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 COPD patients. PATIENTS AND METHODS: We measured plasma levels of thrombin antithrombin III complex (TAT), fibrinopeptide A (FPA), tissue plasminogen activator-plasminogen activator inhibitor (tPA-PAI): markers of coagulation-fibrinolysis-system, and also beta-thromboglobulin (beta-TG): a marker of platelet activation, in 40 COPD patients and in 20 control subjects. Measurements were also repeated 12 months after entry in all patients. RESULTS: TAT, FPA, tPA-PAI, and beta-TG concentrations were significantly higher in COPD than in control subjects. At 12 months follow-up, deltaA-aDO2 and delta%FEV1 were significantly higher in patients with high TAT or tPA-PAI levels than in patients with low levels and TAT, FPA and tPA-PAI levels remained elevated, although beta-TG levels decreased after domiciliary O2 therapy. CONCLUSION: Our results showed an enhanced prothrombotic process in COPD patients, which could potentially account for the increased thrombosis in pulmonary vessels in these patients.
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: We measured plasma levels of thrombin antithrombin III complex (TAT), fibrinopeptide A (FPA), tissue plasminogen activator-plasminogen activator inhibitor (tPA-PAI): markers of coagulation-fibrinolysis-system, and also beta-thromboglobulin (beta-TG): a marker of platelet activation, in 40 COPDpatients and in 20 control subjects. Measurements were also repeated 12 months after entry in all patients. RESULTS: TAT, FPA, tPA-PAI, and beta-TG concentrations were significantly higher in COPD than in control subjects. At 12 months follow-up, deltaA-aDO2 and delta%FEV1 were significantly higher in patients with high TAT or tPA-PAI levels than in patients with low levels and TAT, FPA and tPA-PAI levels remained elevated, although beta-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.
Authors: Adam Wanner; Stephen C Groft; J Russell Teagarden; Jeffrey Krischer; Barry R Davis; Christopher S Coffey; David H Hickam; Jeffrey Teckman; David R Nelson; Michael L McCaleb; Rohit Loomba; Charlie Strange; Robert A Sandhaus; Mark Brantly; Jonathan M Edelman; Albert Farrugia Journal: Chronic Obstr Pulm Dis Date: 2015-04-28
Authors: Benjamin L Nicholas; Paul Skipp; Sheila Barton; Dave Singh; Dinesh Bagmane; Richard Mould; Gilbert Angco; Jon Ward; Binita Guha-Niyogi; Susan Wilson; Peter Howarth; Donna E Davies; Stephen Rennard; C David O'Connor; Ratko Djukanovic Journal: Am J Respir Crit Care Med Date: 2010-01-28 Impact factor: 21.405
Authors: Dawn L Demeo; Thomas J Mariani; Christoph Lange; Sorachai Srisuma; Augusto A Litonjua; Juan C Celedon; Stephen L Lake; John J Reilly; Harold A Chapman; Brigham H Mecham; Kathleen J Haley; Jody S Sylvia; David Sparrow; Avrum E Spira; Jennifer Beane; Victor Pinto-Plata; Frank E Speizer; Steven D Shapiro; Scott T Weiss; Edwin K Silverman Journal: Am J Hum Genet Date: 2005-12-15 Impact factor: 11.025