The Effects of Montelukast on Smokers With Asthma

This study has been completed.
Sponsor:
Information provided by (Responsible Party):
Chang-Keun Kim, Dr., Inje University
ClinicalTrials.gov Identifier:
NCT00712335
First received: July 7, 2008
Last updated: April 18, 2012
Last verified: April 2012

July 7, 2008
April 18, 2012
February 2007
May 2011   (final data collection date for primary outcome measure)
Sputum Neutrophil Percentages [ Time Frame: 24 weeks ] [ Designated as safety issue: No ]
Week 24 sputum neutrophil percentages were measured in active treatment groups.
Sputum neutrophil counts [ Time Frame: 180 days ] [ Designated as safety issue: No ]
Complete list of historical versions of study NCT00712335 on ClinicalTrials.gov Archive Site
  • Sputum Eosinophil Percentages [ Time Frame: 24 weeks ] [ Designated as safety issue: No ]
    Secondary endpoints of inflammatory markers (sputum eosinophil percentages at 24 weeks) were measured in active treatment groups
  • Sputum IL-8 Levels [ Time Frame: 24 weeks ] [ Designated as safety issue: No ]
    Week 24 sputum IL-8 levels in active treatment groups
  • Sputum GM-CSF Levels [ Time Frame: 24 weeks ] [ Designated as safety issue: No ]
    Week 24 sputum GM-CSF levels in active treatment groups were measured.
  • Sputum IFN-gamma/IL-5 Ratios [ Time Frame: 24 weeks ] [ Designated as safety issue: No ]
    Week 24 sputum IFN-gamma/IL-5 ratios were determined in active treatment groups.
  • Sputum Eotaxin Levels [ Time Frame: 24 weeks ] [ Designated as safety issue: No ]
    Week 24 sputum eotaxin levels in active treatment groups were measured.
  • Sputum RANTES Levels [ Time Frame: 24 weeks ] [ Designated as safety issue: No ]
    Week 24 sputum RANTES levels in active treatment groups were measured.
Sputum cells, eosinophil and urinary markers,neutrophils, and Th1/Th2 cytokines [ Time Frame: 180 days ] [ Designated as safety issue: No ]
Not Provided
Not Provided
 
The Effects of Montelukast on Smokers With Asthma
The Effects of Montelukast on Sputum Cells and Inflammatory Markers in Smokers With Asthma

The purpose of this study is:

  1. To compare neutrophilia, eosinophilic inflammatory markers and asthma symptom indices between smokers and non-smokers.
  2. To elucidate the mechanism by which cigarette smokers are resistant to corticosteroids.

Many smokers have insufficient control of their symptoms due to inefficacy of ICS in this subpopulation of asthmatics. Cigarette smoking has been shown to stimulate production of cysLTs. CysLTs could activate production of IL-8 for neutrophilia as well as cause eosinophilia in the airway of asthmatics.

LTRAs are felt to be less efficacious than ICS in smokers with asthma. However, LTRA's unique mechanism of action could be particularly efficacious in preventing worsening symptoms and lung function for smokers with asthma. Given this, along with the fact that ICS are less effective in smokers, targeting cysLT could lead to significant clinical benefits for asthmatic smokers.

Data from this study may possibly serve as crucial data for the significant clinical benefits for asthmatic smokers and determination of the mechanism of corticosteroid resistance in smokers with asthma.

Interventional
Phase 4
Allocation: Randomized
Endpoint Classification: Pharmacodynamics Study
Intervention Model: Parallel Assignment
Masking: Single Blind (Subject)
Primary Purpose: Diagnostic
  • Asthmatic Smokers
  • Non-asthmatic Smokers
  • Drug: Fluticasone Propionate
    DPI 250 mcg BID for 3 weeks
    Other Name: inhaled corticosteroid
  • Drug: Montelukast
    PO 10 mg QHS for 3 weeks
    Other Name: leukotriene receptor antagonist
  • Drug: Salmeterol
    DPI 50mg BID for 3 weeks
    Other Name: long-acting beta-agonist
  • Experimental: 1

    Asthmatic smokers treated with combination therapy:

    Fluticasone propionate dosage - DPI 250 mcg BID for 3 months Salmeterol dosage - DPI 50 mcg BID for 3 months

    Interventions:
    • Drug: Fluticasone Propionate
    • Drug: Salmeterol
  • Experimental: 2

    Asthmatic smoker treated with Montelukast only:

    Montelukast dosage: PO 10 mg QHS for 3 months

    Intervention: Drug: Montelukast
  • Active Comparator: 3

    Non-smoking asthmatics treated with combination therapy:

    Fluticasone propionate dosage - DPI 250 mcg BID for 3 months Salmeterol dosage - DPI 50 mcg BID for 3 months

    Interventions:
    • Drug: Fluticasone Propionate
    • Drug: Salmeterol
  • Active Comparator: 4

    Non-smoking asthmatic treated with Montelukast only:

    Montelukast dosage: PO 10 mg QHS for 3 months

    Intervention: Drug: Montelukast
  • No Intervention: 5
    Normal controls
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
105
May 2011
May 2011   (final data collection date for primary outcome measure)

Inclusion Criteria:

Asthmatics:

  • clinical history of asthma for at least 1 year
  • with evidence of reversible airway obstruction,
  • two documented FEV1 between 60-85%,
  • PC20 < 4mg/ml by methacholine challenge test
  • and average baseline β-agonist use of 2 puffs/day

Smokers:

  • smoke 1/2 to 2 packs a day
  • with a smoking history of 5-30 pack years

Non-smokers:

  • Non-smokers will have either never smoked or have stopped smoking cigarettes over 5 years ago

Exclusion Criteria:

  • positive HCG (for females)
  • have a respiratory tract infection or need oral corticosteroids within the preceding 6 weeks
  • history of COPD or respiratory disorder other than asthma
  • history of psychiatric illness
  • allergy to fluticasone propionate, salmeterol, montelukast or any of their components
  • significant, unstable medical condition other than asthma
  • history of life-threatening asthma exacerbation requiring intubation and mechanical ventilation in the last ten years
Both
18 Years to 45 Years
Yes
Contact information is only displayed when the study is recruiting subjects
Korea, Republic of
 
NCT00712335
MASK2008
Yes
Chang-Keun Kim, Dr., Inje University
Inje University
Not Provided
Principal Investigator: Chang-Keun Kim, MD, PhD Asthma and Allergy Center, Inje University Sanggye Paik Hospital
Inje University
April 2012

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP