Making a literature seach in terms of differences between asthma and COPD (especially their inflammatory response) I found a review performed by Peter K. Jeffery (Thorax 1998;53:129-136).
Asthma and COPD may look alike…
There is a clear overlap between some COPD patients and some asthmatics. The reason for the overlap is mainly based on the similaties found among COPD patients with some reversibility in their obstructive component and asthma patients with some fixed component at the same parameters.
The degree of slow motion when a different approach is being looked for has impacted guidelines, research, academic opinions, and so farth. However, Jeffery points out several structural and inflammatory changes particularly seen in COPD or in asthma. Unfortunately, these diseases have a diagnosis mainly based in physiological than hystological parameters.
Inflammation and obstruction
What it is clear is that airways in in both clinical conditions are or have been markedly inflamed but the type and place of response seems to be inequal.
Some locations are relevant in COPD. For example in the proximal bronchi there is a reaction called Chronic Bronchitis where there are changes in the amount and composition if secretions. These secretions are composed by glycosaminoglycans, glycoproteins, lypids, and transudate and their proportion may change after the continous irritation by smoke or other pollutants. The glands and cells responsible for their production get large and hyperplasic respectively. In asthma. Jeffery points out the presence of plugs in the airways as well as “patchy loos of surface epithelium” among other features.
Getting the cells
Most of the new characterisitcs on the cells at the surface of the airways favor the bacterial colonisation too.
The assessment of sputum tend to show what is happening up to the sixth generations of bronchial branching. Beyond that, the material need to be obtained by bronchoalveolar lavage. The transformation of the cellular composition (mucous metaplasia) lead to other noxious effects that potentiate the proteolytic destruction of the lung tissue. This is due to the imbalance between the protective and reparing process.
The effect in the lung tissue is Emphysema which is also definitively associated to smoking. This is a consequence (together with the right heart effect) typical in COPD but not in asthma.
Proportions as a clue
The cellular population involved in both entities may vary importantly. Tobacco smoke recruit more netrophils to the lung and their transit time at this level is increased (delayed) due to their reduced deformability at the local capillary level. COPD patients have more mononuclear cells including: lumphocytes, plasma cells, and macrophages. From lymphocytes, T lymphocytes (CD8+) are predominant while tissue eosinophils found in COPD do not degranulate.
Patients with asthma also have an inflammatory infiltrate but it comprises other population of lymphocytes (CD25+ and CD4+) activated and T helper as wells as activated eosinophils.
Of course, this structural changes are different in many ways and the chemical mediators tend to differ also in proportions with a different response that may require more specific mechanisms.
The suggested conclusion: there’s a difference like in many diferential diagnosis and, although it is not easy to stablish it clinically or physiologically, it is important to keep this in mind when assessing, managing, and follow up these overlapped gropu of patients.
Making a literature seach in terms of differences between asthma and COPD (especially their inflammatory response) I found a review performed by Peter K. Jeffery (Thorax 1998;53:129-136).
Asthma and COPD may look alike…
There is a clear overlap between some COPD patients and some asthmatics. The reason for the overlap is mainly based on the similaties found among COPD patients with some reversibility in their obstructive component and asthma patients with some fixed component at the same parameters.
The degree of slow motion when a different approach is being looked for has impacted guidelines, research, academic opinions, and so farth. However, Jeffery points out several structural and inflammatory changes particularly seen in COPD or in asthma. Unfortunately, these diseases have a diagnosis mainly based in physiological than hystological parameters.
Inflammation and obstruction
What it is clear is that airways in in both clinical conditions are or have been markedly inflamed but the type and place of response seems to be inequal.
Some locations are relevant in COPD. For example in the proximal bronchi there is a reaction called Chronic Bronchitis where there are changes in the amount and composition if secretions. These secretions are composed by glycosaminoglycans, glycoproteins, lypids, and transudate and their proportion may change after the continous irritation by smoke or other pollutants. The glands and cells responsible for their production get large and hyperplasic respectively. In asthma. Jeffery points out the presence of plugs in the airways as well as “patchy loos of surface epithelium” among other features.
Getting the cells
Most of the new characterisitcs on the cells at the surface of the airways favor the bacterial colonisation too.
The assessment of sputum tend to show what is happening up to the sixth generations of bronchial branching. Beyond that, the material need to be obtained by bronchoalveolar lavage. The transformation of the cellular composition (mucous metaplasia) lead to other noxious effects that potentiate the proteolytic destruction of the lung tissue. This is due to the imbalance between the protective and reparing process.
The effect in the lung tissue is Emphysema which is also definitively associated to smoking. This is a consequence (together with the right heart effect) typical in COPD but not in asthma.
Proportions as a clue
The cellular population involved in both entities may vary importantly. Tobacco smoke recruit more netrophils to the lung and their transit time at this level is increased (delayed) due to their reduced deformability at the local capillary level. COPD patients have more mononuclear cells including: lumphocytes, plasma cells, and macrophages. From lymphocytes, T lymphocytes (CD8+) are predominant while tissue eosinophils found in COPD do not degranulate.
Patients with asthma also have an inflammatory infiltrate but it comprises other population of lymphocytes (CD25+ and CD4+) activated and T helper as wells as activated eosinophils.
Of course, this structural changes are different in many ways and the chemical mediators tend to differ also in proportions with a different response that may require more specific mechanisms.
The suggested conclusion: there’s a difference like in many diferential diagnosis and, although it is not easy to stablish it clinically or physiologically, it is important to keep this in mind when assessing, managing, and follow up these overlapped gropu of patients.