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Notes: Blood eosinophils, and serum levels of the eosinophil proteins, eosinophil cationic protein (ECP) and eosinophil protein X (EPX) were measured in childhood asthma. Seventeen patients mean age 11–9 years who were symptomatic with asthma, were enrolled in a study examining the eosinophil counts and eosinophil proteins at the onset of study and after treatment in relation to changes in their baseline forced expiratory volume at 1 second (FEV1) and % predicted FEV1. The patients with symptomatic asthma were compared with 17 patients mean age 12.0 years with asymptomatic asthma maintained on daily inhaled steroid and 13 patients, mean age 12.0 years, without asthma but with urticaria who served as non-asthma controls. Patients with symptomatic asthma did not have significantly higher initial eosinophil counts compared with those with asymptomatic asthma (0.43 × 109/1 vs 0.26 × 109/1, P= 0.09) but had higher serum ECP levels (28.9 μ/1 vs 18.5 μg/1). Both asthma patient groups had significantly higher serum ECP levels (P〈0.01) than the controls (9.8 μg/1). After therapy consisting of increased dose of inhaled steroids and/or oral steroids, patients in the symptomatic asthma group demonstrated a significant rise in FEV1 (1.67 1/sec at Visit 1 vs 2.08 1/ sec at Visit 2, 1〈0.01). A similar rise was seen for % predicted FEV1. Patients in the asymptomatic asthma group showed no significant change in FEV1 between visits (2.23 1/sec vs 2.37 1/sec), which was verified with the % predicted FEV1, Patients in the symptomatic asthma group showed a significant decrease in ECP level following treatment (28.9 μ/1 to 9.6 μ/1. P〈0.001) while the values in the asymptomatic group did not change (18.6 μ/1 to 15.2 μ/1 not significant). There was a significant correlation between the initial ECP level in the symptomatic asthma group and the change in the FEV| with treatment. Serum EPX levels showed similar trends but there was no significant correlation between the initial EPX levels and the changes in FEV1. Neither did blood eosinophil counts show such a correlation. This data suggests that the changes in serum ECP levels correlate with the changes in lung function subsequently to anti-inflammation therapy.

Notes: Bronchoalveolar lavage (BAL) greatly improved our understanding of asthma allowing to demonstrate the key role of inflammation in the pathogenesis of the disease. BAL is a safe procedure, even in severe patients when properly performed. BAL samples large and small airways and alveoli. Cells and mediators may be measured in BALF but they only represent an indirect estimation of the bronchial inflammation. Before performing BAL, the clinical status of the patients should be ascertained and drugs taken may have to be withdrawn. BALF markers should follow some requirements: (I) markers should be released by cells that are pertinent to airways inflammation (and reparation) in asthma, and, if possible they should be specific of a single cell type, (2) the enumeration of cells or titration of the marker or of its metabolites should be specific and sensitive, (3) if possible the titration should not be modified by the sampling procedure, (4)pilot studies should have demonstrated that the cell is incrcased or the secretory product is released during challenge in asthmatic subjects, (5) studies in a large number of patients should have demonstrated that the levels of the marker are increased in chronic asthmatics, that these levels are correlated with the severity of the disease and are decreased during effective anti-inflammatory treatment, and (6) if possible the cell or marker should be specific to asthma (but at present there is no such cell or marker). Eosinophils and granule secretory products follow most of these requirements. BAL represents an important research tool to assess the effects of therapeutic interventions.