A Phase 1 interventional study of Pulmicort in Asthma, sponsored by University of California, San Francisco. Completed at 1 site in United States. Open to participants aged 18 Years to 70 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2014-01-20.
Sponsored by University of California, San Francisco · Phase 1, Interventional, and Basic science
The purpose of this study is to identify the causes of asthma that were not previously suspected, to better understand the effects of inhaled steroids on asthma and to identify new way to treat asthma. In order to take advantage of the most current scientific expertise, we (scientists at UCSF) plan to work together with Genentech Inc. We believe that working with Genentech will provide the best chance of developing new treatments for asthma.
Asthma is a common airway disease with persistent unmet needs on terms of treatment. Although many asthmatics enjoy good control of their disease by using regularly scheduled corticosteroid treatment, a significant minority do not achieve optimal control with steroids and suffer asthma exacerbations which can be severe and even fatal. Asthma pathophysiology is complex and involves multiple cell types and multiple signaling mechanisms. One approach to this complexity has been to study responses of isolated airway cells to experimental conditions which model asthmatic inflammation; another has been genetic manipulations of candidate mediators of asthma in inbred mice. These studies have yielded important insights about possible mechanisms of asthma in humans, but the relevance of these mechanisms to human disease has not always been proven, and it is possible that unsuspected mechanism have not yet been revealed by these approaches. In the studies proposed here we will take an experimental approach which takes advantage of the distinct clinical phenotype of human asthma, the ability to measure steroid response in asthma, the relative ease of collecting airway cells and tissues by bronchoscopy, and the availability of new technologies such as high density microarrays which have probes for all genes in the genome or proteomics which can identify all proteins present in a biologic sample. Using this approach, we will identify differential expression of genes and proteins in airway cells and tissues in asthma that can then be explored further in cell and animal model systems to determine their potential as drug targets in asthma. We further believe that our approach will identify previously unsuspected mechanisms of action of corticosteroids in airway cells and tissues in asthma. Presently, relatively little is known about why some asthmatics respond well and some poorly to steroids and closing this gap in knowledge will help identify candidate genes and proteins to target in order to address unmet therapeutic needs in asthmatics with steroid resistant asthma.
3,921 studies on the registry are indexed under Asthma; 507 are open to participants now.
This study's enrollment of 127 is above the median of 83 across 2,752 interventional studies indexed under Asthma.
Browse Asthma studies →University of California, San Francisco is the lead sponsor of 2,133 studies on the registry; 376 are open to participants now.
Of its 262 completed or terminated interventional studies of FDA-regulated products, 196 (75%) have results posted.
Counted across the registry records on this site, refreshed daily.
Group C:
Exclusion Criteria:
At least one of the following symptoms, beta agonist use, or FEV1 criteria:
Asthmatics not on inhaled corticosteroids who will be put on an inhaled steroid during the study
Drug: Pulmicort
Healthy, non-asthmatics who will not be put on any intervention
Asthmatics, who are already on inhaled corticosteroids who will be put on standardized dose of inhaled corticosteroids
Drug: Pulmicort
inhaled powder of inhaled corticosteroid, 1 puff (180mcg) twice a day for 8-10 weeks
Also known as: Budesonide
Gene Expression in Airway Secretions and Tissues
The primary outcome measure for this study is the scaled mean value of three gene expression markers of IL-13 in the airway: PERIOSTIN, calcium-activated chloride channel regulator 1 (CLCA1), and plasminogen activator inhibitor-2 (SERPINB2). First, for each of the three interleukin-13 (IL-13) signature genes, the log (base-2) transformed relative expression value for each subject is measured using real-time polymerase chair reaction (PCR) and normalized with the geometric mean of 5 housekeeping genes. Next, these values are centered (by subtracting the mean for that gene) and scaled (by dividing by the standard deviation for that gene) so that each gene makes an equal, assay-independent contribution to the Th2 phenotype. Then, for each subject, the arithmetic mean of the three centered \& scaled genes is calculated, producing the "three-gene-mean" metric.
