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ENFUMOSA: The European Network For Understanding Mechanisms Of Severe Asthma (investigators: B. Abraham, J.M. Antó, E. Barreiro, E.H.D. Bel, J. Bousquet, J. Castellsagud, P. chanez, B. Dahién, S.E. Dahién,
. Dews, R. Djukanovic, L.M. Fabbri, G. Folkerts, M. Gaga, C. Gratziou, S.T. Holgate, P.H. Howarth, S.L. Johnston, F. Kanniess),
CORRESPONDENCE: S.T. Holgate, Respiratory Cell and Molecular Biology Research Division, Mail Point 810, Level D, Centre Block, Southampton General Hospital, Southampton, SO16 6YD, UK. Fax: 44 2380796960. E-mail: sth@soton.ac.uk
Keywords: asthma, atopy, clinical characteristics, disease severity, inflammatory biomarkers, sex-related disease
Received: July 19, 2001
Accepted May 29, 2003
This work was supported by a Concerted Action Grant for the European Union Framework IV Biomed Programme No. BMH4-96-1471, National Research Foundations in the participating countries, and unconditional support from several corporations including AstraZeneca, Bayer AG, Jaeger GmbH, Novartis Epidemiology, Pharmacia & Upjohn Diagnostics and SmithKline Beecham.
Since severe asthma is a poorly understood, major health problem, 12 clinical specialist centres in nine European countries formed a European Network For Understanding Mechanisms Of Severe Asthma (ENFUMOSA).
In a cross-sectional observational study, a total of 163 subjects with severe asthma were compared with 158 subjects whose asthma was controlled by low doses of inhaled corticosteroids (median dose of beclomethasone equivalents 666 µg). Despite being treated with higher doses of inhaled corticosteroids (median dose 1773 µg) and for a third of the severe asthmatics also being treated with regular, oral-steroid therapy (median daily dose 19 mg), the subjects with severe asthma met the inclusion criteria. The criteria required subjects to have undergone at least one asthma exacerbation in the past year requiring oral steroid treatment. Females dominated the severe asthma group (female/male ratio 4.4:1 versus 1.6:1 in the controlled asthmatics), and compared with controlled asthmatics, they had a predominantly neutrophilic inflammation (sputum neutrophils, 36 versus 28%) and evidence of ongoing mediator release but less atopy.
From these findings and other physiological and clinical data reported in this paper, it is suggested that severe asthma might be a different form of asthma rather than an increase in asthma symptoms. The findings prompt for longitudinal studies and interventions to define the mechanisms in severe asthma.
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