Beruflich Dokumente
Kultur Dokumente
DOI 10.1007/s11239-007-0073-1
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Introduction
Chronic obstructive pulmonary disease (COPD) is a
preventable and treatable disease state characterized by
airflow limitation that is not fully reversible. The airflow
limitation is usually progressive and is associated with an
abnormal inflammatory response of the lungs to noxious
particles or gases, especially those of tobacco smoking.
Despite its major pulmonary effects, COPD have also
systemic effects that may contribute to the severity in
individual patients [1].
In COPD, the systemic effects of the disease reflect the
structural and/or biochemical alterations occurring in
the structures or organs other than the lungs in relation to
the characteristics of the primary disease. As in many other
inflammatory diseases, may COPD occur with systemic
symptoms [2].
Reflecting the multicomponent nature of the disorder,
there is extensive heterogeneity among patients with COPD
in terms of clinical presentation, disease severity and rate of
disease progression. It is increasingly apparent that a single
marker is unlikely to be predictive of clinical outcome in all
patients with COPD, given the diverse range of pathological
mechanisms involved. Furthermore, with the variable clinical presentation of COPD, a single outcome is unlikely to
provide a full assessment of the impact of COPD across all
patients [3]. COPD exacerbation definition is based on only
clinical findings such as cough, sputum color and dyspnea
according to recent guidelines. Assessment of the severity of
an exacerbation depends on the patients medical history
before the exacerbation, preexisting comorbidities, symptoms, physical examination, arterial blood gas measurements, and other laboratory tests [1].
Endothelial cells in the human body play a central role
in the control of vascular tone, permeability, blood flow,
coagulation, thrombolysis, inflammation, tissue repair and
growth [4]. The disorders of endothelial structures due to
COPD may lead vascular pathologies, such as ischemic
heart disease, stroke, to occur more commonly in those
with COPD [5].
Evidence suggests that proteinuria does not solely reflect
renal pathology but is also associated with a systemic increase in vascular permeability. One possible mechanism
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M. Polatli et al.
Results
In the present study, 59 patients with COPD (33 SCOPD,
26 COPDAE) and 16 controls of the same age group were
evaluated. The mean age was 63.42 10.29, 68.00 9.77
and 59.63 14.10 years in SCOPD, COPDAE, and CG,
respectively.
99
Discussion
In the present study, the level of microalbuminuria was
found to be much higher in COPD exacerbation group than
in both stable COPD and the control group, and that elevation in the level of microalbuminuria is statistically
significant compared with that of the controls. Significantly
lower PaO2 in the AECOPD compared with those of the
controls and a significant inverse correlation between SaO2
and microalbuminuria indicates that hypoxemia has an
effect on microalbuminuria.
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M. Polatli et al.
Table 1 Demographic variables, smoking history, lung function, microalbuminuria, fibrinogen, vWF, arterial blood gas values in the study
groups
SCOPD
(n = 33)
AECOPD
(n = 26)
Control group(CG)
(n = 16)
SCOPDAECOPD
(P*)
SCOPDCG
(P**)
AECOPDCG
(P***)
Age
63.42 10.29
68.00 9.77
59.63 14.10
NS
NS
NS
Smoking history
(Pack-years)
33.64 10.33
45.04 10.36
21.56 13.13
0.0001
0.002
0.001
FVC (L)
FVC % predicted
3.03 0.86
79.62 15.53
2.40 0.66
66.68 18.92
3.54 0.76
94.64 17.32
0.005
0.009
0.001
0.0001
0.0001
0.0001
FEV1(L)
1.69 0.59
1.03 0.38
2.71 0.57
FEV1 % predicted
56.89 15.13
37.11 13.79
91.66 15.47
FEV1/FVC
55.94 10.54
43.55 12.93
76.67 3.74
0.0001
0.0001
0.0001
Microalbuminuria
20.98 28.74
34.99 46.35
10.47 8.08
NS
NS
0.004
289.99 39.9
0.001
0.013
0.0001
142.85 57.16
0.017
NS
0.004
Fibrinogen
346.88 92.3
vWF
447.67 128
PaO2
80.59 7.80
58.07 8.36
0.0001
SaO2
95.24 2.39
89.10 6.68
0.0001
PaCO2
38.18 4.31
43.55 12.49
NS
pH
HCO3
7.42 0.002
24.69 2.12
7.411 0.006
NS
26.66 4.63
NS
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