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Author Kreiner-Moller, E.; Bisgaard, H.; Bonnelykke, K. url  doi
  Title Prenatal and postnatal genetic influence on lung function development Type Journal Article
  Year (down) 2014 Publication The Journal of Allergy and Clinical Immunology Abbreviated Journal J Allergy Clin Immunol  
  Volume 134 Issue 5 Pages 1036-42.e15  
  Keywords Adult; Age Factors; Bronchoconstrictor Agents/administration & dosage; Case-Control Studies; Child; Child, Preschool; Female; Forced Expiratory Volume/drug effects/*genetics; Humans; Infant; Infant, Newborn; Lung/*growth & development/*physiopathology; Lung Volume Measurements/methods; Male; Methacholine Chloride/administration & dosage; Polymorphism, Single Nucleotide; Pregnancy; Prenatal Exposure Delayed Effects/*genetics/physiopathology; Prospective Studies; Spirometry/methods; Child; asthma; genetics; respiratory function tests  
  Abstract BACKGROUND: It is unknown to what extent adult lung function genes affect lung function development from birth to childhood. OBJECTIVE: Our aim was to study the association of candidate genetic variants with neonatal lung function and lung function development until age 7 years. METHODS: Lung function measurement by means of spirometry with the raised-volume thoracoabdominal compression technique and bronchial responsiveness to methacholine challenge were assessed in 411 high-risk newborns from the Copenhagen Prospective Study on Asthma in Childhood 2000 (COPSAC2000) cohort. Measures were repeated at age 7 years. Genetic risk scores were calculated based on reported single nucleotide polymorphisms for adult lung function (FEV1/forced expiratory vital capacity [FVC] ratio and FEV1) as the number of risk alleles weighted on known effect size. These genetic risk scores were analyzed against lung function measures as z scores at birth (forced expiratory volume in 0.5 seconds [FEV0.5], forced expiratory flow at 50% of functional vital capacity [FEF50], and provocative dose of methacholine causing a 15% decrease in lung function [PD15]) and at age 7 years (FEV1, FEF50, and provocative dose of methacholine causing a 20% decrease in lung function [PD20]) and with development from birth to age 7 years (FEV0.5/1, FEF50, and PD15/20). RESULTS: The genetic risk scores were not associated with lung function measures at age 1 month, but the FEV1/FVC genetic risk score was associated with reduced FEF50 values at age 7 years (P = .01) and similarly with reduced growth in FEF50 from birth to age 7 years (P = .02). This score was also associated with increased bronchial responsiveness (reduced PD20) at age 7 years (P = .02) and change in responsiveness from birth to age 7 years (P = .05). CONCLUSION: Lung function genetic variants identified in adults were not associated with neonatal lung function or bronchial responsiveness but with the development of these lung function measures during early childhood, suggesting a window of opportunity for interventions targeting these genetic mechanisms.  
  Address COPSAC, the Copenhagen Prospective Studies on Asthma in Childhood, Faculty of Health Sciences, University of Copenhagen, and the Danish Pediatric Asthma Center, Copenhagen University Hospital, Gentofte, Copenhagen, Denmark  
  Corporate Author Thesis  
  Impact Factor 11,476 First Author Kreiner-Moller, E. Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Senior Author Bonnelykke, K.  
  ISSN 0091-6749 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:24857373 Approved no  
  Call Number Serial 44  
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