BACKGROUND: Serum eosinophil cationic protein (ECP) is suggested to reflect the degree of bronchial inflammation and hyperreactivity in patients with asthma. We measured serum ECP levels before and 1 and 5 months after treatment with inhaled budesonide (n = 10) or sodium cromoglycate (SCG) (n = 7) in children with asthma. METHODS: The daily dose of budesonide was 800 micrograms/m2 during the first month and 400 micrograms/m2 during the next 4 months. ECP levels were determined by radioimmunoassay. RESULTS: ECP decreased during the 5 months of treatment (p = 0.020 for treatment groups combined; p = 0.049 for the budesonide group; p = NS for the SCG group). The higher the serum ECP level at entry, the more it decreased during treatment, both in the budesonide group (r = -0.697, p < 0.05) and in the SCG group (r = -0.893, p < 0.05). No correlation was found between the ECP level and the ratio of forced expiratory volume in 1 second to forced vital capacity (FEV1%) or between changes in these. However, basal pulmonary function was reduced in 8 of 16 subjects only, and FEV1% did not change significantly in either group. Thus the absence of a correlation is understandable. CONCLUSIONS: The clinical value of the sensitive decrease in serum ECP remains to be established.
BACKGROUND: Serum eosinophil cationic protein (ECP) is suggested to reflect the degree of bronchial inflammation and hyperreactivity in patients with asthma. We measured serum ECP levels before and 1 and 5 months after treatment with inhaled budesonide (n = 10) or sodium cromoglycate (SCG) (n = 7) in children with asthma. METHODS: The daily dose of budesonide was 800 micrograms/m2 during the first month and 400 micrograms/m2 during the next 4 months. ECP levels were determined by radioimmunoassay. RESULTS:ECP decreased during the 5 months of treatment (p = 0.020 for treatment groups combined; p = 0.049 for the budesonide group; p = NS for the SCG group). The higher the serum ECP level at entry, the more it decreased during treatment, both in the budesonide group (r = -0.697, p < 0.05) and in the SCG group (r = -0.893, p < 0.05). No correlation was found between the ECP level and the ratio of forced expiratory volume in 1 second to forced vital capacity (FEV1%) or between changes in these. However, basal pulmonary function was reduced in 8 of 16 subjects only, and FEV1% did not change significantly in either group. Thus the absence of a correlation is understandable. CONCLUSIONS: The clinical value of the sensitive decrease in serum ECP remains to be established.