According to Peter K. Jeffery, there has been some difficulty distinguishing COPD from asthma. The main reason is the occurrence of patients who have some reversibility in their airway obstruction having COPD and patients with asthma whose airflow limitation is more fixed. Some other patients may also have COPD plus asthma.
The key obstructive features in COPD
The main conditions contributing to obstruction in COPD are: Chronic bronchitis, emphysema, and chronic bronchiolitis (affecting small airways of less than 2 mm in diameter). As the airway in chronic bronchitis is inflamed, this feature leads to more difficulty in getting the diagnosis of COPD from presumptive patients with asthma (where inflammation is a key component).
The easy difference
What seems to be clear is the main risk factor for developing COPD: the long-term exposure to inhaled noxious gases and particles, having cigarette smoke accounting for more than 90 percent of cases. In some circumstances the inhalation of smoke different to that from cigarettes (e.g. burning of wood during cooking) represents an important cause of COPD.
A key clue to have also in mind is that all smokers don’t develop COPD. It is considered that 10 to 20 percent of heavy smokers will become COPD sufferers. This indicates the relevance of some individual susceptibility to cigarette smoking. Unfortunately, there are different diseases that may appear in those who don’t develop COPD: lung cancer, cardiovascular conditions, etc.
Everybody exposed to some irritants will have a local response in the lungs. The inflammatory response seen in COPD patients is in fact an exaggeration of what is seen in everybody who inhale the irritating cigarette smoke.
Trying to target inflammation in COPD
Inhaled corticosteroids (ICS) are being prescribed for COPD. However, spirometric evidence of benefits in patients with a clearly defined diagnosis of COPD is still lacking. This is absolutely different in patients wit asthma, where the outstanding response to inhaled corticosteroids is amazing.
These findings lead to claim steroid resistance in COPD inflammation. However patients in advanced stages of COPD and with frequent exacerbations have shown beneficial effects of ICS mainly reducing the exacerbation rate.
Then, why is it so beneficial to use ICS in asthma and not in COPD? One of the reasons is that the predominant inflammatory cell type as well as the precise site of inflammation in both conditions are different.
The structural differences between COPD and asthma
While COPD airflow obstruction tends to deteriorate progressively, in asthma it occurs in a variable mode. Post mortem findings in COPD include excessive mucus and emphysema but in asthma emphysema is not a frequent finding.
The sputum of patients with asthma is crowded with eosinophils while neutrophils are more seen in COPD. The surface of the airway in asthma is deteriorated with fragility an loss of epithelium and the changes of bronchiolar mucous cells is still under debate in asthma.
COPD lungs have metaplasia and hyperplasia of bronchiolar mucous cells and the fragility of the surface epithelium is undetermined.
Some other differences between COPD and asthma have been seen in the reticular basement membrane (which tends to be thickened in asthma), local edema (also more more typical for asthma), bronchial smooth muscle (enlarged in small airways in COPD and in large airways in asthma), and bronchial glands (no change in mucin histochemistry in asthma but increased acidic glycoprotein in COPD).
Finally, the cellular infiltrate and the cytokines profile is different between both conditions: more neutrophils, CD8+ T-cells, and macrophages in COPD. In asthma, eosinophils, CD4+ T-cells are increased particularly in large airways.
For more details about COPD structural changes comparison with asthma, Peter K. Jeffery’ s review in Thorax is a good source (Thorax 1998;53;129-136)
According to Peter K. Jeffery, there has been some difficulty distinguishing COPD from asthma. The main reason is the occurrence of patients who have some reversibility in their airway obstruction having COPD and patients with asthma whose airflow limitation is more fixed. Some other patients may also have COPD plus asthma.
The key obstructive features in COPD
The main conditions contributing to obstruction in COPD are: Chronic bronchitis, emphysema, and chronic bronchiolitis (affecting small airways of less than 2 mm in diameter). As the airway in chronic bronchitis is inflamed, this feature leads to more difficulty in getting the diagnosis of COPD from presumptive patients with asthma (where inflammation is a key component).
The easy difference
What seems to be clear is the main risk factor for developing COPD: the long-term exposure to inhaled noxious gases and particles, having cigarette smoke accounting for more than 90 percent of cases. In some circumstances the inhalation of smoke different to that from cigarettes (e.g. burning of wood during cooking) represents an important cause of COPD.
A key clue to have also in mind is that all smokers don’t develop COPD. It is considered that 10 to 20 percent of heavy smokers will become COPD sufferers. This indicates the relevance of some individual susceptibility to cigarette smoking. Unfortunately, there are different diseases that may appear in those who don’t develop COPD: lung cancer, cardiovascular conditions, etc.
Everybody exposed to some irritants will have a local response in the lungs. The inflammatory response seen in COPD patients is in fact an exaggeration of what is seen in everybody who inhale the irritating cigarette smoke.
Trying to target inflammation in COPD
Inhaled corticosteroids (ICS) are being prescribed for COPD. However, spirometric evidence of benefits in patients with a clearly defined diagnosis of COPD is still lacking. This is absolutely different in patients wit asthma, where the outstanding response to inhaled corticosteroids is amazing.
These findings lead to claim steroid resistance in COPD inflammation. However patients in advanced stages of COPD and with frequent exacerbations have shown beneficial effects of ICS mainly reducing the exacerbation rate.
Then, why is it so beneficial to use ICS in asthma and not in COPD? One of the reasons is that the predominant inflammatory cell type as well as the precise site of inflammation in both conditions are different.
The structural differences between COPD and asthma
While COPD airflow obstruction tends to deteriorate progressively, in asthma it occurs in a variable mode. Post mortem findings in COPD include excessive mucus and emphysema but in asthma emphysema is not a frequent finding.
The sputum of patients with asthma is crowded with eosinophils while neutrophils are more seen in COPD. The surface of the airway in asthma is deteriorated with fragility an loss of epithelium and the changes of bronchiolar mucous cells is still under debate in asthma.
COPD lungs have metaplasia and hyperplasia of bronchiolar mucous cells and the fragility of the surface epithelium is undetermined.
Some other differences between COPD and asthma have been seen in the reticular basement membrane (which tends to be thickened in asthma), local edema (also more more typical for asthma), bronchial smooth muscle (enlarged in small airways in COPD and in large airways in asthma), and bronchial glands (no change in mucin histochemistry in asthma but increased acidic glycoprotein in COPD).
Finally, the cellular infiltrate and the cytokines profile is different between both conditions: more neutrophils, CD8+ T-cells, and macrophages in COPD. In asthma, eosinophils, CD4+ T-cells are increased particularly in large airways.
For more details about COPD structural changes comparison with asthma, Peter K. Jeffery’ s review in Thorax is a good source (Thorax 1998;53;129-136)