title: Changes in inflammatory markers following treatment of acute exacerbations of obstructive pulmonary disease.
abstract: The aim ofthe study was to investigate changes in inflammatory markers following emergency treatment of obstructive pulmonary disease. The study comprised 43 patients. After acute treatment, they were given either 30 mg of prednisolone p.o. or 1600 microg of inhaled budeson de daily for 1 week. Over the following 3 weeks, all the patients were given 1600 microg of inhaled budesonide daily. Blood samples for measurements of eosinophil cationic protein (S-ECP), eosinophil peroxidase (S-EPO), total eos nophil count (B-Eos), myeloperoxidase (S-MPO) and human neutrophil lipocaline (HNL) were taken and spirometry was performed before emergency treatment and after 1 and 4 weeks. There was no difference in the improvement in forced expiratory volume in 1 sec (FEV1) between patients given prednisolone or budesonide. Patients with an improvement in FEV1 of >20% of baseline after 1 and 4 weeks displayed a larger decrease in eosinophil markers. The correlation between deltaFEV1 and deltaS-ECP was r= -0.37, P < 0.05, deltaS-EPO -0.40, P < 0.01 and deltaB-Eos -0.44, P < 0.01, after 4 weeks. This correlation was highly significant in patients who had smoked < or = 5 pack-years, while the correlation was not significant in patients with a longer smoking history and chronic airflow limitation (best FEV <80% of predicted). We conclude that the change in eosinophil markers is correlated to the improvement in lung function in non-smokers or short-term smokers following the emergency treatment of obstructive pulmonary disease. This study indicates that following eosinophil markers is more useful in patients with asthma than patients with COPD.
authors.affiliation: Deptartment of Medical Sciences, Respiratory Medicine and Allergology, Uppsala University Hospital, Sweden. inger.dahlen@medsci.uu.se
authors.forename: I
authors.initials: I
authors.lastname: Dahlén
authors.forename: C
authors.initials: C
authors.lastname: Janson
authors.forename: E
authors.initials: E
authors.lastname: Björnsson
authors.forename: G
authors.initials: G
authors.lastname: Stålenheim
authors.forename: C G
authors.initials: CG
authors.lastname: Peterson
authors.forename: P
authors.initials: P
authors.lastname: Venge
mesh_terms: D000208:Acute Disease; D000209:Acute-Phase Proteins; D000328:Adult; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood*; D001798:Blood Proteins / Q000032:analysis; D001993:Bronchodilator Agents / Q000627:therapeutic use; D019819:Budesonide / Q000627:therapeutic use; D002352:Carrier Proteins / Q000097:blood; D016009:Chi-Square Distribution; D047091:Eosinophil Granule Proteins; D047209:Eosinophil Peroxidase; D004804:Eosinophils / Q000378:metabolism; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D000071068:Lipocalin-2; D054834:Lipocalins; D008297:Male; D008875:Middle Aged; D015513:Oncogene Proteins; D009195:Peroxidase / Q000097:blood; D010544:Peroxidases / Q000097:blood; D011239:Prednisolone / Q000627:therapeutic use; D011518:Proto-Oncogene Proteins; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood* / Q000188:drug therapy; D012260:Ribonucleases; D012907:Smoking / Q000097:blood; D018709:Statistics, Nonparametric
chemical_list: D000209:Acute-Phase Proteins; D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D001798:Blood Proteins; D001993:Bronchodilator Agents; D002352:Carrier Proteins; D047091:Eosinophil Granule Proteins; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D015513:Oncogene Proteins; D011518:Proto-Oncogene Proteins; D019819:Budesonide; D011239:Prednisolone; D047209:Eosinophil Peroxidase; D010544:Peroxidases; D009195:Peroxidase; D012260:Ribonucleases