title: [The influence oc glycocorticoid therapy on sputum ECP concentration in symptomatic patients with bronchial asthma].
abstract: ECP released from the granules of activated eosinophils is regarded to be a marker of airway inflammation in asthma. The study was performed to compare the usefulness of measuring serum and sputum ECP for monitoring the asthma treatment. 29 subjects with mild to moderate asthma (mean age 41 +/- 17) were admitted in exacerbation (FEV1 55.54 +/- 87.49% N). 10 subjects with grass pollen asymptomatic asthma and 10 healthy subjects were also enrolled in the study. Patients with symptomatic asthma were ordered 30 mg prednisone for 2 weeks and they continued during next 2 weeks inhaled budesonide therapy. The concentrations of ECP (mcg/L) were determined by CAP-system (Pharmacia). The total eosinophil count and serum ECP in all subjects treated orally and next by inhaled GKS didn't differ statistically. The highest sputum ECP concentration was determined in exacerbation of asthma 84.5 +/- 78 mcg/L and statistically were reduced after 2-weeks of prednisone treatment 24.4 +/- 12.1 mcg/L (p = 0.05). In following 2 weeks of budesonide treatment sputum ECP concentration was statistically negligible in relation to previous treatment in spite of increasing tendency (50 +/- 61.3 mcg/L (p = 0.2394). In asymptomatic grass pollen asthma sputum ECP concentration was 19.7 +/- 9.4 mcg/L, higher than in controls 12 +/- 5.8 mcg/L (p = 0.04). There were a significant correlations between total eosinophil count and serum (r = 0.6396) and sputum ECP(r = 0.4683) in exacerbation.
  
  
  CONCLUSIONS
  1. In asthma exacerbation elevated sputum ECP concentration was observed. 2. In consequence of prednisone treatment the sputum ECP concentration was reduced. 3. Sputum ECP measurement is more accurate than serum ECP for monitoring the effectiveness of treatment. 4. Sputum ECP concentration is a sensitive parameter which discriminate asymptomatic patients with asthma from healthy subjects.
authors.affiliation: Klinika i Katedra Chorób Wewnetrznych, Pneumonologii i Alergologii Akademii Medycznej w Warszawie.
authors.forename: Joanna
authors.initials: J
authors.lastname: Hermanowicz-Salamon
authors.forename: Hanna
authors.initials: H
authors.lastname: Grubek-Jaworska
authors.forename: Jolanta
authors.initials: J
authors.lastname: Wrońska
authors.forename: Wacław
authors.initials: W
authors.lastname: Droszcz
authors.forename: Ryszarda
authors.initials: R
authors.lastname: Chazan
mesh_terms: D000328:Adult; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage*; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology*; D015415:Biomarkers / Q000032:analysis; D001798:Blood Proteins / Q000378:metabolism*; D019819:Budesonide / Q000008:administration & dosage; D016022:Case-Control Studies; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000378:metabolism; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D011241:Prednisone / Q000008:administration & dosage; D012260:Ribonucleases; D013183:Sputum / Q000378:metabolism*; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D019819:Budesonide; D012260:Ribonucleases; D011241:Prednisone