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Original Research: COPD |

The Effects of Hypoxia on Markers of Coagulation and Systemic Inflammation in Patients With COPD

Ramsey Sabit, MD; Paul Thomas, HTec; Dennis J. Shale, MD, FCCP; Peter Collins, MD; Seamus J. Linnane, MB, BCh
Author and Funding Information

From the Department of Respiratory Medicine (Drs Sabit, Shale, and Linnane), Academic Department, and the Department of Lung Function (Mr Thomas), University Hospital Llandough, Penarth, Vale of Glamorgan, Wales; the Department of Haematology and Coagulation (Dr Collins), University Hospital of Wales, Cardiff, Wales; and the Blackrock Clinic (Dr Linnane), Blackrock, Dublin, Ireland.

Correspondence to: Ramsey Sabit, MD, Department of Respiratory Medicine, University Hospital Llandough, Penarth, CF64 2XX, Wales; e-mail: ramsey.sabit@gmail.com


Funding/Support: This study was supported by a Cardiff and Vale Lung Function Fund and GlaxoSmithKline Global. Dr Sabit was a Cardiff and Vale NHS Trust Clinical Research Fellow.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(1):47-51. doi:10.1378/chest.09-2764
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Background:  It has been demonstrated that there is an increased risk of venous thromboembolism (VTE) during air travel on flights of long duration. Patients with COPD are also at increased risk of VTE, particularly during exacerbations, possibly because of a hypercoagulable state secondary to hypoxia and/or heightened systemic inflammation. We investigated the effects of hypoxia on indices of coagulation and systemic inflammation in patients with COPD.

Methods:  Twenty clinically stable patients with mild COPD were recruited. Patients were randomized to receive either medical air or 100% nitrogen through a 40% venturi mask at a flow rate of 10 L/min for 2 h. Blood was sampled for thrombin-antithrombin complex (TAT), prothrombin activation fragments 1 + 2 (F1 + 2), von Willebrand factor antigen (VWF:Ag), D-dimer, and interleukin-6 (IL-6) at baseline and after 2 h.

Results:  Patients in the hypoxia and control groups were similar in terms of age, sex, pack-years smoked, and severity of airflow obstruction. There was no difference in baseline TAT, F1 + 2, VWF:Ag, D-dimer, or IL-6 levels between groups. In the control group, there was no change in markers of coagulation or systemic inflammation over the 2-h study. In patients who underwent hypoxic challenge, there was an increase in TAT (P < .001), F1 + 2 (P < .01), and IL-6 (P < .01), whereas D-dimer and VWF:Ag levels were unchanged.

Conclusions:  This study demonstrates that a 2-h hypoxic challenge in patients with COPD results in coagulation activation in conjunction with an increase in systemic inflammation.

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