Asthma is a disease characterised by reversible airways obstruction, bronchial hyper-responsiveness (BHR), and chronic inflammation of the bronchial mucosal lining. Structural changes in the airway wall, collectively known as airway wall remodelling, include, subbasement membrane thickening, smooth muscle hyperplasia/hypertrophy, and collagen deposition. These changes may be responsible for an increased decline in lung function, irreversible airflow obstruction and BHR seen in chronic asthma.
Conditions
Interventions
Trade Name: Pulmicort
Product Name: Budesonide
Pharmaceutical Form: Inhalation powder
INN or Proposed INN: BUDESONIDE
CAS Number: 51333223
Other descriptive name: pulmicort
Concentration unit: µg micr
Sponsors
Imperial College
Eligibility
Sex/Gender
All
Inclusion criteria
Inclusion criteria: Physician diagnosis of asthma Age 18-60 Intermittent asthma symptoms 80% of predicted Not on inhaled corticosteroid therapy Are the trial subjects under 18? no Number of subjects for this age range: F.1.2 Adults (18-64 years) yes F.1.2.1 Number of subjects for this age range F.1.3 Elderly (>=65 years) no F.1.3.1 Number of subjects for this age range
Exclusion criteria
Exclusion criteria: Previous long-term use of inhaled corticosteroids (within 1 year of entry into study) Past History of hypersensitivity to budesonide Current smokers, or less than 3 years since quitting smoking Less than 4 weeks from an exacerbation On steroid-sparing agent or immunosuppressant such as azathioprine, methotrexate and ciclosporin Concomitant anti-IgE therapy Pregnancy Previous bronchoscopy within three months of this study
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Main Objective: The main objective is to evaluate how treatment with inhaled corticosteroids affects the characteristics of airway smooth muscle cells. Our hypothesis is that airway smooth muscle cell dysfunction plays an important role in the pathogenesis of asthma, and that treatment with inhaled corticosteroids reverses the abnormalities in airway smooth muscle cell function.;Secondary Objective: ;Primary end point(s): Primary endpoints: 1. Changes in airway smooth muscle (ASM) mass, proliferation and migration after inhaled corticosteroid therapy 2. Changes in chemokine release after inhaled corticosteroid therapy Secondary endpoints: 1. Changes in sub-basement membrane thickness and inflammatory cell count after inhaled corticosteroid therapy 2. Correlation between ASM mass and airway hyper-responsiveness | — |
Countries
United Kingdom
Outcome results
None listed