Risk analysis of early childhood eczema - 15/08/11
Abstract |
Background |
The increasing prevalence of eczema suggests the role of environmental factors triggering a genetic predisposition.
Objective |
To analyze the effect of environmental exposures in early life and genetic predisposition on the development of eczema before age 3 years.
Methods |
The Copenhagen Study on Asthma in Childhood is a prospective clinical study of a birth cohort of 411 children born of mothers with asthma. Eczema was diagnosed, treated, and monitored at the clinical research unit, and complete follow-up for the first 3 years of life was available for 356 children. Risk assessments included filaggrin loss-of-function mutation; parent’s atopic disease; sex; social status; previous deliveries; third trimester complications and exposures; anthropometrics at birth; month of birth; duration solely breast-fed; introduction of egg, cow’s milk, and fish; time spent in day care; cat and dog at home; feather pillow; nicotine in infant’s hair; and temperature and humidity in bedroom.
Results |
Eczema developed in 43.5% of the infants. Filaggrin mutation (odds ratio [OR], 3.20; 95% CI, 1.46-7.02; P = .004), mother’s eczema (OR, 2.80; 95% CI, 1.70-4.63; P < .0001), and father’s allergic rhinitis (OR, 1.91; 95% CI, 1.09-3.33; P = .02) were directly associated with risk of eczema. Risk of eczema was significantly reduced by birth length (OR per cm increase, 0.87; 95% CI, 0.78-0.97; P = .02), increased bedroom temperature (probably inverse causality; OR, 0.80; 95% CI, 0.66-0.97; P = .02), and dog living in the home (OR, 0.44; 95% CI, 0.23-0.87; P = .02).
Conclusions |
Dog exposure reduced the risk of eczema, whereas short length at birth, filaggrin mutation, and parental atopy increased the risk of eczema by age 3 years.
Le texte complet de cet article est disponible en PDF.Key words : Length at birth, breast-feeding, dog, eczema, filaggrin, risk factor
Abbreviations used : COPSAC, FLG, OR
Plan
Supported by the Lundbeck Foundation, the Pharmacy Foundation of 1991, the Danish Medical Research Council, the Danish Pediatric Asthma Center, the Danish Lung Association, the Hans Skoubys og hustru Emma Skoubys Fond, and Oda Pedersens Legat. |
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Disclosure of potential conflict of interest: H. Bisgaard has been a consultant to and paid lecturer for and holds sponsored grants from Aerocrine, AstraZeneca, Altana, GSK, Merck, MedImmune, NeoLab, and Pfizer; in addition, he is a lecturer for AstraZeneca and Merck, receives grant support from AstraZeneca, Merck, MedImmune, and GSK, and has provided expert witness testimony/legal consultation services to NeoLab. The Danish Pediatric Asthma Center has received unrestricted institutional grants from Aerocrine, AstraZeneca, GSK, Merck, and MedImmune. The rest of the authors have declared that they have no conflict of interest. |
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COPSAC is funded by private and public research funds; see www.copsac.com. Grants above 100.000 Euro were donated by the Lundbeck Foundation, the Pharmacy Foundation of 1991, the Augustinus Foundation, the Danish Medical Research Council, and the Danish Pediatric Asthma Centre. The funding agencies did not have any role in study design, data collection and analysis, decision to publish, or preparation of the article. |
Vol 123 - N° 6
P. 1355 - juin 2009 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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