Prevalence of Different Haptoglobin Phenotypes in Patients With COPD- Frequent Exacerbators Versus Non Exacerbators
Chronic obstructive pulmonary disease (COPD) is a common disease in smokers. COPD has a slowly deteriorating course, punctuated by exacerbations- acute events characterized by increasing shortness of breath and putrid sputum. Exacerbations of COPD may be precipitated by several factors, most commonly infections.
Exacerbation frequency generally increases with declining lung function. However, some patients with COPD consistently experience a higher rate of exacerbations than others despite similar severity of COPD. This has led researchers to postulate the existence of a distinct subgroup of "frequent exacerbators" . Recent work has also brought attention to a subset of patients who experience remarkably few exacerbations despite significantly impaired lung function. Careful characterization of both of these extreme subgroups of COPD may offer additional insights into why certain patients are prone to frequent exacerbations while others remain relatively protected.
Haptoglobin (Hp) is a protein produced predominately by the liver . In humans two types of genes for Hp exist (1 and 2) with possible combinations of these two genes- 1-1, 1-2, or 2-2. The Hp 2 gene is believed to have arisen from the Hp 1 gene in human evolution. Subsequently the prevalence of the Hp 2 allele has spread throughout the world, probably as a result of its ability to provide a selective advantage against infectious disease. The Hp 1-2 combination is a very common one. In most western countries, the prevalence of the Hp genotypes is 16% Hp 1-1, 36% Hp 2-2 and 48% Hp 2-1.
The Hp gene form has been shown to be associated with disease. Specifically, Hp phenotypes have been found to affect propensity to atherosclerosis in Diabetic individuals. There have been several studies suggesting that the Hp 2-2 phenotype is associated with a protection against infectious complications.
In view of the importance of respiratory infections on COPD exacerbations, and of the gained knowledge of Haptoglobin subtypes on propensity to infection, we propose to investigate whether Haptoglobin subtypes are in correlation with the "frequent exacerbator" phenotype of COPD. We postulate that, since people with Hp 1-1 are more prone to infection, the frequency of the Hp 1-1 phenotype will be higher in "frequent exacerbators" of COPD than in "non- exacerbators".
To test our hypothesis we propose to determine Hp phenotype in two groups of COPD patients: one with frequent exacerbations and one with no exacerbations, and compare the relative frequency of the 1-1 phenotype in the two groups.
Pulmonary Disease, Chronic Obstructive
|Study Design:||Observational Model: Case Control
Time Perspective: Retrospective
|Official Title:||Prevalence of Different Haptoglobin Phenotypes in Patients With COPD- Frequent Exacerbators Versus Non Exacerbators|
- Prevalence of Hp 1-1 phenotype [ Time Frame: 1 visit- approximately 2 hours. ]Prevalence as percentage of Hp 1-1 phenotypes in each group of patients
Biospecimen Retention: Samples Without DNA
|Study Start Date:||January 2013|
|Study Completion Date:||June 2016|
|Primary Completion Date:||January 2015 (Final data collection date for primary outcome measure)|
COPD Frequent Exacerbators
COPD patients having experienced at least two episodes of acute exacerbations in the former 12 months. (Acute exacerbations are defined as worsening symptoms requiring treatment with systemic steroids (oral or parenteral) or antibiotics, a visit to the emergency room, and/or admission to a hospital. Events separated by at least 21 days are considered as separate events of exacerbation.)
COPD non- exacerbators
COPD patients who have not experienced exacerbations in the former 24 months. (Acute exacerbations are defined as worsening symptoms requiring treatment with systemic steroids (oral or parenteral) or antibiotics, a visit to the emergency room, and/or admission to a hospital. Events separated by at least 21 days are considered as separate events of exacerbation.)
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Please refer to this study by its ClinicalTrials.gov identifier: NCT01745419
|Pulmonology Institute, Carmel Medical Center|
|Haifa, Israel, 34362|
|Principal Investigator:||Michal Shteinberg, MD, PhD||Pulmonology Institute, Carmel Medical Center|