title: Enhanced prostaglandin E2 secretion in sputum from asthmatic patients after zafirlukast therapy.
abstract: OBJECTIVE
  Leukotrienes are important inflammatory mediators of bronchial asthma that cause bronchoconstriction, mucous secretion, and increased vascular permeability. Current guidelines recommend anti-leukotriene agents as alternative treatments for asthma; however, data on their anti-inflammatory effect is lacking.
  
  
  METHODS
  The purpose of this study was to determine the anti-inflammatory effect of zafirlukast, a leukotriene antagonist, in patients with bronchial asthma. A total of 30 adult patients with mild persistent asthma received 6 weeks of zafirlukast treatment. Peak expiratory flow rate (PEFR) was determined before and after therapy to assess clinical efficacy. Both serum and sputum samples were collected before and after therapy and concentrations of eosinophil cationic protein (ECP), prostaglandin E2 (PGE2), and leukotriene E4 (LTE4) were measured.
  
  
  RESULTS
  A significant improvement in PEFR was found after zafirlukast therapy (p = 0.017). There was also a significant reduction in serum ECP concentration (13.6 +/- 2.4 micrograms/L vs 10.3 +/- 2.1 micrograms/L, p < 0.025) and a significant increase in sputum PGE2 concentration (112.7 +/- 14.0 pg/mL vs 176.8 +/- 32.1 pg/mL, p < 0.01). The percentage eosinophil count and the concentrations of ECP and LTE4 in the sputum were not significantly different after therapy.
  
  
  CONCLUSIONS
  This study found a significant reduction in serum ECP and a significant increase in sputum PGE2 concentrations in asthmatic patients after zafirlukast treatment, both of which were significantly associated with improvement in PEFR. The modulation of PGE2 and ECP production might occur through the anti-inflammatory effect of zafirlukast.
authors.affiliation: Section of Allergy and Clinical Immunology, Cathay General Hospital, 280, Section 4, Jen-Ai Road, Taipei, Taiwan.
authors.forename: J J
authors.initials: JJ
authors.lastname: Tsai
authors.forename: Y C
authors.initials: YC
authors.lastname: Su
authors.forename: S C
authors.initials: SC
authors.lastname: Chan
authors.forename: C K
authors.initials: CK
authors.lastname: Ho
authors.forename: T C
authors.initials: TC
authors.lastname: Feng
mesh_terms: D000328:Adult; D000368:Aged; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy* / Q000378:metabolism; D001798:Blood Proteins / Q000032:analysis; D015232:Dinoprostone / Q000378:metabolism*; D047091:Eosinophil Granule Proteins; D006801:Humans; D007211:Indoles; D020024:Leukotriene Antagonists / Q000627:therapeutic use*; D017999:Leukotriene E4 / Q000378:metabolism; D008448:Maximal Expiratory Flow Rate / Q000187:drug effects; D008875:Middle Aged; D048448:Phenylcarbamates; D012260:Ribonucleases; D013183:Sputum / Q000378:metabolism*; D013449:Sulfonamides; D014105:Tosyl Compounds / Q000627:therapeutic use*
chemical_list: D018927:Anti-Asthmatic Agents; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D007211:Indoles; D020024:Leukotriene Antagonists; D048448:Phenylcarbamates; D013449:Sulfonamides; D014105:Tosyl Compounds; D017999:Leukotriene E4; D012260:Ribonucleases; D015232:Dinoprostone; C062735:zafirlukast