title: Effect of inhaled steroids on increased collagen synthesis in asthma.
abstract: BACKGROUND
  We previously reported that sputum levels of procollagen type I C-terminal peptide (PICP), a marker of ongoing collagen type I deposition, are increased in proportion to airway inflammation in asthma patients.
  
  
  OBJECTIVE
  In this study, we examined the effect of inhaled corticosteroids on increased collagen synthesis in step 2-4 asthmatics.
  
  
  METHODS
  We compared the sputum PICP concentrations of 25 steroid-naive asthmatics, 25 normal volunteers, and 10 subjects with chronic obstructive pulmonary disease. Asthma subjects were also instructed to start fluticasone propionate treatment, and the percentage of forced expiratory volume in 1 s, sputum eosinophil counts, sputum PICP concentrations, and sputum transforming growth factor-beta-positive cell counts before treatment were compared with those 1 month after treatment.
  
  
  RESULTS
  Sputum PICP concentrations were detected in the following order: asthma group >or= chronic obstructive pulmonary disease group > control group. Asthma patients showing high sputum PICP belonged to step 4, although there was no correlation between sputum PICP and asthma severity. Treatment with fluticasone propionate not only significantly improved the mean percentage of forced expiratory volume in 1 s (from 66.7 to 87.2%), but also decreased the mean sputum eosinophil counts (from 13.4 to 5.8%), the mean sputum PICP concentrations (from 30.8 to 10.2 ng/ml), and the mean sputum tumor growth factor-beta-positive cells (from 11.3 to 2.8%). Nevertheless, a significant difference in sputum PICP concentrations was still observed between the control group and the steroid-treated asthma group.
  
  
  CONCLUSIONS
  The present results suggest that inhaled corticosteroid treatment might reduce sputum indexes of collagen metabolism and eosinophilic inflammation in asthma patients.
authors.affiliation: Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
authors.forename: Sachiko
authors.initials: S
authors.lastname: Kai
authors.forename: Akihiro
authors.initials: A
authors.lastname: Nomura
authors.forename: Yuko
authors.initials: Y
authors.lastname: Morishima
authors.forename: Yukio
authors.initials: Y
authors.lastname: Ishii
authors.forename: Tohru
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Takumi
authors.initials: T
authors.lastname: Kiwamoto
authors.forename: Takashi
authors.initials: T
authors.lastname: Iizuka
authors.forename: Kiyohisa
authors.initials: K
authors.lastname: Sekizawa
mesh_terms: D000280:Administration, Inhalation; D000328:Adult; D000368:Aged; D001249:Asthma / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D015415:Biomarkers / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D005938:Glucocorticoids / Q000008:administration & dosage*; D006801:Humans; D007150:Immunohistochemistry; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000096:biosynthesis* / Q000187:drug effects; D011347:Procollagen / Q000096:biosynthesis* / Q000187:drug effects; D011379:Prognosis; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D012720:Severity of Illness Index; D013183:Sputum / Q000166:cytology / Q000378:metabolism*; D016211:Transforming Growth Factor alpha / Q000378:metabolism
chemical_list: D015415:Biomarkers; D005938:Glucocorticoids; D010446:Peptide Fragments; D011347:Procollagen; D016211:Transforming Growth Factor alpha; C042813:procollagen type I carboxy terminal peptide