Biomedical Engineering Reference
In-Depth Information
HRCT emphysema score in patients with fixed airflow obstruction due to
COPD suggest that parenchymal destruction, i.e., emphysema, is present
in subjects with fixed airflow limitation due to COPD but not in subjects
with fixed airflow limitation due to asthma (Table 2).
IV. CHARACTERISTICS OF INFLAMMATION IN COPD
AND ASTHMA
A. COPD
Many studies have been conducted in the last 20 years on the pathology of
asthma and COPD, mainly directed to understand the mechanisms of these
two complex syndromes. The studies on the pathology have revealed quite
remarkable differences between the pathology of asthma and the pathology
of COPD, so that there has been an increasing interest in using cellular
and
=
or biochemical markers for the diagnosis, differential diagnosis, and
management of these two diseases.
The pathology of COPD and asthma is markedly different (4,5,29,30). In
general, in COPD the fixed airflow obstruction is associated with an airway
inflammatory profile consisting mainly of an increased number of T-lympho-
cytes (predominantly CD8
þ
), macrophages, and neutrophils (31,32). In con-
trast, the variable airflow obstruction in asthma is associated with a
characteristic airway inflammation consisting of an increased number of T-lym-
phocytes (predominantly CD4
þ
) and eosinophils and an increased thickness of
the reticular layer of the epithelial basement membrane (19,25) (Table 3).
COPD is associated with inflammation of central and peripheral
airways, lung parenchyma, and pulmonary vessels. In the central airways,
the characteristics of inflammation are: (1) an increased number of mono-
nuclear cells, particularly macrophages and T-lymphocytes of the CD8
þ
type, associated in few cases with neutrophils, eosinophils, and mast cells
in the airway mucosa; (2) increased number of neutrophils and, in few cases,
of eosinophils in lavage fluid; (3) infiltration of submucosal glands by neu-
trophils; (4) hyperplasia of goblet cells and enlarged mucous glands; (5)
metaplasia of airway epithelium that is otherwise well preserved; (6) no
change of the structure of the lamina reticularis of the basement membrane.
The contribution of these pathological abnormalities to airflow limitation
and gas-exchange abnormalities remains unclear. However, as airflow lim-
itation progresses, the number of T-lymphocytes and macrophages increases
in the submucosa, and a particular subset of T-lymphocytes, the CD8
þ
type,
correlates significantly with the evolution of airflow limitation (33,34).
Peripheral airways show pathological abnormalities similar to the ones
present in central airways with an increased number of mononuclear cells
in the airway mucosa, and, similar to central airways, a particular subset
of T-lymphocytes, the CD8
þ
, that correlates significantly with the evolution
of airflow limitation (33,34), an increased number of neutrophils in the
