‐slope (DRS). Results Fourteen subjects (12%) developed airway symptoms to work allergens, of whom 12 had nasal symptoms. A positive SPT to work allergens occurred in 64%, and was the strongest predictor of airway symptoms [relative risk (RR) 7.5, 95% confidence interval (CI) 2.0–28.6]. Other predictors were airway symptoms to common allergens (RR 4.3, 95% CI 1.4–12.8), blood hypereosinophilia (RR 4.4, 95% CI 1.2–15.4) and BHR, with a slightly higher risk estimate for AMP than for methacholine (RRAMP 3.7, 95% CI 1.1–12.5 and RRmeth 2.8, 95% CI 1.0–8.5). The difference was more distinct analysing airway responsiveness by DRS, for which AMP predicted symptoms better than methacholine (P
Published: 2003

40. Provocation with adenosine 5 '-monophosphate increases sputum eosinophils

Author: van den Berge, M, Kerstjens, HAM, Kauffman, HF, Koeter, GH, Postma, DS, and Groningen Research Institute for Asthma and COPD (GRIAC)
Published: 2003

41. Guidelines and shared care for asthma and COPD

Author: Postma, DS and Groningen Research Institute for Asthma and COPD (GRIAC)
Abstract: Shared-care constructions between general practitioners and pulmonary physicians are seemingly attractive for asthma and COPD patients. Thus they have to be implemented in further guidelines. However, anticipation that rapid changes will occur in treatment options towards optimal disease management justifies rapid adjustments in these strategies and requires investigations as to their ultimate benefit in disease outcome.
Published: 2003

42. Sibling effect on atopy in children of patients with asthma

Author: Koppelman, GH, Jansen, DF, Schouten, JP, van der Heide, S, Bleecker, ER, Meyers, DA, Postma, DS, and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: HAY-FEVER, BIRTH-ORDER, sibling effect, atopy, skin test, specific IgE, CHILDHOOD, FAMILY-SIZE, SIBSHIP SIZE, ALLERGIC SENSITIZATION, asthma, RESPIRATORY SYMPTOMS, HIGH-RISK, CD14 GENE, IgE, SERUM IMMUNOGLOBULIN-E
Abstract: Background Multiple population studies have shown the presence of a sibling effect on atopic disease. However, it is unclear if the sibling effect is also of importance in subjects who are genetically at high risk for the development of atopy. Objective To study the presence of a sibling effect on markers of atopy (serum total IgE, specific IgE, skin tests) and asthma (bronchial hyper-responsiveness to histamine) in families ascertained through a parent with asthma. Methods First-degree offspring in 200 asthma families were studied (n = 541). Mixed effects regression models were used to account for the dependence of the observations within a family, and to adjust for possible confounding variables. Results Multiple regression analysis showed that having older siblings was inversely related to atopy, defined as greater than or equal to 2, greater than or equal to 3, greater than or equal to 4, or greater than or equal to 5 skin tests (P = 0.07-0.009). In addition, family size (number of siblings) had a significant protective effect on the presence of specific IgE to common aeroallergens (P = 0.03). Exposure to cigarette smoke in the first 3 years of life significantly increased the risk of having specific IgE to common aeroallergens (P = 0.04). No sibling effect was detected for serum total IgE or bronchial hyper-responsiveness to histamine. Conclusions This study shows a protective sibling effect on the presence and severity of atopy but not on bronchial hyper-responsiveness in children who are genetically at risk. The identification of the sibling effect in high-risk families stresses the need to understand the basis of this effect, in order to design future prevention programmes.
Published: 2003

43. In memoriam - Benjamin Burrows, MD, 1927-2002

Author: Postma, DS, Pride, N, Viegi, G, University of Groningen, and Groningen Research Institute for Asthma and COPD (GRIAC)
Published: 2003

