Peripheral Blood Eosinophil Counts and Serum ECP in Adolescents with Long-term Asthma Remission and Persistent Bronchial Hyperresponsiveness: Comparison with Adolescents with Symptomatic Asthma

Kang, Hee; Yoo, Young; Yu, Jinho; Park, Yang; Koh, Young Yull

Abstract

PURPOSE
Bronchial hyperresponsiveness(BHR) in asthma is thought to be a consequence of underlying airway inflammation. But the mechanism responsible for persistent BHR in adolescents with long-term asthma remission is poorly understood. The aim of this study was to examine whether BHR in adolescents with asthma remission is associated with peripheral blood eosinophilia and/or increased serum levels of eosinophil cationic protein(ECP).
METHODS
We studied 35 adolescents with long-term asthma remission(neither symptoms nor medication during the previous two years) who have persistent BHR(remission group) and 35 adolescents with symptomatic asthma(symptomatic group) who were matched for methacholine provocative concentration producing a 20% fall in FEV1(PC20) with subjects in the remission group. The peripheral blood eosinophil counts and serum ECP concentrations were compared between these two groups. Correlations between PC20 and peripheral blood eosinophil counts or serum ECP concentrations were assessed in these two groups.
RESULTS
Peripheral blood eosinophil counts and serum ECP concentrations were significantly lower in the remission group than in the symptomatic group(273+/-108 vs. 365+/-178/microliter; 16.3+/-9.4 vs. 26.5+/-15.1 microgram/L, both, P<0.05). PC20 was correlated with peripheral blood eosinophil counts and serum ECP concentrations in the symptomatic group(r=-0.385, P=0.022; r=-0.439, P=0.008), but not in the remission group(r=-0.292, P=0.089; r=-0.243, P=0.159).
CONCLUSION
BHR in adolescents with long-term asthma remission is not associated with peripheral blood eosinophilia or an increase in serum ECP concentration, which suggests that BHR in this clinical setting may not be attributed to airway eosinophilic inflammation. Further studies including direct assessment of airway inflammation are needed to confirm this conclusion.