Thromb Haemost 2009; 101(02): 312-316
DOI: 10.1160/TH08-06-0347
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

Factor XIII-A subunit Val34Leu polymorphism is associated with the risk of thrombosis in patients with antiphospholipid antibodies and high fibrinogen levels[*]

Gloria de la Red
1   Department of Autoimmune Diseases, Institut Clínic de Medicina i Dermatologia, Barcelona, Catalonia, Spain
,
Dolores Tàssies
2   Department of Hemotherapy and Hemostasis, Hospital Clinic, Barcelona, Catalonia, Spain
,
Gerard Espinosa
1   Department of Autoimmune Diseases, Institut Clínic de Medicina i Dermatologia, Barcelona, Catalonia, Spain
,
Joan Monteagudo
2   Department of Hemotherapy and Hemostasis, Hospital Clinic, Barcelona, Catalonia, Spain
,
Albert Bové
1   Department of Autoimmune Diseases, Institut Clínic de Medicina i Dermatologia, Barcelona, Catalonia, Spain
,
Joan Plaza
1   Department of Autoimmune Diseases, Institut Clínic de Medicina i Dermatologia, Barcelona, Catalonia, Spain
,
Ricard Cervera
1   Department of Autoimmune Diseases, Institut Clínic de Medicina i Dermatologia, Barcelona, Catalonia, Spain
,
Joan-Carles Reverter
2   Department of Hemotherapy and Hemostasis, Hospital Clinic, Barcelona, Catalonia, Spain
› Author Affiliations

Financial support: Dr. de la Red’s work was supported by a grant from the Hospital Clínic of Barcelona (2004). The study was supported by Spanish grants FIS 02/0711, FIS 02/0696, FIS 05/0204, and PI 030280.
Further Information

Publication History

Received: 02 June 2008

Accepted after major revision: 16 November 2008

Publication Date:
23 November 2017 (online)

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Summary

Recent reports have described the factor XIII A subunit (FXIII-A) Val34Leu polymorphism as a protective factor against venous and arterial thrombosis. The aim of this study was to investigate the association between the FXIII-A Val34Leu polymorphism, its interaction with fibrinogen concentration, and thrombosis in patients with antiphospholipid antibodies (aPL). We included 172 consecutive patients with aPL: 88 with primary antiphospholipid syndrome (APS), 38 with APS associated with systemic lupus erythematosus (APS-SLE), 32 with SLE and aPL but without APS (SLE-aPL), and 14 asymptomatic individuals with aPL (A-aPL). The FXIII-A Val34Leu polymorphism was assessed by polymerase chain reaction techniques. We found no significant differences in FXIII-A Leu34 allele frequencies between primary APS (allele frequency 0.22), APS-SLE (0.23), SLE-aPL (0.22) and A-aPL (0.32) patients, or between patients with (0.21) and without thrombosis (0.26). FXIII-A Leu34 allele frequencies were significantly lower in patients with thrombosis and those in the upper fibrinogen tertile (>3.40 g/l) (allele frequency 0.07) compared with patients without thrombosis in the upper fibrinogen tertile (0.29) and patients with (0.29) and without (0.25) thrombosis in the mid- and lower fibrinogen tertiles. The FXIII-A Leu34 allele had a protective effect against thrombosis in patients in the upper fibrinogen tertile (odds ratio [OR]=0.20, 95% confidence interval [CI] 0.07–0.60) but not in those in the other tertiles (OR=1.20, 95% CI 0.67–2.16). The FXIII-A Leu34 allele seems to have a protective effect on the development of thrombosis in patients with aPL, but only in those with high plasma fibrinogen values.

* This work is dedicated to the memory of Josep Font, who passed away on July 26, 2006 while this study was in progress.