Serum eosinophil cationic protein (ECP) as a mediator of inflammation in acute asthma, during resolution and during the monitoring of stable asthmatic patients treated with inhaled steroids according to a dose reduction schedule

Citation
G. Kunkel et Ac. Ryden, Serum eosinophil cationic protein (ECP) as a mediator of inflammation in acute asthma, during resolution and during the monitoring of stable asthmatic patients treated with inhaled steroids according to a dose reduction schedule, INFLAMM RES, 48(2), 1999, pp. 94-100
Citations number
21
Categorie Soggetti
Immunology
Journal title
INFLAMMATION RESEARCH
ISSN journal
10233830 → ACNP
Volume
48
Issue
2
Year of publication
1999
Pages
94 - 100
Database
ISI
SICI code
1023-3830(199902)48:2<94:SECP(A>2.0.ZU;2-G
Abstract
Objective and Design: The main objective was to establish the level of seru m ECP in a group of adult asthmatic patients with acute exacerbation and th e following resolution and in another group of adult, stable asthmatic pati ents during reduction of inhaled steroids. Subjects and Treatment: Acute group: Twenty-one asthmatic patients admitted to the asthma clinic with acute deterioration of their asthma were set on oral steroids which were reduced to 0 within one week. Reduction group: For ty-four stable asthmatic patients on maintenance inhaled steroids were incl uded and, on the basis of their peak expiratory flow (PEF) values, adjustme nts in the doses of steroids were made. Control group: Twenty stable asthma tics on a constant dose of inhaled steroids were enrolled as controls. Methods: All patients registered daily PEF measurements and spirometry was performed at each visit. Blood samples were drawn and analysed for eosinoph il cationic protein (ECP), myeloperoxidase (MPO), eosinophils and neutrophi ls. Results: ECP was low and within the normal range for all three groups at st udy entry. (Acute group = 8.4 mu g/l, reduction group = 3.7 mu g/l and cont rol group = 4.6 mu g/l). Nevertheless, the value in the acute group was sig nificantly higher than in the control group (p = 0.005). The levels in the acute group decreased significantly (p = 0.004) after one week on oral ster oids. No significant changes in ECP were observed in the reduction group or in the control group during the follow-up period. The lung function was lo w in the acute group at inclusion, forced expiratory volume in one second ( FEV1) = 47.1% of predicted, and increased significantly during the treatmen t period (p = 0.006). The patients in the reduction- and control group show ed small variations in lung function during the whole study, FEV1 > 70% and PEF > 80% of predicted, respectively. No correlation between atopy and ECP was found in the patients irrespective of the stage of disease. Conclusions: This study suggests that the resolution of acute asthma exacer bations during treatment could be followed using ECP determinations. In sta ble asthmatics on inhaled steroids and with normal ECP levels, a dose reduc tion could be indicated. A longer period after tapering off steroids is pro posed to confirm the benefit of ECP measurements for controlling asthma.