Thromb Haemost 2003; 90(03): 434-438
DOI: 10.1160/TH03-07-0031
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

Role of blood coagulation factor XIII in patients with acute pulmonary embolism. Correlation of factor XIII antigen levels with pulmonary occlusion rate, fibrinogen, D-dimer, and clot firmness

Nils Kucher
1   Cardiology, Swiss Cardiovascular Center Bern, and Laboratory for Thrombosis Research, Department of Clinical Research, Inselspital, University Hospital of Bern, Switzerland
,
Verena Schroeder
1   Cardiology, Swiss Cardiovascular Center Bern, and Laboratory for Thrombosis Research, Department of Clinical Research, Inselspital, University Hospital of Bern, Switzerland
,
Hans P. Kohler
1   Cardiology, Swiss Cardiovascular Center Bern, and Laboratory for Thrombosis Research, Department of Clinical Research, Inselspital, University Hospital of Bern, Switzerland
› Author Affiliations

Financial support: This work was supported by a grant from the Swiss National Science Foundation.
Further Information

Publication History

Received 17 January 2003

Accepted after resubmission 20 May 2003

Publication Date:
05 December 2017 (online)

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Summary

In patients with acute pulmonary embolism (PE), pulmonary occlusion rate is directly related to D-dimer and inversely related to fibrinogen levels. The role of coagulation factor XIII (FXIII) levels in acute venous thromboembolism is not known. A total of 120 consecutive patients with suspected PE and VIDAS D-dimer levels >500 μg/L were investigated by helical computed tomography (CT). Pulmonary occlusion rate was assessed by CT using the modified Miller index. D-dimer, fibrinogen, and FXIII A- and B-subunit antigen levels were taken on admission. Thrombelastography (TEG) was performed in a subset of patients (n=12).

The 71 patients with PE had lower FXIII A-subunit levels than the 49 patients with excluded PE (78.6±24.5% vs. 91.3±28.8%, p=0.01). In both groups, FXIII A-subunit was inversely related to D-dimer levels. FXIII A-subunit correlated with fibrinogen levels in patients with PE but not in patients without PE. FXIII A-subunit decreased with increasing pulmonary occlusion rate. The risk of PE was increased in the presence of A-subunit levels < 60% (OR 7.0 [95% CI 1.4-35.3], p=0.019). Clot firmness determined by TEG was lower in patients with PE than in patients without PE.

In patients with PE, circulating FXIII A-subunit is decreased compared to patients with suspected but excluded PE. The higher the clot burden within the pulmonary arteries the lower the FXIII antigen. In these patients, direct relation of FXIII A-subunit to fibrinogen levels argues for significant consumption of these coagulation factors in PE. This consumption of FXIII can also be detected by a global coagulation test like TEG.