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Relationship between childhood atopy and wheeze: what mediates wheezing in atopic phenotypes?

Relationship between childhood atopy and wheeze: what mediates wheezing in atopic phenotypes?
Relationship between childhood atopy and wheeze: what mediates wheezing in atopic phenotypes?
Background: the nature of the relationship between childhood wheeze and atopy remains uncertain.

Objective: to characterize childhood wheeze among atopic phenotypes in a longitudinal birth cohort study.

Methods: a whole population birth cohort (N = 1,456) was recruited in 1989. Children were seen at birth and at 1, 2, 4, and 10 years of age to obtain information on asthma and allergic disease development and relevant risk factors for these states. Skin prick testing at ages 4 (n = 980) and 10 (n = 1,036) years was used to define atopic phenotypes. Wheezing in these states was characterized, and logistic regression was used to identify independent risk factors for wheeze onset in different atopic phenotypes.

Results: wheeze ever occurred in 37% of never atopics, 38% of early childhood atopics, 65% of chronic childhood atopics, and 52% of delayed childhood atopics. Chronic childhood atopics had significant wheezing morbidity and bronchial hyperresponsiveness. Their wheezing was associated with male sex, early eczema, family history of eczema, and early tobacco exposure. Never atopic wheeze was related to maternal asthma, parental smoking, and respiratory tract infections. Exclusive breastfeeding protected against early childhood atopic wheeze. Maternal asthma, family history of urticaria, and dog ownership increased delayed childhood atopic wheeze.

Conlusions: in many respects, chronic childhood atopy is the atopic phenotype associated with the most significant forms of childhood wheezing. In such children, heritable drive, allergens, and synergy with other environmental triggers seem to be crucial determinants of wheeze onset. Where such sensitization is absent, numerous environmental factors plus genetic predisposition may assume importance for wheezing.
Age of Onset, Allergens/adverse effects, Animals, Cohort Studies, Comorbidity, Eczema/epidemiology, Female, Follow-Up Studies, Genetic Predisposition to Disease, Humans, Hypersensitivity, Immediate/complications, Infant, Newborn, Male, Phenotype, Respiratory Sounds/etiology, Respiratory Tract Infections/epidemiology, Risk Factors, Sex Factors, Tobacco Smoke Pollution/statistics & numerical data
1081-1206
84-91
Kurukulaaratchy, Ramesh J
9c7b8105-2892-49f2-8775-54d4961e3e74
Matthews, Sharon
da71ceaa-c974-4fda-aea0-13c7cdecaf04
Arshad, S Hasan
795d8599-b77d-44e5-bb9c-67db78822057
Kurukulaaratchy, Ramesh J
9c7b8105-2892-49f2-8775-54d4961e3e74
Matthews, Sharon
da71ceaa-c974-4fda-aea0-13c7cdecaf04
Arshad, S Hasan
795d8599-b77d-44e5-bb9c-67db78822057

Kurukulaaratchy, Ramesh J, Matthews, Sharon and Arshad, S Hasan (2006) Relationship between childhood atopy and wheeze: what mediates wheezing in atopic phenotypes? Annals of Allergy, Asthma and Immunology, 97 (1), 84-91. (doi:10.1016/S1081-1206(10)61375-0).

Record type: Article

Abstract

Background: the nature of the relationship between childhood wheeze and atopy remains uncertain.

Objective: to characterize childhood wheeze among atopic phenotypes in a longitudinal birth cohort study.

Methods: a whole population birth cohort (N = 1,456) was recruited in 1989. Children were seen at birth and at 1, 2, 4, and 10 years of age to obtain information on asthma and allergic disease development and relevant risk factors for these states. Skin prick testing at ages 4 (n = 980) and 10 (n = 1,036) years was used to define atopic phenotypes. Wheezing in these states was characterized, and logistic regression was used to identify independent risk factors for wheeze onset in different atopic phenotypes.

Results: wheeze ever occurred in 37% of never atopics, 38% of early childhood atopics, 65% of chronic childhood atopics, and 52% of delayed childhood atopics. Chronic childhood atopics had significant wheezing morbidity and bronchial hyperresponsiveness. Their wheezing was associated with male sex, early eczema, family history of eczema, and early tobacco exposure. Never atopic wheeze was related to maternal asthma, parental smoking, and respiratory tract infections. Exclusive breastfeeding protected against early childhood atopic wheeze. Maternal asthma, family history of urticaria, and dog ownership increased delayed childhood atopic wheeze.

Conlusions: in many respects, chronic childhood atopy is the atopic phenotype associated with the most significant forms of childhood wheezing. In such children, heritable drive, allergens, and synergy with other environmental triggers seem to be crucial determinants of wheeze onset. Where such sensitization is absent, numerous environmental factors plus genetic predisposition may assume importance for wheezing.

Full text not available from this repository.

More information

Accepted/In Press date: 16 November 2005
Published date: July 2006
Keywords: Age of Onset, Allergens/adverse effects, Animals, Cohort Studies, Comorbidity, Eczema/epidemiology, Female, Follow-Up Studies, Genetic Predisposition to Disease, Humans, Hypersensitivity, Immediate/complications, Infant, Newborn, Male, Phenotype, Respiratory Sounds/etiology, Respiratory Tract Infections/epidemiology, Risk Factors, Sex Factors, Tobacco Smoke Pollution/statistics & numerical data

Identifiers

Local EPrints ID: 59362
URI: http://eprints.soton.ac.uk/id/eprint/59362
ISSN: 1081-1206
PURE UUID: fa82d3dd-9d82-4d0e-9851-6c12b09eee35
ORCID for Ramesh J Kurukulaaratchy: ORCID iD orcid.org/0000-0002-1588-2400

Catalogue record

Date deposited: 03 Sep 2008
Last modified: 18 Feb 2021 16:54

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