Tags

Type your tag names separated by a space and hit enter

Early-life risk factors for childhood wheeze phenotypes in a high-risk birth cohort.
J Pediatr. 2014 Feb; 164(2):289-94.e1-2.JPed

Abstract

OBJECTIVE

To define longitudinal childhood wheeze phenotypes and identify their early-life risk factors.

STUDY DESIGN

Current wheeze was recorded 23 times up to age 7 years in a birth cohort at high risk for allergy (n = 620). Latent class analysis of wheeze responses identified 5 classes. Multinomial logistic regression estimated associations of probability-weighted wheezing classes with early-life factors. All phenotypes were compared with never/infrequent wheezers.

RESULTS

Lower respiratory tract infection (LRTI) by 1 year (relative risk [RR], 3.00; 95% CI, 1.58-5.70), childcare by 1 year (RR, 1.51; 95% CI, 1.02-2.22), and higher body mass index (RR, 2.51; 95% CI, 1.09-5.81) were associated with increased risk of early transient wheeze, whereas breastfeeding was protective (RR, 0.54; 95% CI, 0.32-0.90). LRTI (RR, 6.54; 95% CI, 2.55-16.76) and aeroallergen sensitization (RR, 4.95; 95% CI, 1.74-14.02) increased the risk of early persistent wheeze. LRTI (RR, 5.31; 95% CI, 2.71-10.41), eczema (RR, 2.77; 95% CI, 1.78-4.31), aeroallergen sensitization (RR, 5.60; 95% CI, 2.86-10.9), and food sensitization (RR, 2.77; 95% CI, 1.56-4.94) increased the risk of intermediate-onset wheeze, whereas dog exposure at baseline (RR, 0.52; 95% CI, 0.32-0.84) and first-born status (RR, 0.49; 95% CI, 0.32-0.76) were protective. Heavy parental smoking at birth (RR, 3.18; 95% CI, 1.02-9.88) increased the risk of late-onset wheeze, whereas breastfeeding reduced it (RR, 0.34; 95% CI, 0.12-0.96). All wheeze classes except early transient had greater risk of wheeze at age 12 years compared with never/infrequent wheezers.

CONCLUSION

We found distinct early-life risk factor profiles for each wheeze phenotype. These findings provide insight into possible wheeze mechanisms and have implications for identifying preventive strategies and addressing clinical management of early-life wheeze.

Authors+Show Affiliations

Center for Molecular, Environmental, Genetic, and Analytic Epidemiology, School of Population and Global Health, University of Melbourne, Melbourne, Australia. Electronic address: clodge@unimelb.edu.au.Center for Molecular, Environmental, Genetic, and Analytic Epidemiology, School of Population and Global Health, University of Melbourne, Melbourne, Australia.Center for Molecular, Environmental, Genetic, and Analytic Epidemiology, School of Population and Global Health, University of Melbourne, Melbourne, Australia; Murdoch Children's Research Institute, Royal Children's Hospital, Parkville, Australia.Center for Molecular, Environmental, Genetic, and Analytic Epidemiology, School of Population and Global Health, University of Melbourne, Melbourne, Australia.Center for Molecular, Environmental, Genetic, and Analytic Epidemiology, School of Population and Global Health, University of Melbourne, Melbourne, Australia.Murdoch Children's Research Institute, Royal Children's Hospital, Parkville, Australia.Deakin Population Health, Deakin University, Burwood, Australia.Murdoch Children's Research Institute, Royal Children's Hospital, Parkville, Australia.Department of Pediatrics, John Hunter Children's Hospital, Newcastle, Australia.Bergen Respiratory Research Group, Center of International Health, University of Bergen, Bergen, Norway; Department of Occupational Medicine, Haukeland University Hospital, Bergen, Norway.Department of Epidemiology and Preventive Medicine, The Alfred Hospital, Monash University, Melbourne, Australia.Murdoch Children's Research Institute, Royal Children's Hospital, Parkville, Australia; Department of Allergy and Immunology, Royal Children's Hospital, Parkville, Australia.Center for Molecular, Environmental, Genetic, and Analytic Epidemiology, School of Population and Global Health, University of Melbourne, Melbourne, Australia; Murdoch Children's Research Institute, Royal Children's Hospital, Parkville, Australia.

