【Objective】 To investigate the association between variation in a disintegrin and metalloprotease with thrombospondin type 1 repeats (ADAMTS-13) and prothrombotic state (PTS) and inflammatory biomarkers in patients with chronic obstructive pulmonary disease (COPD). 【Methods】 In this case-control study

67 patients with COPD were consecutively recruited from the inpatient respiratory unit and outpatient respiratory clinic of the First Affiliated Hospital of Sun Yat-sen University (40 with AECOPD and 27 with stable COPD). In addition

21 healthy subjects from physical examination center served as a reference population (11 smokers and 10 non-smokers). An commercial enzyme-linked immunosorbent assay (ELISA) kit (USCNK

China) was used to detect plasma ADAMTS-13

vWF

IL-6 and biomarkers of PTS

D-Dimer and fibrinogen. 【Results】 VWF levels in plasma in AECOPD group

stable COPD group

healthy smokers group and healthy non-smokers group were 12.5 ± 1.9 pg/mL

9.8 ± 1.5 pg/mL

5.5 ± 1.9 pg/mL

3.8 ± 1.3 pg/mL

respectively

decreasing progressively in order from AECOPD group to healthy non-smoker group. The differences between any two groups were statistically significant (all P < 0.05). ADAMTS-13 levels in plasma in AECOPD group

stable COPD group

healthy smokers group and healthy non-smokers group were 261 ± 59 ng/mL

396 ± 74 ng/mL

668 ± 138 ng/mL and 913 ± 131 ng/mL

respectively

increasing progressively in order from AECOPD group to healthy non-smoker group. The differences between any two groups were statistically significant (all P < 0.05). Multiple linear regression analysis showed that plasma ADAMTS-13 level was significantly correlated with vWF (partial correlation coefficient t = -0.661

P < 0.001)

D-Dimer (partial correlation coefficient t = -0.357

P = 0.028)

fibrinogen (partial correlation coefficient t = -0.402

P = 0.004) and IL-6 (partial correlation coefficient t = -0.275

P = 0.001).【Conclusion】 Patients with COPD have significantly lower levels of ADAMTS-13 in plasma than the reference group

which may play a role in the development of PTS. Systemic inflammation and cigarette smoking are possibly involved in the pathogenesis of decreased plasma ADAMTS-13 levels.