Elevated Plasma Procoagulant and Fibrinolytic Markers in Patients with Chronic Obstructive Pulmonary Disease.

Abstract

Objective There is clinical and pathological evidence of thrombosis in pulmonary vessels of patients with chronic obstructive pulmonary disease (COPD). The purpose of this study was to investigate the presence of hypercoagulability and determine the extent of this abnormality in COPDpatients.Patients and Methods Wemeasured plasma levels of thrombin antithrombin III complex (TAT), fibrinopeptide A (FPA), tissue plasminogen activator-plasminogen activator inhibitor (tPA-PAI) : markers of coagulation-fibrinolysis-systeni, and also (3-thromboglobulin (p-TG): a marker of platelet activation, in 40 COPDpatients and in 20 control subjects. Measurementswere also repeated 12 months after entry in all patients. Results TAT, FPA, tPA-PAI, and p-TG concentrations were significantly higher in COPDthan in control subjects. At 12 months follow-up, AA-aDO2and A^jFEVj were significantly higher in patients with high TATor tPA-PAI levels than in patients with low levels and TAT, FPAand tPA-PAI levels remained elevated, although p-TG levels decreased after domiciliary O2 therapy.Conclusion Our results showed an enhanced prothrombotic process in COPDpatients, which could potentially account for the increased thrombosis in pulmonary vessels in these patients.

An in vitro analysis of the effect of acidosis on coagulation in chronic disease states – a thromboelastograph study

“…Others have noted increased thrombin-antithrombin III complex, fibrinopeptide A, β-thromboglobulin and tissue plasminogen activator concentrations. 21 Wedzicha and colleagues found increased interleukin 6 and fibrinogen levels in keeping with increased inflammation. 22 During exacerbations, there is evidence of an enhanced inflammation, with an increase in acute phase proteins, complement components, endothelial dysfunction, and variations of haemostasis mechanisms favouring coagulation.…”

Thrombocytopenia as a Marker of Outcome in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease

“…COPD patients show a higher number of platelet-monocyte aggregates, which is indicative of platelet activation; this further increases in AECOPD [21]. Ashitani et al [22] reported an increase in a marker of platelet activation (beta-thromboglobulin) and markers of coagulation-fibrinolysis-system (fibrinopeptide A, thrombin antithrombin III complex, and tissue plasminogen activator-plasminogen activator inhibitor) in 40 COPD patients compared to the control group. They concluded that this clotting factor is an independent predictor of an acute exacerbation [22].…”

“…Ashitani et al [22] reported an increase in a marker of platelet activation (beta-thromboglobulin) and markers of coagulation-fibrinolysis-system (fibrinopeptide A, thrombin antithrombin III complex, and tissue plasminogen activator-plasminogen activator inhibitor) in 40 COPD patients compared to the control group. They concluded that this clotting factor is an independent predictor of an acute exacerbation [22]. During AECOPD, an exaggerated shift in the hemostatic balance occurs due to an increase in platelet aggregation, which was caused by acute disturbances in gas exchange and hypoxemia.…”

Mechanisms of atherothrombosis in chronic obstructive pulmonary disease

“…Hypercoagulable state (Table 2) Some case-control studies have clearly established that, independent of current smoking, plasma levels of fi brinogen and other markers of coagulation are signifi cantly higher in stable COPD patients than in healthy subjects (Alessandri et al 1994;Xie and Wang 1998;Wedzicha et al 2000;Ashitani et al 2002). The increased procoagulant activity in COPD may primarily result from infl ammation.…”