Biomedical Engineering Reference
In-Depth Information
Respiratory viral infections are also associated with a systemic inflam-
matory response. Plasma fibrinogen is an independent risk factor for
cardiovascular disease (38) and we have shown that plasma fibrinogen is
increased in COPD, suggesting that COPD patients with moderate-to-severe
disease more susceptible to ischaemic events (39). At exacerbation, we found
further increased levels of plasma fibrinogen and IL-6 that are produced by
blood monocytes and stimulate the production of fibrinogen in the liver
(40). We found that plasma fibrinogen levels were higher in the presence
of colds and respiratory viral infections at COPD exacerbation (8,40). This
suggests that respiratory viral infection may predispose to an increased risk
from vascular disease. Epidemiological studies have suggested that infec-
tions especially those of the respiratory tract may be involved in the onset
of myocardial infarction and stroke (41) and thus patients who are frequent
exacerbators with their recurrent infections may be particularly susceptible
to cardiovascular disease.
IV. ROLE OF BACTERIAL INFECTIONS
The precise role of bacteria at COPD exacerbation has been difficult to eval-
uate as airway bacterial colonization in the stable state has been found in
approximately 30% of COPD patients. The commonest organism isolated
is Haemophilus influenzae, but others isolated include Streptococcus pneumo-
niae, Branhamella cattarhalis, Staphylococcus aureus,andPseudomonas aer-
uginosa. Bacterial colonization has been shown to be related to the degree of
airflow obstruction, current cigarette smoking status, and also associated
with an increased exacerbation frequency (42-45). Soler et al. (43) showed
that the presence of potentially pathogenic organisms in bronchoalveolar
lavage from COPD patients at bronchoscopy was associated with a greater
degree of neutrophilia and higher TNF
a
levels. Hill et al. (46) in a larger
study showed that the airway bacterial load was related to inflammatory
markers. They also found that the bacterial species was related to the degree
of inflammation, with P. aeruginosa colonization showing greater myeloper-
oxidase activity (an indirect measure of neutrophil activation).
Evidence for the involvement of bacteria at COPD exacerbation has
come from studies of antibiotic therapy. Acute exacerbations of COPD
often present with increased sputum purulence and volume and antibiotics
have traditionally been used as first line therapy in such exacerbations. A
study investigating the benefit of antibiotics in over 300 acute exacerbations
demonstrated a greater treatment success rate in patients treated with anti-
biotics, especially if their initial presentation was with the symptoms of
increased dyspnoea, sputum volume, and purulence (47). Patients with mild
COPD obtained less benefit from antibiotic therapy. A meta-analysis
of trials of antibiotic therapy in COPD identified only nine studies of
