Duration of postviral airway hyperresponsiveness in children with asthma: Effect of atopy
Received 11 November 2004; received in revised form 28 March 2005; accepted 4 April 2005. published online 24 May 2005.
Background
Respiratory viruses induce asthma exacerbations and airway hyperresponsiveness (AHR). Atopy is an important risk factor for asthma persistence.
Objective
We sought to evaluate whether atopy is a risk factor for prolonged AHR after upper respiratory tract infections (URIs).
Methods
Twenty-five children (13 atopic and 12 nonatopic children) with intermittent virus-induced asthma were studied. Clinical evaluation, skin prick tests, methacholine bronchoprovocation, questionnaires, and a nasal wash specimen were obtained at baseline. For 9 months, subjects completed diary cards with respiratory symptoms. During their first reported cold, a nasal wash specimen was obtained. Methacholine provocation was performed 10 days and 5, 7, 9, and 11 weeks later. In case a new cold developed, the provocation schedule was followed from the beginning.
Results
Viruses were detected in 17 (68%) of 25 patients during their first cold, with rhinovirus being most commonly identified (82%). AHR increased significantly 10 days after the URI, equally in both groups (P=.67), and remained so up to the fifth week. Duration of AHR in subjects experiencing a single URI ranged from 5 to 11 weeks, without a significant difference between groups. In the duration of the study, atopic children experienced more colds and asthma exacerbations than nonatopic children. Thus for duration of AHR, significant prolongation was noted in the atopic group when assessed cumulatively.
Conclusion
In asthmatic children the duration of AHR after a single natural cold is 5 to 11 weeks. However, an increased rate of symptomatic cold and asthma episodes in atopic children is associated with considerable cumulative prolongation of AHR, which might help explain the role of atopy as a risk factor for asthma persistence.
Disclosure of potential conflict of interest: N. Papadopoulos has received grants–research support from GlaxoSmithKline and AstraZeneca. P. Saxoni-Papageorgiou has received grants–research support from Novartis and Schering-Plough. All other authors—none disclosed.
∗ Drs Xepapadaki and Papadopoulos contributed equally to this work.
ABSTRACT