title: Montelukast, a leukotriene receptor antagonist, reduces the concentration of leukotrienes in the respiratory tract of children with persistent asthma.
abstract: BACKGROUND
  Leukotrienes are bronchoactive mediators secreted by inflammatory cells in the respiratory mucosa on exposure to asthma triggers.
  
  
  OBJECTIVE
  We investigated the effect of montelukast, a leukotriene receptor antagonist, on the release of leukotrienes in the respiratory mucosa of children with persistent asthma.
  
  
  METHODS
  Twenty-three children aged 6 to 11 years with moderately severe asthma were treated in a cross-over design starting, after a 2-week run in period, with either montelukast (n = 12) or cromolyn (n = 11) for 4 weeks with a 2-week washout period between treatments. Twelve of them were then treated with either montelukast or beclomethasone for 6 months. The use of beta(2)-agonists was recorded on a diary card. The concentration of leukotriene C(4) (LTC(4)) was measured by HPLC in nasal washes obtained before and at the end of each treatment period. Eosinophilic cationic protein (ECP) was measured in the nasal washes by RIA.
  
  
  RESULTS
  The LTC(4) concentration significantly decreased in the children treated for the first 4 weeks with montelukast, from 5.03 +/- 1.17 to 1.42 +/- 0.33 ng/mL (P <.005), and a nonsignificant increase was noted in children treated with cromolyn, from 3.37 +/- 1.11 to 5.88 +/- 2.17 ng/mL (P =.17). ECP concentration also decreased in the children receiving montelukast (P =.12). The concentration of LTC(4) remained low after 3 and 6 months of treatment with montelukast (0.8 +/- 0.7 and 1.0 +/- 0.3 microg/mL) and was lower than with beclomethasone. Children treated with montelukast required significantly fewer beta(2)-agonists (P <.04),
  
  
  CONCLUSIONS
  Montelukast reduces the concentration of leukotrienes in the respiratory tract of children with persistent asthma parallel to reduction in ECP and clinical improvement. This effect was not observed when the same children were treated with cromolyn.
authors.affiliation: Schneider Children's Medical Center of Israel, Petah Tikva.
authors.forename: B
authors.initials: B
authors.lastname: Volovitz
authors.forename: E
authors.initials: E
authors.lastname: Tabachnik
authors.forename: M
authors.initials: M
authors.lastname: Nussinovitch
authors.forename: B
authors.initials: B
authors.lastname: Shtaif
authors.forename: H
authors.initials: H
authors.lastname: Blau
authors.forename: I
authors.initials: I
authors.lastname: Gil-Ad
authors.forename: A
authors.initials: A
authors.lastname: Weizman
authors.forename: I
authors.initials: I
authors.lastname: Varsano
mesh_terms: D000085:Acetates / Q000494:pharmacology*; D001249:Asthma / Q000188:drug therapy*; D001507:Beclomethasone / Q000627:therapeutic use; D001798:Blood Proteins / Q000378:metabolism; D002648:Child; D004205:Cromolyn Sodium / Q000494:pharmacology / Q000627:therapeutic use; D018592:Cross-Over Studies; D003521:Cyclopropanes; D047091:Eosinophil Granule Proteins; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D020024:Leukotriene Antagonists / Q000494:pharmacology*; D015289:Leukotrienes / Q000378:metabolism*; D008297:Male; D011804:Quinolines / Q000494:pharmacology*; D012137:Respiratory System / Q000737:chemistry*; D012260:Ribonucleases; D013440:Sulfides
chemical_list: D000085:Acetates; D001798:Blood Proteins; D003521:Cyclopropanes; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D020024:Leukotriene Antagonists; D015289:Leukotrienes; D011804:Quinolines; D013440:Sulfides; D012260:Ribonucleases; D001507:Beclomethasone; C093875:montelukast; D004205:Cromolyn Sodium