Effect of oral glucocorticoid treatment on serum inflammatory markers in acute asthma.

Background: Acute asthma is associated with elevated serum concentrations of products of activated T cells and eosinophils.
Aims: To compare the changes in concentrations of these products with disease severity and changes in lung function following oral prednisolone treatment.
Methods: Twenty patients (mean age 8.7 years) were recruited on admission with acute asthma to a district general hospital. Disease severity was recorded before and after treatment with oral prednisolone using a validated pulmonary index score. Serum concentrations of interleukin (IL)-4, IL-5, soluble (s)CD25 (soluble IL-2 receptor), using a specific enzyme linked immunosorbent assay, and eosinophil cationic protein (ECP), using radioimmunoassay, were measured concomitantly. Non-asthmatic children (n = 6, mean age 9.2 years) undergoing elective surgery were recruited as controls, and serum samples were obtained on one occasion without treatment. Main outcome measures were changes in serum concentrations of cytokines and ECP, clinical asthma severity score, and peak expiratory flow rate.
Results: As expected, oral glucocorticoid treatment in the children with asthma was associated with clinical improvement and also with significant reductions in serum concentrations of IL-5 (mean 5.59 to 2.19 pg/ml, p = 0.0001), sCD25 (mean 2236 to 1772 pg/ml, p = 0.002), and ECP (mean 54.3 to 33. 1 pg/ml, p = 0.0001). Serum IL-4 concentrations, in most patients and all the controls, remained below the sensitivity of the assay. However, serum concentrations of IL-5, sCD25, and ECP remained significantly higher than in controls, even after treatment with oral glucocorticoids (p = 0.03).
Conclusions: These data suggest that T cell mediated inflammation may persist in childhood asthma despite apparent clinical remission associated with conventional doses of prednisolone. The long term consequences of persistent inflammation after an apparently treated acute attack of asthma require clarification. Clinical assessment and pulmonary function are inadequate surrogates for airway inflammation.