Time frame: Healthy Control: Visit 2 (at 1 week); Steroid Naive Asthmatics: Visit 2 (at 1 week); Steroid Treated Asthmatics: Visit 5 (at 9 weeks)
The MAST study enrolled 103 adults with asthma and 24 healthy controls between 8/2007 to 6/2011. Participants were seen in a clinical research center.
| Milestone | Healthy Control | Steroid Naive Asthmatics | Asthmatics on ICS Treatment |
|---|---|---|---|
| Started | 24 | 42 | 61 |
| Completed | 20 | 26 | 36 |
| Not completed | 4 | 16 | 25 |
The primary outcome measure for this study is the scaled mean value of three gene expression markers of IL-13 in the airway: PERIOSTIN, calcium-activated chloride channel regulator 1 (CLCA1), and plasminogen activator inhibitor-2 (SERPINB2). First, for each of the three interleukin-13 (IL-13) signature genes, the log (base-2) transformed relative expression value for each subject is measured using real-time polymerase chair reaction (PCR) and normalized with the geometric mean of 5 housekeeping genes. Next, these values are centered (by subtracting the mean for that gene) and scaled (by dividing by the standard deviation for that gene) so that each gene makes an equal, assay-independent contribution to the Th2 phenotype. Then, for each subject, the arithmetic mean of the three centered \& scaled genes is calculated, producing the "three-gene-mean" metric.
| Relative gene expression level | Healthy Control | Steroid Naive Asthmatics | Asthmatics on ICS Treatment |
|---|---|---|---|
| Gene Expression in Airway Secretions and Tissues | -0.66 ± 0.36 | 0.54 ± 0.87 | -0.30 ± 0.60 |
Non-serious events are listed at a 5% frequency threshold.
| Group | Deaths | Serious | Other |
|---|---|---|---|
| Healthy Control | — | 0/24 (0%) | 6/24 (25%) |
| Steroid Naive Asthmatics | — | 0/42 (0%) | 5/42 (11.9%) |
| Asthmatics on ICS Treatment | — | 0/61 (0%) | 15/61 (24.6%) |
| Event | Healthy Control | Steroid Naive Asthmatics | Asthmatics on ICS Treatment |
|---|---|---|---|
| Respiratory symptoms/decreased lung function following bronchoscopyRespiratory, thoracic and mediastinal disorders | 6/24 | 5/42 | 5/61 |
| Increased asthma symptoms following medication holdRespiratory, thoracic and mediastinal disorders | — | 0/42 | 5/61 |
| Did not tolerate switch of asthma controller medicationRespiratory, thoracic and mediastinal disorders | — | 0/42 | 5/61 |
| Age, Categorical(Participants) | Healthy Control | Steroid Naive Asthmatics | Asthmatics on ICS Treatment | Total |
|---|---|---|---|---|
| <=18 years | 0 | 0 | 0 | 0 |
| Between 18 and 65 years | 24 | 42 | 61 | 127 |
| >=65 years | 0 | 0 | 0 | 0 |
| Age, Continuous(years) | Healthy Control | Steroid Naive Asthmatics | Asthmatics on ICS Treatment | Total |
|---|---|---|---|---|
| Mean | 34.5 ± 9.0 | 32.0 ± 11.6 | 39.0 ± 11.9 | 35.9 ± 11.7 |
| Sex: Female, Male(Participants) | Healthy Control | Steroid Naive Asthmatics | Asthmatics on ICS Treatment | Total |
|---|---|---|---|---|
| Female | 10 | 27 | 34 | 71 |
| Male | 14 | 15 | 27 | 56 |
| Region of Enrollment(participants) | Healthy Control | Steroid Naive Asthmatics | Asthmatics on ICS Treatment | Total |
|---|---|---|---|---|
| United States | 24 | 42 | 61 | 127 |
This study is completed, as verified in Dec 2013. You cannot join it, but the record below documents what was studied.
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University of California, San Francisco