Maximal Airway Response in Adolescents With Long-term Asthma Remission and Persisting Airway Hypersensitivity: Conclusion
It is not known whether persistent BHR in adolescents with asthma remission is associated with airway inflammation or is linked to another mechanism. The only study on the presence of airway inflammation in BHR of this clinical setting was performed by Van den Toorn et al, who showed that adolescents with atopic asthma in clinical remission had an increased exhaled nitric oxide level, like that of symptomatic asthmatics. However, this does not provide definite evidence for ongoing airway inflammation, since atopic status independent of asthma diagnosis may be an important determinant of increased nitric oxide production in the airways. Reduction of airway sensitivity or maximal airway response to metha-choline through inhaled corticosteroid treatment is mainly a result of improvements in various measures of airway inflammation. The lack of improvement in either maximal airway response or airway hypersensitivity with inhaled corticosteroid treatment therefore may suggest that airway inflammation does not play an important role in persisting BHR in adolescents with clinical remission. It has been shown that BHR may be the result of a chronic inflammatory process, with increased airway wall thickness and hypertrophy of the airway smooth muscle. BHR caused by such airway remodeling would not be influenced by corticosteroids. However, genetic factors could offer another possible explanation. The importance of a familial predisposition, and therefore a possible genetic transmission of BHR, has been demonstrated by several studies. Inasmuch as this genetic factor exists in subjects, it could explain the observed lack of improvement in BHR with inhaled corticosteroids.
In conclusion, adolescents with asthma remission showed a relatively low level of maximal airway response, compared to symptomatic asthmatic adolescents with a similar degree of airway sensitivity to methacholine. Budesonide inhaled regularly for 6 months did not lead to a significant improvement in maximal airway response in adolescents with asthma remission. These findings suggest that the mechanism underlying bronchial hyperresponsiveness in this clinical setting may be different from that in symptomatic asthma.