Background:The prevalence of asthma has increased in developed countries in the past 2 decades. The effectiveness of intervention measures on the primary prevention of asthma has not been well studied.

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Polymorphisms in the TNF-alpha (A-308G), IL-4 (C-589T), and Fcalpha RIbeta (E237G) genes have been associated with asthma and related phenotypes. To determine the predictive value of these polymorphisms we have assessed their relative risk (RR) for the development of atopy, asthma, and rhinitis in a high-risk infant population that is being followed longitudinally from birth. DNA was extracted and genotyped for 373 infants and 572 parents for each polymorphism. Phenotypic data were collected for atopy and allergic diseases in the infants at 12 mo of age. The prevalence of these phenotypes in the 281 white infants was compared in each genotypic group. There were no differences in the prevalence of any phenotype between genotypes of the TNF-alpha and Fcalpha RIbeta polymorphisms. However, we found that the IL4-589*T allele was associated with "probable" asthma (RR = 4.1) and that homozygotes for the IL4-589*T allele had an increased risk for the development of rhinitis (RR = 2.4). Using the transmission disequilibrium test, an association of IL4-589*T with atopy was found. We conclude that IL-4-589*T, but not TNF-alpha-308*2 or Fcalpha RIbeta*G, is a risk factor for the development of atopy, asthma, and rhinitis by 12 mo of age.

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Changes in symptom score and peak expiratory flow (PEF) and the use of medications during the first acute exacerbation of asthma were studied in 41 patients and matched controls who took part in a panel study. An acute exacerbation was defined as the presence of at least one of the following: any unscheduled physician visit, visit to an emergency room, or hospitalization for treatment of asthma; a decrease in PEF by 30% from the patient's best reading; an increase in asthma symptoms during the day and night for over 48 h and not responding to usual medications; and the commencement or doubling of the dose of oral or inhaled steroids for any of the foregoing reasons. Data from -9 to -7 d before the onset of an acute exacerbation were taken as the baseline data, with which the values of the subsequent 14 d were compared. Significant increases in symptoms occurred before a significant reduction in PEF. None of the patients had a decrease of more than 30% in PEF before the onset of symptoms. Daily variation in PEF was not significantly increased from the baseline. Our results suggest that PEF monitoring is not as sensitive as a symptom diary for revealing acute exacerbations of asthma, and that a 30% decrease in PEF is too stringent a criterion for defining an acute exacerbation.

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We studied a cohort containing 368 children at high risk of developing atopy and atopic disorders and 540 parents of those children to investigate whether the IL13 Arg130Gln and CÀ1112 T polymorphisms were associated with these outcomes. We also investigated whether haplotypes consisting of any two polymorphisms of IL13 Arg130Gln, IL13 CÀ1112 T and IL4 CÀ589 T were associated with these phenotypes. In 288 white children, the IL13 130Gln allele was associated with atopy (RR ¼ 1.9, P ¼ 0.047), and with atopic dermatitis (RR ¼ 2.5, P ¼ 0.014). The associations were confirmed using a family-based test of association (P ¼ 0.027 and 0.030, respectively) in all subjects. In white subjects there were associations of haplotypes consisting of IL13 Arg130Gln and IL4 CÀ589 T with atopic dermatitis (P ¼ 0.006) and with atopy (P ¼ 0.009). Our data suggest that the IL13 Arg130Gln polymorphism and haplotypes consisting of IL13 Arg130Gln and IL4 CÀ589 T were associated with the development of atopy and atopic dermatitis at 24 months of age.