J Asthma Allergy Clin Immunol.
1998 Dec;18(4):647-655.
Tthe influences of parental atopy and bronchial hyperresponsiveness on the development
of asthma agter early childhood wheezing
Abstract
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BACKGROUND: Many young children suffer from wheezing illness during viral respiratory infection, and
some of them experience wheezing many years later and ultimately develop bronchial asthma. It is not
clear whether atopy or bronchial hyperresponsiveness in the family is a significant risk factor for
asthma in this clinical setting. Objective : To examine the genetic basis for the development of asthma
after early childhood wheezing. Materials and
METHODS
A measurement of serum total IgE concentration, skin prick test to common inhalant allergens,
and methacholine bronchial provocation test were performed in 29 asthmatic children and their parents,
and 22 non-asthmatic children with the past history of wheezing illness during the first three years of
age and their parents. A questionnaire was performed to assess the presence of asthma and allergic
rhinitis in the parents.
RESULTS
Positive skin test response to common inhalant allergens was more prevalent in asthmatics than
in non-asthmatics(67.8% vs. 27.2%). Serum total IgE concentration was significantly higher in asthmatics
than in non-asthmatics(geometric mean: 173 vs. 83 IU/ ml). Positive skin test response to comman inhalant
allergens was more prevalent in parents of asthmatics than in thoae of non-asthmatics(51.7% vs. 25.0%),
but serum total IgE level was not different between the two groups(geometric mean: 132 vs. 120 IU/ml).
Positive rate of methacholine bronchial provocation test, geometric mean of PC20-methacholine, and BR
index were not different between the parents of asthmatics and non-asthmatics (18.1% vs. 13.9%; 164 vs.
180 mg/ml; 1.154+-0.077 vs. 1.055+-0.068, respectively).
CONCLUSION
It is suggested that personal atopy is important in the development of asthma after early
childhood wheezing, and parental atopy rather than bronchial hyperresponsiveness is a risk factor for
the development of childhood asthma in this clinical setting.