44. Risk factors for atopic dermatitis in infants at high risk of allergy: the PIAMA study

Author: Kerkhof, M, Koopman, Laurens, van Strien, RT, Wijga, A, Smit, HA, Aalberse, RC, Neijens, HJ (Herman), Brunekreef, B, Postma, DS, Gerritsen, J, Landsteiner Laboratory, Faculteit Medische Wetenschappen/UMCG, Groningen Research Institute for Asthma and COPD (GRIAC), Pediatrics, and Internal Medicine
Subjects: atopic dermatitis, breastfeeding, infants, BIRTH, CHILDHOOD, birth weight, hygiene hypothesis, SENSITIZATION, day care attendance, LIFE, body regions, SIZE, INFECTIONS, FOOD, DISEASES, risk factors, ASTHMA, epidemiology, IGE
Abstract: Background It has been suggested that the period immediately after birth is a sensitive period for the development of atopic disease. Objective We investigated whether birth characteristics and environmental factors are associated with the development of atopic dermatitis in the first year of life. Methods Seventy-six children with and 228 without atopic dermatitis, all children of mothers with respiratory allergy or asthma (PIAMA birth cohort study) were included in the study. Atopic dermatitis was defined as a positive history of an itchy skin condition with at least two of the following characteristics: visible dermatitis, history of outer arms/leg involvement, or general dry skin. Multiple logistic regression analysis was performed to study the independent effects of various risk factors. Results A birth weight greater than or equal to4000 g compared to 3000 - 4000 g was a significant risk factor for atopic dermatitis ( odds ratio (OR) = 2.4; 95% CI: 1.1 - 5.1) as was day care attendance (OR = 2.9; 95% CI: 1.5 - 5.9). Exclusive breastfeeding in the first 3 months was negatively associated with atopic dermatitis (OR = 0.6; 95% CI: 0.3 - 1.2), especially with visible dermatitis (OR = 0.4; 95% CI: 0.2-1.0). Gender, gestational age, the presence of siblings or pets, and parental smoking were not significantly associated with atopic dermatitis. Conclusion This study shows that a high birth weight and day care attendance increase the risk of atopic dermatitis in the first year of life, while exclusive breastfeeding is a protective factor when dermatitis is found on inspection.
Published: 2003

45. Interaction between nitric oxide and subsets of human T lymphocytes with differences in glutathione metabolism

Author: Roozendaal, R, Kauffman, HF, Dijkhuis, AJ, Ommen, ETV, Postma, DS, de Monchy, JGR, Vellenga, E, Guided Treatment in Optimal Selected Cancer Patients (GUTS), Stem Cell Aging Leukemia and Lymphoma (SALL), and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: EXPRESSION, ACTIVATION, LEUKEMIA-CELLS, RESISTANCE PROTEINS MRP1, S-NITROSOGLUTATHIONE, HEPATOCARCINOGENESIS, LINES, GAMMA-GLUTAMYL-TRANSPEPTIDASE, TRANSPORT, APOPTOSIS
Abstract: Nitric oxide (NO) modulates human T-lymphocyte responses through several mechanisms. In the current study we show that interactions between NO and glutathione (GSH) metabolism are related to the selective persistent inhibition of interferon-gamma (IFN-gamma) production by NO, which we previously identified. T cells were exposed to NO using the NO-donor compound Spermine-nonoate (Sper) and activated using anti-CD3 plus anti-CD28 monoclonal antibodies. Persistent inhibition of IFN-gamma by Sper was prevented by addition of the GSH precursor L-Cysteine, which inhibits Sper induced GSH depletion. Subsets of cells were either susceptible (GSH(low)) or resistant (GSH(high)) to NO-induced GSH depletion. The GSH(low) subset was characterized by enhanced numbers of CD4(+) cells, reduced numbers of activated cells as characterized by CD25 and CD69, and reduced numbers of memory (CD45RO(+)) cells relative to the GSH(high) population. Rather than directly affecting susceptibility to NO, these surface markers reflected different expression patterns. Particularly, the GSH(low) subset was further characterized by decreased activity of the GSH synthesis related enzymes multi-drug resistance related protein (MRP)-1 and gamma-glutamyltranspeptidase (gamma-GT). Blocking gamma-GT, using acivicin was shown to exacerbate NO-induced GSH depletion and NO-induced apoptosis. Since NO induced apoptosis selectively affects IFN-gamma production these findings implicate GSH metabolism in the modulation and maintenance of the T helper (Th) 1/Th2 balance.
Published: 2002

46. Chronic obstructive pulmonary disease

Author: Kerstjens, HA, Postma, DS, Faculteit Medische Wetenschappen/UMCG, and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: WOMEN, COPD, SMOKING
Published: 2002

