Resistance to activated protein C caused by a factor V gene mutation
(1995) In Current Opinion in Hematology 2(5). p.358-364- Abstract
Each year, approximately one in 1000 individuals suffers from venous thromboembolism. The pathogenesis of the disease is multifactorial and a thrombotic event is the result of a combination of genetic and circumstantial risk factors. Until recently, genetic defects could only be identified in a minority of thrombosis patients. The discovery of inherited resistance to activated protein C as a risk factor for thrombosis changed the situation for the better. In Western countries, activated protein C resistance is found in 20% to 60% of patients with thrombosis. Activated protein C resistance is caused by a single point mutation in the Factor V gene, leading to replacement of Arg(R)506 in the activated protein C cleavage site of Factor V... (More)
Each year, approximately one in 1000 individuals suffers from venous thromboembolism. The pathogenesis of the disease is multifactorial and a thrombotic event is the result of a combination of genetic and circumstantial risk factors. Until recently, genetic defects could only be identified in a minority of thrombosis patients. The discovery of inherited resistance to activated protein C as a risk factor for thrombosis changed the situation for the better. In Western countries, activated protein C resistance is found in 20% to 60% of patients with thrombosis. Activated protein C resistance is caused by a single point mutation in the Factor V gene, leading to replacement of Arg(R)506 in the activated protein C cleavage site of Factor V with a Gln(Q). As a result, the activated protein C-mediated cleavage and inhibition of mutated Factor V (FV:Q506) is impaired, which leads to increased thrombin generation, a hypercoagulable state, and a life-long increased risk of thrombosis.
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- author
- Zöller, Bengt LU and Dahlbäck, Björn LU
- organization
- publishing date
- 1995-09
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- anticoagulant agent, blood clotting factor 5, protein C, aged, drug resistance, genetic predisposition, genetics, human, point mutation, review, risk factor, thrombophlebitis
- in
- Current Opinion in Hematology
- volume
- 2
- issue
- 5
- pages
- 7 pages
- publisher
- Lippincott Williams & Wilkins
- external identifiers
-
- pmid:9372020
- scopus:0029361437
- ISSN
- 1065-6251
- language
- English
- LU publication?
- yes
- id
- 649c2da4-a895-48ae-8534-2e377d7b580c
- date added to LUP
- 2017-10-19 15:26:20
- date last changed
- 2024-01-14 08:02:21
@article{649c2da4-a895-48ae-8534-2e377d7b580c, abstract = {{<p>Each year, approximately one in 1000 individuals suffers from venous thromboembolism. The pathogenesis of the disease is multifactorial and a thrombotic event is the result of a combination of genetic and circumstantial risk factors. Until recently, genetic defects could only be identified in a minority of thrombosis patients. The discovery of inherited resistance to activated protein C as a risk factor for thrombosis changed the situation for the better. In Western countries, activated protein C resistance is found in 20% to 60% of patients with thrombosis. Activated protein C resistance is caused by a single point mutation in the Factor V gene, leading to replacement of Arg(R)506 in the activated protein C cleavage site of Factor V with a Gln(Q). As a result, the activated protein C-mediated cleavage and inhibition of mutated Factor V (FV:Q506) is impaired, which leads to increased thrombin generation, a hypercoagulable state, and a life-long increased risk of thrombosis.</p>}}, author = {{Zöller, Bengt and Dahlbäck, Björn}}, issn = {{1065-6251}}, keywords = {{anticoagulant agent; blood clotting factor 5; protein C; aged; drug resistance; genetic predisposition; genetics; human; point mutation; review; risk factor; thrombophlebitis}}, language = {{eng}}, number = {{5}}, pages = {{358--364}}, publisher = {{Lippincott Williams & Wilkins}}, series = {{Current Opinion in Hematology}}, title = {{Resistance to activated protein C caused by a factor V gene mutation}}, volume = {{2}}, year = {{1995}}, }