PT  - JOURNAL ARTICLE
AU  - Feriyl Bhaijee
AU  - Brenda Jordan
AU  - Dominique J. Pepper
AU  - Rodney Leacock
AU  - William A. Rock, Jr.
TI  - Venous Thrombosis with Both Heterozygous Factor V Leiden (R507Q) and Factor II (G20210A) Mutations
AID  - 10.29074/ascls.25.4.199
DP  - 2012 Oct 01
TA  - American Society for Clinical Laboratory Science
PG  - 199--205
VI  - 25
IP  - 4
4099  - http://hwmaint.clsjournal.ascls.org/content/25/4/199.short
4100  - http://hwmaint.clsjournal.ascls.org/content/25/4/199.full
SO  - Clin Lab Sci2012 Oct 01; 25
AB  - Both hereditary and acquired factors increase the risk of venous thromboembolism, thus the clinical management of affected patients involves evaluation of genetic factors that predispose to hypercoagulability. Factor V Leiden (R507Q) and factor II (prothrombin) mutation (G20210A) are the two most common inherited hypercoagulability disorders among populations of European origin. Both factor V Leiden and factor II mutation (G20210A) represent gain-of-function mutations: factor V Leiden causes resistance to activated protein C, and factor II mutation (G20210A) results in higher levels of plasma prothrombin. Herein, we present an uncommon case of combined factor V Leiden mutation (R507Q) and factor II mutation (G20210A), and discuss the prevalence and features of each entity, as well as their role in the clinical management of affected patients.ABBREVIATIONSEDTA–ethylenediaminetetraacetic acid, VTE–venous thromboembolism, APC–activated protein C,