Association of idiopathic venous thromboembolism with single point-mutation at Arg506 of factor V

The Lancet

Volumn 343, Issue 8912, 1994, Pages 1535-1536

  Voorberg, J ^a   Roelse, J ^a   Mertens, K ^a   van Mourik, J A ^a   Koopman, R ^b   Buller H ^b   Berends, F ^b   ten Cate, J W ^b  

^a CENTRAL LABORATORY   (Netherlands)

^b Departments of Internal Medicine and Cardiology   (Netherlands)

Author keywords

[No Author keywords available]

Indexed keywords

ACTIVATED PROTEIN C; BLOOD CLOTTING FACTOR 5;

ADULT; AGED; ARTICLE; CLINICAL ARTICLE; FEMALE; HUMAN; MALE; POINT MUTATION; PRIORITY JOURNAL; THROMBOEMBOLISM;

EID: 0028243401     PISSN: 01406736     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0140-6736(94)92939-4     Document Type: Article

References (10)

1. Inherited predisposition to thrombosis
2. Deficiencies of coagulation-inhibiting and fibrinolytic proteins in outpatients with deep vein thrombosis
3. Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C prediction of a cofactor to activated protein C
4. Anticoagulant protein C pathway defective in majority of thrombophilic patients
5. Venous thrombosis due to poor anticoagulant response to activated protein C: Leiden Thrombophilia Study.
6. Resistance to activated protein C as a basis for venous thrombosis
7. Inherited resistance to activated protein C is corrected by anticoagulant cofactor activity found to be a property of factor V
8. Storage conditions of blood samples and primer selection affect the yield of cDNA-polymerase chain reaction products of hepatitis C virus
9. Role of the membrane in inactivation of factor Va by activated protein C
10. Hypercoagulability—a new cofactor in the protein C anticoagulant pathway