Fibrinogen Is not an Additional Risk Factor of Thromboembolic Disease in Factor V Leiden Patients

Thromb Haemost 1999; 81(04): 659-660
DOI: 10.1055/s-0037-1614543

Letters to the Editor

Schattauer GmbH

Sandrine Billon

¹From the Molecular Genetic Laboratory, CHU Morvan, Boulevard Tanguy Prigent, Brest, France

²Hematology Department, C.H.U Morvan. and the Centre de Biogénétique, Brest, France

,

Martine Escoffre-Barbe

²Hematology Department, C.H.U Morvan. and the Centre de Biogénétique, Brest, France

,

Bernard Mercier

¹From the Molecular Genetic Laboratory, CHU Morvan, Boulevard Tanguy Prigent, Brest, France

³E.T.S.B.O., Brest, France

,

Jean François Abgrall

²Hematology Department, C.H.U Morvan. and the Centre de Biogénétique, Brest, France

,

Claude Ferec

¹From the Molecular Genetic Laboratory, CHU Morvan, Boulevard Tanguy Prigent, Brest, France

³E.T.S.B.O., Brest, France

References
1 Kierkegaard. Incidence of acute deep vein thrombosis in two districts. A phlebographic study. Acta Chir Scand 1980; 146: 267-9.
2 Koster T, Rosendaal FR, Reitsma PH, van der Velden PA, Briët E, Vandenbroucke JP. Factor VII and fibrinogen levels as risk factors for venous thrombosis. Thromb Haemost 1994; 71: 719-22.
3 Bertina RM, Koeleman BPC, Koster T. Mutation in blood coagulation factor V is associated with resistance to activated protein C. Nature 1994; 369: 64-7.
4 Leroyer C, Mercier B, Escoffre M and al. Factor V Leiden prevalence in venous thromboembolism patients. Chest 1997; 111: 1603-6.
5 Thomas A, Lamlun H, Humpries S, Green F. Linkage disequilibrium across the fibrinogen locus as shown by five genetic polymorphisms, G/A^-455 (Hae III), C/T^-148 (Hind III/ Alu I), T/G⁺¹⁶⁸⁹ (Ava II), and Bcl I (β fibrinogen) and Taq I (α fibrinogen), and their detection by PCR. Human Mutation 1994; 3: 79-81.