Elevated plasma fibrinogen associated with reduced pulmonary function and increased risk of chronic obstructive pulmonary disease

被引:178
作者
Dahl, M
Tybjærg-Hansen, A
Vestbo, J
Lange, P
Nordestgaard, BG
机构
[1] Herlev Univ Hosp, Dept Clin Biochem 54M1, DK-2730 Herlev, Denmark
[2] Copenhagen Univ Hosp, Dept Clin Biochem, Copenhagen, Denmark
[3] Hvidovre Univ Hosp, Dept Resp Med, Copenhagen, Denmark
[4] Univ Copenhagen, Bispebjerg Univ Hosp, Copenhagen City Heart Study, Copenhagen, Denmark
关键词
fibrinogen; pulmonary function; epidemiology; airway inflammation; COPD;
D O I
10.1164/ajrccm.164.6.2010067
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
We tested whether increased concentrations of the acute-phase reactant fibrinogen correlate with pulmonary function and rate of chronic obstructive pulmonary disease (COPD) hospitalization. We measured plasma fibrinogen and forced expiratory volume in 1 s (FEV1), and assessed prospectively COPD hospitalizations in 8,955 adults from the Danish general population. Smokers with plasma fibrinogen in the upper and middle tertile (>3.3 and 2.7-3.3 g/L) had 7% (95% confidence interval [CI]: 5-8%) and 2% (0-3%) lower percentage predicted FEV1 than smokers with fibrinogen in the lower tertile (<2.7 g/L). The equivalent decreases in nonsmokers were 6% (4-7%) and 0% (-1-2%), respectively. Individuals with plasma fibrinogen in the upper and middle tertile had COPD hospitalization rates of 93 and 60 compared with 52 per 10,000 person-years in individuals with fibrinogen in the lower tertile (log-rank: p < 0.001 and p = 0.31). After adjusting for age, body mass index, sex, pack-years, and recent respiratory infections, relative risks for COPD hospitalization were 1.7 (95% Cl: 1.1-2.6) and 1.4 (0.9-2.1) in individuals with fibrinogen in the upper and middle versus lower tertile. In conclusion, elevated plasma fibrinogen was associated with reduced FEV1 and increased risk of COPD. This could not be explained by smoking alone.
引用
收藏
页码:1008 / 1011
页数:4
相关论文
共 25 条
[21]  
SPSS Inc, 1998, SPSS BAS 8 0 WIND US
[22]   Interleukin-6 changes deformability of neutrophils and induces their sequestration in the lung [J].
Suwa, T ;
Hogg, JC ;
Klut, ME ;
Hards, J ;
van Eeden, SF .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2001, 163 (04) :970-976
[23]   Association of mutations in the apolipoprotein B gene with hypercholesterolemia and the risk of ischemic heart disease [J].
Tybjaerg-Hansen, A ;
Steffensen, R ;
Meinertz, H ;
Schnohr, P ;
Nordestgaard, BG .
NEW ENGLAND JOURNAL OF MEDICINE, 1998, 338 (22) :1577-1584
[24]   Signal transduction by tumor necrosis factor and gene regulation of the inflammatory cytokine interleukin-6 [J].
Vanden Berghe, W ;
Vermeulen, L ;
De Wilde, G ;
De Bosscher, K ;
Boone, E ;
Haegeman, G .
BIOCHEMICAL PHARMACOLOGY, 2000, 60 (08) :1185-1195
[25]  
WELLE I, 1999, EUR RESPIR J, V14, pS133