Biomedical Engineering Reference
In-Depth Information
ment is less characterized. Some data suggest that in addition to the typical
eosinophilic airway inflammation observed in patients with asthma, smok-
ing asthmatics develop a neutrophilic airway inflammation that has been
suggested to be responsible for the development of resistance to steroid
treatment in these subjects (44). Only one study has assessed airway inflam-
mation in nonsmoking subjects and COPD, suggesting that two phenotypes
may exist, with and without airway eosinophilia (10). COPD patients
presenting with a certain degree of reversibility of airflow limitation show
some inflammatory abnormalities similar to asthmatics, i.e. higher airway
eosinophilia (9,37), and higher levels of exhaled NO (37).
D. Asthmatics with Developed Fixed Airflow Limitation
The inflammatory characteristics of asthmatic patients who have developed
fixed airflow limitation, and thus, functionally similar to COPD patients,
has been poorly investigated. Previous studies have compared airway
inflammation in predefined patients with either asthma or COPD (45-47).
The limitation of those studies is that they compared young asthmatics with
variable airflow obstruction with older COPD patients with fixed airflow
obstruction. The results of those studies showed that, in asthma, the variable
airflow obstruction is associated with a characteristic airway inflammation
consisting of an increased number of T-lymphocytes (predominantly
CD4
þ
) and eosinophils and an increased thickness of the reticular layer of
the epithelial basement membrane (25). In contrast, in COPD the fixed
airflow obstruction is associated with an airway inflammatory profile
consisting mainly of an increased number of T-lymphocytes (predominantly
CD8
þ
), macrophages, and neutrophils (31,32).
Based on this evidence, one could predict that in asthmatics develop-
ing fixed airflow limitation, airway inflammation would also change with
the development of fixed airflow limitation and become similar to the air-
way inflammation present in COPD. If so, asthma could become COPD
not only functionally but also pathologically. The recent investigation
(28) of subjects with fixed airflow limitation with history of asthma or
COPD, has shown that, compared with the patients with a history of
COPD, patients with a history of asthma have more eosinophils in periph-
eral blood, sputum, BALF, and airway mucosa (Fig. 1) and have fewer neu-
trophils in sputum and BALF. Patients with a history of asthma have more
bronchoalveolar lymphocytes and more CD4
þ
cells, a higher CD4
þ
=
CD8
þ
ratio, and a thicker reticular layer of the basement membrane in bronchial
biopsy specimens. Finally, they have a higher level of exhaled NO. More-
over, the statistical analysis showed that both the percentage of sputum
and BALF eosinophils and the NO level were good predictors of a history
of asthma (28).
