The inflammatory marker serum eosinophil cationic protein (ECP) compared with PEF as a tool to decide inhaled corticosteroid dose in asthmatic patients.
The objective of this study was to compare the inflammatory marker eosinophil cationic protein (ECP) with peak expiratory flow (PEF) in determining the therapeutic needs of inhaled corticosteroids in asthma patients assessed as asthma symptoms. A randomized, single-blind study over 6 months was performed at six specialist centres in Europe. In total, 164 adult patients with moderate to severe symptomatic asthma and regular use of inhaled corticosteroids were included. After a run-in period of 2 weeks patients were randomly allocated to the ECP or the PEF monitoring group. The dose of inhaled cort costeroids was adjusted every fourth week based on the current serum ECP value or pre-bronchodilator morning PEF values as surrogate markers of therapeutic needs. At the end of the study there were no statistically significant differences in the mean daily symptom score or the percentage of symptom-free days between the two groups. The mean daily dose of inhaled corticosteroids was similar in the two groups at the start of the study but the algorithms used to adjust the dose of inhaled corticosteroids resulted in an increased use of inhaled corticosteroids in both groups. The mean daily dose of inhaled corticosteroids over the whole study period was significantly lower in the ECP group compared withthe PEF group (1246 vs. 1667 microg, P = 0.026). In the ECP group, forced expiratory volume in I sec (FEV)% predicted was lower at the end ofthe study compared with the begining (92% vs. 87%, P = 0 .0009), although there was no significant difference between the two groups. None of the used algorithms for ECP and PEF led to improvement in symptom scores, in spite of increased doses of inhaled corticosteroids. In this respect, both methods were equivalent and insufficient. Recommendations suggesting lung function tests in current guidelines may be difficult to translate into clinical practice, however, a combination of inflammatory markers, lung function and symptoms may still improve asthma control.
Löwhagen
O
O
Asthma and Allergy Research Group, Sahlgrenska University Hospital, Gothenburg, Sweden. olle.lowhagen@lungall.gu.se
Wever
A M
AM
Lusuardi
M
M
Moscato
G
G
De Backer
W A
WA
Gandola
L
L
Donner
C F
CF
Ahlstedt
S
S
Larsson
L
L
Holgate
S T
ST
D000280:Administration, Inhalation; D000287:Administration, Topical; D000328:Adult; D000704:Analysis of Variance; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage*; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001798:Blood Proteins / Q000032:analysis*; D004334:Drug Administration Schedule; D047091:Eosinophil Granule Proteins; D004804:Eosinophils; D005260:Female; D005938:Glucocorticoids; D006801:Humans; D007958:Leukocyte Count; D008168:Lung / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010366:Peak Expiratory Flow Rate; D016016:Proportional Hazards Models; D012260:Ribonucleases; D016037:Single-Blind Method; D018709:Statistics, Nonparametric
D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D005938:Glucocorticoids; D012260:Ribonucleases