E. Grebski et al., Does eosinophil cationic protein in sputum and blood reflect bronchial inflammation and obstruction in allergic asthmatics?, J INVES ALL, 9(2), 1999, pp. 82-88
Citations number
29
Categorie Soggetti
Clinical Immunolgy & Infectious Disease
Journal title
JOURNAL OF INVESTIGATIONAL ALLERGOLOGY & CLINICAL IMMUNOLOGY
In the assessment of asthma severity and monitoring of asthma drug therapy
eosinophils and eosinophil cationic protein (ECP) have been identified in b
lood but rarely in sputum. The aim of our study was to determine ii ECP con
centrations in blood and sputum reflect bronchial inflammation and obstruct
ion in allergic asthmatics and if inhaled steroids influence this relations
hip. We carried out a descriptive, cross-sectional study of 42 allergic ast
hmatic outpatients from a respiratory medicine department, of whom 22 were
on beta(2)-adrenergic agonists only and 20 were treated with low doses of i
nhaled steroids. Spirometry and methacholine challenge were performed and e
osinophils and ECP values in induced sputum and blood were determined The a
ge and FEV1 were similar in both groups. If was found that in patients rece
iving inhaled steroids, the methacholine PD20 was higher than in patients o
n beta(2)-adrenergic agonists only. However, there were no significant diff
erences in serum and sputum ECP between the groups (median 14.5 mu g/l vs.
17.2 mu g/l and 235 mu g/l vs. 301 mu g/l respectively). In patients not re
ceiving steroids, sputum ECP correlated positively with eosinophils in sput
um (r = 0.61, p <0.01) and inversely with FEV1 (r = -0.43, p <0.05). Serum
ECP correlated with blood eosinophils and methacholine PD20. In patients tr
eated with inhaled steroids most correlations were no longer significant. W
e concluded that ECP in sputum, rather than in blood, seems to reflect both
eosinophilic inflammation and bronchial obstruction in asthmatics not rece
iving inhaled steroids. Asthmatics on low doses of inhaled steroids had inc
reased ECP levels in sputum and serum, indicating persistent eosinophilic i
nflammation of the airways.