Relationships of bronchial responsiveness assessed by methacholine to serum IgE, lung function, symptoms, and diagnoses in 11-year-old New Zealand children*,**

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The relationship of bronchial responsiveness (BR), assessed by methacholine challenge, to serum IgE, baseline ventilatory function, and symptoms or diagnoses suggesting an atopic disorder were examined in 522 11-year-old New Zealand children. BR was assessed by the presence or absence of a PC20 25 mg/ml or less and by calculating a continuous index of the decline of the FEV1 during the methacholine test. The latter facilitated multivariate analyses and revealed significant relationships to predictor variables even in those considered “nonresponsive” by PC20 criteria. There was a close relationship of BR to the baseline FEV1/vital capacity ratio, seen even in patients with known asthma, but this relationship was seen only in subjects with at least moderate levels of serum IgE. There was a less close relation of BR to percent predicted FEV1, but this persisted even after accounting for the FEV1/vital capacity ratio and was present regardless of the level of serum IgE. Reported asthma was associated with increased BR independent of all other factors, but other diagnoses and symptoms contributed relatively little to the prediction of BR once the serum IgE and lung function were taken into account. The overall results are compatible with the concept that IgE is a critical factor in the development of bronchial responsiveness in childhood.

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    Similarly, individual symptoms of nocturnal cough and exercise-induced cough were not predictive, whereas coexistence of these 2 symptoms displayed the most significant association with AHR. A number of studies in children, including birth cohorts, have reported an association between AHR and atopy.20–23 Moreover, early-onset atopy has been reported as a particularly strong risk factor for subsequent development of AHR.24

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*

Data collection and processing in New Zealand supported by grants from the Medical Research Council of New Zealand and the Otago Medical Research Foundation.

**

Data analyses in Arizona supported by a Specialized Center of Research Grant from the Lung Division, National Heart, Lung, and Blood Institute (HL-14136)

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