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Summary: Background: Understanding of adolescent-onset asthma remains limited. We sought to characterise this state and identify associated factors within a longitudinal birth cohort study. Methods: The Isle of Wight Whole Population Birth Cohort was recruited in 1989 (N =1456) and characterised at 1, 2, 4, 10 and 18-years. “Adolescent-onset asthma” was defined as asthma at age 18 without prior history of asthma, “persistent-adolescent asthma” as asthma at both 10 and 18 and “never-asthma” as those without asthma at any assessment. Results: Adolescent-onset asthma accounted for 28.3% of asthma at 18-years and was of similar severity to persistent-adolescent asthma. Adolescent-onset asthmatics showed elevated bronchial hyper-responsiveness (BHR) and atopy at 10 and 18 years. BHR in this group at 10 was intermediate to that of never-asthmatics and persistent-adolescent asthma. By 18 their BHR, bronchodilator reversibility and sputum eosinophilia was greater than never-asthmatics and comparable to persistent-adolescent asthma. At 10, males who later developed adolescent-onset asthma had reduced FEV1 and FEF25–75, while females had normal lung function but then developed impaired FEV1 and FEF25–75 in parallel with adolescent asthma. Factors independently associated with adolescent-onset asthma included atopy at 10 (OR=2.35; 95% CI=1.08–5.09), BHR at 10 (3.42; 1.55–7.59), rhinitis at 10 (2.35; 1.11–5.01) and paracetamol use at 18-years (1.10; 1.01–1.19). Conclusions: Adolescent-onset asthma is associated with significant morbidity. Predisposing factors are atopy, rhinitis and BHR at age 10 while adolescent paracetamol use is also associated with this state. Awareness of potentially modifiable influences may offer avenues for mitigating this disease state. [ABSTRACT FROM AUTHOR]

Background: The parent-of-origin effect is important in understanding the genetic basis of childhood allergic diseases and improving our ability to identify high-risk children. Objective: We sought to investigate the parent-of-origin effect in childhood allergic diseases. Methods: The Isle of Wight Birth Cohort (n = 1456) has been examined at 1, 2, 4, 10, and 18 years of age. Information on the prevalence of asthma, eczema, rhinitis, and environmental factors was obtained by using validated questionnaires. Skin prick tests were carried out at ages 4, 10, and 18 years, and total IgE measurement was carried out at 10 and 18 years. Parental history of allergic disease was assessed soon after the birth of the child, when maternal IgE levels were also measured. Prevalence ratios (PRs) and their 95% CIs were estimated, applying log-linear models adjusted for confounding variables. Results: When stratified for sex of the child, maternal asthma was associated with asthma in girls (PR, 1.91; 95% CI, 1.34-2.72; P = .0003) but not in boys (PR, 1.29; 95% CI, 0.85-1.96; P = .23), whereas paternal asthma was associated with asthma in boys (PR, 1.99; 95% CI, 1.42-2.79; P < .0001) but not in girls (PR, 1.03; 95% CI, 0.59-1.80; P = .92). Maternal eczema increased the risk of eczema in girls (PR, 1.92; 95% CI, 1.37-2.68; P = .0001) only, whereas paternal eczema did the same for boys (PR, 2.07; 95% CI, 1.32-3.25; P = .002). Similar trends were observed when the effect of maternal and paternal allergic disease was assessed for childhood atopy and when maternal total IgE levels were related to total IgE levels in children at ages 10 and 18 years. Conclusions: The current study indicates a sex-dependent association of parental allergic conditions with childhood allergies, with maternal allergy increasing the risk in girls and paternal allergy increasing the risk in boys. This has implications for childhood allergy prediction and prevention. [ABSTRACT FROM AUTHOR]