Ming Zhang1, Jie Zhang1, Qiuhong Zhang1, Xia Yang1, Hu Shan1, Zongjuan Ming1, Haijuan Chen1, Yanqin Liu1, Jiafeng Yin2, Yali Li3. 1. Department of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. 2. Department of Laboratory Examination, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. 3. Department of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. Electronic address: 81276894@qq.com.
Abstract
BACKGROUND: D-dimer is a manifestation of endogenous fibrinolytic activity and associated with inflammation process. Despite chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by a hypercoagulable state, D-dimer levels in COPD patients are still conflicting. METHODS: Forty-three participants were investigated at admission for an acute exacerbation of COPD, and reassessed when stable. Forty-three controls were matched for age, gender, body mass index, smoking index, comorbidities and medication use. Participants underwent pulmonary function and laboratory testing, including the measurements of D-dimer and high-sensitivity C-reactive protein (hsCRP). RESULTS: The median of D-dimer was 2839 μg/l (IQR: 2078-4389 μg/l) and 1799 μg/l (IQR: 1205-2196 μg/l) in exacerbated and stable COPD patients respectively. The median of D-dimer in the control subjects was 433 μg/l (IQR: 369-456 μg/l). D-dimer level was significantly increased in stable COPD patients compared with healthy controls, and further increased in those patients with an acute exacerbation (both P<0.001). D-dimer was positively correlated with the well-known inflammatory marker hsCRP both in the exacerbated and stable phases of COPD (r=0.392 P=0.009 and r=0.411 P=0.006, respectively), and negatively correlated with FEV1% predicted and FEV1/FVC in stable COPD (r=-0.409 P=0.006 and r=-0.343 P=0.024, respectively). CONCLUSIONS: D-dimer is increased in COPD patients, and could be considered as an inflammatory marker for the assessment of inflammation in the progression of COPD.
BACKGROUND: D-dimer is a manifestation of endogenous fibrinolytic activity and associated with inflammation process. Despite chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by a hypercoagulable state, D-dimer levels in COPDpatients are still conflicting. METHODS: Forty-three participants were investigated at admission for an acute exacerbation of COPD, and reassessed when stable. Forty-three controls were matched for age, gender, body mass index, smoking index, comorbidities and medication use. Participants underwent pulmonary function and laboratory testing, including the measurements of D-dimer and high-sensitivity C-reactive protein (hsCRP). RESULTS: The median of D-dimer was 2839 μg/l (IQR: 2078-4389 μg/l) and 1799 μg/l (IQR: 1205-2196 μg/l) in exacerbated and stable COPDpatients respectively. The median of D-dimer in the control subjects was 433 μg/l (IQR: 369-456 μg/l). D-dimer level was significantly increased in stable COPDpatients compared with healthy controls, and further increased in those patients with an acute exacerbation (both P<0.001). D-dimer was positively correlated with the well-known inflammatory marker hsCRP both in the exacerbated and stable phases of COPD (r=0.392 P=0.009 and r=0.411 P=0.006, respectively), and negatively correlated with FEV1% predicted and FEV1/FVC in stable COPD (r=-0.409 P=0.006 and r=-0.343 P=0.024, respectively). CONCLUSIONS: D-dimer is increased in COPDpatients, and could be considered as an inflammatory marker for the assessment of inflammation in the progression of COPD.