title: Childhood wheeze phenotypes show less than expected growth in FEV1 across adolescence.
abstract: BACKGROUND
  Better characterization of childhood wheeze phenotypes using newer statistical methods provides a basis for addressing the heterogeneity of childhood asthma. Outcomes of these phenotypes beyond childhood are unknown.
  
  
  OBJECTIVE
  To determine if adolescent respiratory symptoms, lung function, and changes in lung function over adolescence differ by childhood wheeze phenotypes defined through latent class analysis.
  
  
  METHODS
  A prospective birth cohort (Melbourne Atopy Cohort Study) followed 620 high allergy-risk children, recording respiratory symptoms and spirometry at 12 and 18 years. Regression analyses identified relationships between wheeze phenotypes (never/infrequent, early transient, early persistent, intermediate onset, and late onset) and lung function, change in lung function (12-18 yr), respiratory symptoms, and asthma. The baseline classification was never/infrequent wheeze.
  
  
  RESULTS
  Deficits in expected growth of lung function, measured by change in prebronchodilator FEV1 between 12 and 18 years, were found for early persistent (reduced 290 ml; 95% confidence interval [CI], 82-498), intermediate-onset (reduced 210 ml; 95% CI, 62-359), and late-onset wheeze (reduced 255 ml; 95% CI, 69-442). Intermediate-onset wheezers had persistent FEV1 deficit after bronchodilator at 18 years (reduced 198 ml; 46,350). Current asthma risk was increased for all phenotypes except early transient, which was also not associated with lung function deficits at 12 or 18 years.
  
  
  CONCLUSIONS
  Persistent wheeze phenotypes in childhood were associated with reduced growth in prebronchodilator FEV1 over adolescence. Intermediate-onset wheezers showed irreversible airflow limitation by 18 years. Conversely, early transient wheeze was a benign condition with no sequelae for respiratory health by age 18.
authors.affiliation: 1 Centre for Epidemiology and Biostatistics, School of Population and Global Health, University of Melbourne, Melbourne, Australia.
authors.forename: Caroline J
authors.initials: CJ
authors.lastname: Lodge
authors.forename: Adrian J
authors.initials: AJ
authors.lastname: Lowe
authors.forename: Katrina J
authors.initials: KJ
authors.lastname: Allen
authors.forename: Sophie
authors.initials: S
authors.lastname: Zaloumis
authors.forename: Lyle C
authors.initials: LC
authors.lastname: Gurrin
authors.forename: Melanie C
authors.initials: MC
authors.lastname: Matheson
authors.forename: Christine
authors.initials: C
authors.lastname: Axelrad
authors.forename: Liam
authors.initials: L
authors.lastname: Welsh
authors.forename: Catherine M
authors.initials: CM
authors.lastname: Bennett
authors.forename: John
authors.initials: J
authors.lastname: Hopper
authors.forename: Paul S
authors.initials: PS
authors.lastname: Thomas
authors.forename: David J
authors.initials: DJ
authors.lastname: Hill
authors.forename: Cliff S
authors.initials: CS
authors.lastname: Hosking
authors.forename: Cecilie
authors.initials: C
authors.lastname: Svanes
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Abramson
authors.forename: Shyamali C
authors.initials: SC
authors.lastname: Dharmage
mesh_terms: D000293:Adolescent; D001249:Asthma / Q000150:complications / Q000175:diagnosis* / Q000453:epidemiology / Q000235:genetics / Q000503:physiopathology*; D001315:Australia / Q000453:epidemiology; D002648:Child; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005541:Forced Expiratory Volume; D006801:Humans; D006967:Hypersensitivity / Q000175:diagnosis; D008297:Male; D010641:Phenotype; D011379:Prognosis; D011446:Prospective Studies; D012135:Respiratory Sounds / Q000209:etiology* / Q000503:physiopathology; D012307:Risk Factors; D013147:Spirometry; D011795:Surveys and Questionnaires; D013997:Time Factors