BACKGROUND AND OBJECTIVE: Activation of the blood coagulation system is a common observation in inflammatory diseases. The role of coagulation in COPD is underexplored. METHODS: The study included 413 COPD patients and 49 controls from the 3-year Bergen COPD Cohort Study (BCCS). One hundred and forty-eight COPD patients were also examined during AECOPD. The plasma markers of coagulation activation, TAT complex, APC-PCI complex and D-dimer, were measured at baseline and during exacerbations by enzyme immunoassays. Differences in levels of the markers between stable COPD patients and controls, and between stable COPD and AECOPD were examined. The associations between coagulation markers and later AECOPD and mortality were examined by negative binomial and Cox regression analyses. RESULTS: TAT was significantly lower in stable COPD (1.03 ng/mL (0.76-1.44)) than in controls (1.28 (1.04-1.49), P = 0.002). During AECOPD, all markers were higher than in the stable state: TAT 2.56 versus 1.43 ng/mL, APC-PCI 489.3 versus 416.4 ng/mL and D-dimer 763.5 versus 479.7 ng/mL (P < 0.001 for all). Higher D-dimer in stable COPD predicted a higher mortality (HR: 1.60 (1.24-2.05), P < 0.001). Higher TAT was associated with both an increased risk of later exacerbations, with a yearly incidence rate ratio of 1.19 (1.04-1.37), and a faster time to the first exacerbation (HR: 1.25 (1.10-1.42), P = 0.001, all after adjustment). CONCLUSION: Activation of the coagulation system is increased during COPD exacerbations. Coagulation markers are potential predictors of later COPD exacerbations and mortality.
BACKGROUND AND OBJECTIVE: Activation of the blood coagulation system is a common observation in inflammatory diseases. The role of coagulation in COPD is underexplored. METHODS: The study included 413 COPDpatients and 49 controls from the 3-year Bergen COPD Cohort Study (BCCS). One hundred and forty-eight COPDpatients were also examined during AECOPD. The plasma markers of coagulation activation, TAT complex, APC-PCI complex and D-dimer, were measured at baseline and during exacerbations by enzyme immunoassays. Differences in levels of the markers between stable COPDpatients and controls, and between stable COPD and AECOPD were examined. The associations between coagulation markers and later AECOPD and mortality were examined by negative binomial and Cox regression analyses. RESULTS: TAT was significantly lower in stable COPD (1.03 ng/mL (0.76-1.44)) than in controls (1.28 (1.04-1.49), P = 0.002). During AECOPD, all markers were higher than in the stable state: TAT 2.56 versus 1.43 ng/mL, APC-PCI 489.3 versus 416.4 ng/mL and D-dimer 763.5 versus 479.7 ng/mL (P < 0.001 for all). Higher D-dimer in stable COPD predicted a higher mortality (HR: 1.60 (1.24-2.05), P < 0.001). Higher TAT was associated with both an increased risk of later exacerbations, with a yearly incidence rate ratio of 1.19 (1.04-1.37), and a faster time to the first exacerbation (HR: 1.25 (1.10-1.42), P = 0.001, all after adjustment). CONCLUSION: Activation of the coagulation system is increased during COPD exacerbations. Coagulation markers are potential predictors of later COPD exacerbations and mortality.