47. Accuracy of eosinophils and eosinophil cationic protein to predict steroid improvement in asthma

Author: Meijer, RJ, Postma, DS, Kauffman, HF, Arends, Lidia, Koeter, GH, Kerstjens, HAM, Groningen Research Institute for Asthma and COPD (GRIAC), and Neurology
Subjects: NITRIC-OXIDE, AIRWAY INFLAMMATION, FLUTICASONE PROPIONATE, DEPENDENT ASTHMATICS, EXHALED AIR, respiratory system, asthma, clinical response, ECP, respiratory tract diseases, corticosteroids, LUNG-FUNCTION, quality of life, inflammation, nitric oxide, QUALITY-OF-LIFE, CLINICAL ASTHMA, eosinophils, DOSE-RESPONSE, INDUCED SPUTUM
Abstract: Background There is a large variability in clinical response to corticosteroid treatment in patients with asthma. Several markers of inflammation like eosinophils and eosinophil cationic protein (ECP), as well as exhaled nitric oxide (NO), are good candidates to predict clinical response. Aim We wanted to determine whether we could actually predict a favourable response to inhaled corticosteroids in individual patients. Methods One hundred and twenty patients with unstable asthma were treated with either prednisolone 30 mg/day, fluticasone propionate 1000 mug/day b.i.d. or fluticasone propionate 250 mug/day b.i.d., both via Diskhaler. They were treated during 2 weeks, in a double-blind, parallel group, double dummy design. We measured eosinophils and ECP in blood and sputum, and exhaled nitric oxide as inflammatory parameters before and after 2 weeks in order to predict the changes in forced expiratory volume in 1 s (FEV1), provocative concentration of methacholine causing a 20% fall in FEV1 (PC20 Mch), and asthma quality of life (QOL). Secondly, to test whether these results were applicable in clinical practice we determined the individual prediction of corticosteroid response. Results We fond that changes in FEV1, PC20 Mch and QOL with corticosteroids were predominantly predicted by their respective baseline value and to a smaller extent by eosinophils in blood or sputum. ECP, measured in blood or sputum, was certainly not better than eosinophils in predicting clinical response to corticosteroids. Smoking status was an additional predictor for change in FEV1, but not for change in PC20 Mch or QOL. Prediction of a good clinical response was poor. For instance, high sputum eosinophils (greater than or equal to 3%) correctly predicted an improvement in PC20 Mch in only 65% of the patients. Conclusion Our findings show that baseline values of the clinical parameters used as outcome parameters are the major predictors of clinical response to corticosteroids. Eosinophil percentage in blood or sputum adds to this, whereas ECP provides no additional information. Correct prediction of clinical response in an individual patient, however, remains poor with our currently used clinical and inflammatory parameters.
Published: 2002

48. Provocation with adenosine 5 '-monophosphate as a marker of inflammation in asthma, allergic rhinitis and chronic obstructive pulmonary disease

Author: van den Berge, M, Kerstjens, HAM, Postma, DS, and Groningen Research Institute for Asthma and COPD (GRIAC)
Subjects: HUMAN MAST-CELLS, IL-5 MESSENGER-RNA, AIRWAY INFLAMMATION, DEPENDENT HISTAMINE-RELEASE, INDUCED BRONCHOCONSTRICTION, BRONCHIAL BIOPSY SPECIMENS, FC-EPSILON-RI, INHALED IPRATROPIUM BROMIDE, NONATOPIC ASTHMA, NON-ATOPIC ASTHMA
Published: 2002

49. PC20 adenosine 5 '-monophosphate is more closely associated with airway inflammation in asthma than PC20 methacholine - Reply

Author: Van den Berge, M, Kerstjens, HAM, Postma, DS, Faculteit Medische Wetenschappen/UMCG, and Groningen Research Institute for Asthma and COPD (GRIAC)
Published: 2002

50. Possible dual effect of CD14 molecule on atopy - Reply

Author: Koppelman, GH, Postma, DS, Meyers, DA, Bleecker, ER, Faculteit Medische Wetenschappen/UMCG, and Groningen Research Institute for Asthma and COPD (GRIAC)
Published: 2002

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