Pub Type(s)

Comparative Study
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24238860

Citation

Lodge, Caroline J., et al. "Early-life Risk Factors for Childhood Wheeze Phenotypes in a High-risk Birth Cohort." The Journal of Pediatrics, vol. 164, no. 2, 2014, pp. 289-94.e1-2.
Lodge CJ, Zaloumis S, Lowe AJ, et al. Early-life risk factors for childhood wheeze phenotypes in a high-risk birth cohort. J Pediatr. 2014;164(2):289-94.e1-2.
Lodge, C. J., Zaloumis, S., Lowe, A. J., Gurrin, L. C., Matheson, M. C., Axelrad, C., Bennett, C. M., Hill, D. J., Hosking, C. S., Svanes, C., Abramson, M. J., Allen, K. J., & Dharmage, S. C. (2014). Early-life risk factors for childhood wheeze phenotypes in a high-risk birth cohort. The Journal of Pediatrics, 164(2), 289-e1-2. https://doi.org/10.1016/j.jpeds.2013.09.056
Lodge CJ, et al. Early-life Risk Factors for Childhood Wheeze Phenotypes in a High-risk Birth Cohort. J Pediatr. 2014;164(2):289-94.e1-2. PubMed PMID: 24238860.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Early-life risk factors for childhood wheeze phenotypes in a high-risk birth cohort. AU - Lodge,Caroline J, AU - Zaloumis,Sophie, AU - Lowe,Adrian J, AU - Gurrin,Lyle C, AU - Matheson,Melanie C, AU - Axelrad,Christine, AU - Bennett,Catherine M, AU - Hill,David J, AU - Hosking,Clifford S, AU - Svanes,Cecilie, AU - Abramson,Michael J, AU - Allen,Katrina J, AU - Dharmage,Shyamali C, Y1 - 2013/11/14/ PY - 2013/02/10/received PY - 2013/07/15/revised PY - 2013/09/30/accepted PY - 2013/11/19/entrez PY - 2013/11/19/pubmed PY - 2014/3/26/medline KW - BMI KW - Body mass index KW - LCA KW - LRTI KW - Latent class analysis KW - Lower respiratory tract infection KW - MACS KW - Melbourne Atopy Cohort Study KW - RR KW - Relative risk SP - 289-94.e1-2 JF - The Journal of pediatrics JO - J Pediatr VL - 164 IS - 2 N2 - OBJECTIVE: To define longitudinal childhood wheeze phenotypes and identify their early-life risk factors. STUDY DESIGN: Current wheeze was recorded 23 times up to age 7 years in a birth cohort at high risk for allergy (n = 620). Latent class analysis of wheeze responses identified 5 classes. Multinomial logistic regression estimated associations of probability-weighted wheezing classes with early-life factors. All phenotypes were compared with never/infrequent wheezers. RESULTS: Lower respiratory tract infection (LRTI) by 1 year (relative risk [RR], 3.00; 95% CI, 1.58-5.70), childcare by 1 year (RR, 1.51; 95% CI, 1.02-2.22), and higher body mass index (RR, 2.51; 95% CI, 1.09-5.81) were associated with increased risk of early transient wheeze, whereas breastfeeding was protective (RR, 0.54; 95% CI, 0.32-0.90). LRTI (RR, 6.54; 95% CI, 2.55-16.76) and aeroallergen sensitization (RR, 4.95; 95% CI, 1.74-14.02) increased the risk of early persistent wheeze. LRTI (RR, 5.31; 95% CI, 2.71-10.41), eczema (RR, 2.77; 95% CI, 1.78-4.31), aeroallergen sensitization (RR, 5.60; 95% CI, 2.86-10.9), and food sensitization (RR, 2.77; 95% CI, 1.56-4.94) increased the risk of intermediate-onset wheeze, whereas dog exposure at baseline (RR, 0.52; 95% CI, 0.32-0.84) and first-born status (RR, 0.49; 95% CI, 0.32-0.76) were protective. Heavy parental smoking at birth (RR, 3.18; 95% CI, 1.02-9.88) increased the risk of late-onset wheeze, whereas breastfeeding reduced it (RR, 0.34; 95% CI, 0.12-0.96). All wheeze classes except early transient had greater risk of wheeze at age 12 years compared with never/infrequent wheezers. CONCLUSION: We found distinct early-life risk factor profiles for each wheeze phenotype. These findings provide insight into possible wheeze mechanisms and have implications for identifying preventive strategies and addressing clinical management of early-life wheeze. SN - 1097-6833 UR - https://www.unboundmedicine.com/medline/citation/24238860/Early_life_risk_factors_for_childhood_wheeze_phenotypes_in_a_high_risk_birth_cohort_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-3476(13)01227-4 DB - PRIME DP - Unbound Medicine ER -