Thromb Haemost 2000; 83(01): 20-22
DOI: 10.1055/s-0037-1613750
Commentary
Schattauer GmbH

Factor II G20210A and Factor V G1691A Gene Mutations and Peripheral Arterial Occlusive Disease

Autoren

  • Wilfried Renner

    1   From the Department of Medicine, Karl Franzens University, Graz, Austria
  • Herwig Köppel

    1   From the Department of Medicine, Karl Franzens University, Graz, Austria
  • Marianne Brodmann

    1   From the Department of Medicine, Karl Franzens University, Graz, Austria
  • Edmund Pabst

    1   From the Department of Medicine, Karl Franzens University, Graz, Austria
  • Katharina Schallmoser

    1   From the Department of Medicine, Karl Franzens University, Graz, Austria
  • Hermann Toplak

    1   From the Department of Medicine, Karl Franzens University, Graz, Austria
  • Thomas C. Wascher

    1   From the Department of Medicine, Karl Franzens University, Graz, Austria
  • Ernst Pilger

    1   From the Department of Medicine, Karl Franzens University, Graz, Austria
Weitere Informationen

Publikationsverlauf

Received 23. März 1999

Accepted after revision 23. Juni 1999

Publikationsdatum:
06. Dezember 2017 (online)

Summary

Background

G to A mutations at positions 20210 of the prothrombin gene (F2) and 1691 of the factor V gene (F5) are established risk factors for venous thrombosis. Several factors associated with coagulation and/or fibrinolysis have been associated with arterial occlusive disease, but the role of F2 20210A and F5 1691A for arterial occlusive disease remains unclear.

Objective

To investigate if F2 20210A and F5 1691A are associated with peripheral arterial occlusive disease (PAOD).

Methods and Results

We analyzed the prevalence of F2 20210A and F5 1691A alleles in 336 patients with documented PAOD at Fontaine stage II – IV and 300 controls without vascular disease. Allele frequencies in patients and controls were 0.013 and 0.022 for F2 20210A, and 0.042 and 0.045 for F5 1691, respectively, both differences being not statistically significant.

Conclusion

Our data suggest that mutations F2 G20210A and F5 G1691A are not associated with PAOD.