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We used a tracking index to measure the reproducibility of single breath nitrogen test variables (CV/VC, CC/TLC, [ΔN.sub.2]/L) and spirometric variables ([FEV.sub.1] and [FEV.sub.1]/FVC) and to compare the characteristics of [...]

The natural history of lung growth and senescence in individuals with variable air flow obstruction or clinical asthma has been given less attention than the natural history of chronic airflow obstruction. This article reviews the information available on lung growth during childhood in persons with asthma and on the rate of decline of lung function during adult life in individuals with asthma or bronchial hyperresponsiveness. Lung growth appears to be relatively normal in most children with asthma but is reduced throughout childhood and adolescence in those with severe and persistent symptoms. It is not known if this reflects a failure to reach full growth or reversible bronchoconstriction. During adult life, clinical asthma is associated with a slight increase in the rate of decline in FEV1. In the middle-aged and elderly smoker it is virtually impossible to separate chronic bronchitis and asthma. Bronchial hyperresponsiveness appears to be associated with an increase in the rate of decline of lung function but it is not clear if this is a result of airway disease due to smoking or a true risk factor. Further research needs are identified.

Evidence is accumulating that elevated levels of serum IgE may play a role in the pathogenesis of chronic airflow obstruction. We examined this question using data on 863 subjects drawn from two cohort studies which we have followed over a period of nine to 11 years. One, the Portland cohort, represents a working population aged 25 to 55 years at baseline. The second, the Screening center cohort, spans a wider age range (18 to 87 years at baseline) and is biased towards respiratory disease. Spirometric tests and respiratory symptom questionnaires have been administered five times over a nine-year period for the Portland cohort, and over an 11-year period for the Screening center cohort. IgE was measured one time towards the end of the follow-up. Our data confirm the finding that smokers tend to have higher IgE levels than nonsmokers. For the combined sample, geometric mean levels of IgE were 31.0 IU/ml among smokers and 17.4 IU/ml among nonsmokers. Levels among ex-smokers were intermediate. Among smokers, IgE was not related to either amount smoked or pack-years. Cross-sectionally, FEV1was inversely related to IgE in the Screening center cohort, but not in the Portland cohort study. Among smokers, this association was only present for those subjects with symptoms of chronic bronchitis (chronic cough/sputum production). We found no association of IgE with longitudinal rate of decline of FEV, in either cohort. These findings are consistent with other studies and support the hypothesis that serum IgE is inversely related to function level cross-sectionally, but is not predictive of rate of decline of lung function.

We studied 15 nonsmoking, clinically stable asthmatic subjects aged 27 to 39 years to evaluate the potential cardiotoxic effects of combined use of a β-adrenergic agonist drug and theophylline in the treatment of asthma. Subjects underwent a one-week washout period followed by two one-week periods of study receiving either oral terbutaline or sustained-release theophylline during week 1 and both drugs during week 2. Thirty-six-hour Holter monitoring was performed at the end of each period of study. No significant increase in the total number of ventricular premature beats was noted, although the average heart rate increased significantly between each period of study. Although not statistically significant, the number of individuals with multiform or complete and repetitive ventricular premature beats increased from one at baseline to three during each period of study, including one subject with ventricular tachycardia on combined therapy. These data suggest that combined therapy with theophylline and a ß-adrenergic agonist in young, otherwise healthy asthmatic subjects does not lead to an increase in the total number of ectopic beats but may increase the degree of complexity of ventricular premature beats.