RESUMO
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.