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  • Title: Absence of association of peripheral blood eosinophilia or increased eosinophil cationic protein with bronchial hyperresponsiveness during asthma remission.
    Author: Koh YY, Kang H, Nah KM, Kim CK.
    Journal: Ann Allergy Asthma Immunol; 2003 Sep; 91(3):297-302. PubMed ID: 14533663.
    Abstract:
    BACKGROUND: The mechanisms responsible for persistent bronchial hyperresponsiveness (BHR) in adolescents with long-term asthma remission are poorly understood. OBJECTIVE: To determine whether BHR in adolescents with asthma remission is associated with peripheral blood eosinophilia, increased serum levels of eosinophil cationic protein (ECP), or both findings. METHODS: We classified 51 adolescents with long-term asthma remission (neither asthma-related symptoms nor medication during the previous 2 years) into 28 BHR-positive patients (methacholine PC20 [provocative concentration causing a 20% decrease in forced expiratory volume in 1 second] <18 mg/mL) and 23 BHR-negative patients. The peripheral blood eosinophil counts and serum ECP concentrations were compared between these 2 groups. Twenty-eight patients with symptomatic asthma (symptomatic group), matched for methacholine PC20 level with study subjects in the BHR-positive remission group, and 28 healthy adolescents (control group) were also studied. RESULTS: No significant differences in the peripheral blood eosinophil counts (262.1 +/- 117.0/microL vs 253.9 +/- 165.0/microL) and the serum ECP levels (15.6 +/- 10.0 microg/L vs 15.8 +/- 11.9 microg/L) were found between the BHR-positive and BHR-negative remission groups, respectively. The BHR-positive remission group differed from the symptomatic group (372.9 +/- 190.3/microL, P < 0.05; 26.6 +/- 11.3 microg/L, P < 0.01) in both blood indices but resembled the control group (214.6 +/- 118.6/microL and 12.1 +/- 4.8 microg/L; both, no significant difference). CONCLUSIONS: BHR in adolescents with long-term asthma remission is not associated with peripheral blood eosinophilia or an increase in serum ECP concentration. This finding suggests that the mechanism underlying BHR in this clinical setting may differ from that in symptomatic asthma.
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