Effect of Anticoagulant Therapy on the Hypercoagulable State in Patients Carrying the Factor V Arg506Gln Mutation

Resistance to activated protein C, caused by a single point mutation in the factor V gene (Arg506Gln or FV Leiden), is the most prevalent single risk factor associated with venous thromboembolic disease. The aim of this study was to investigate the effectiveness of standard oral anticoagulant therap...

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Bibliographic Details
Published in:Thrombosis research 1998-11, Vol.92 (4), p.157-162
Main Authors: Larsen, Torben B., Lassen, Jens F., Dahler-Eriksen, Bjarne S., Petersen, Per Hyltoft, Brandslund, Ivan
Format: Article
Language:English
Subjects:
Activated Protein C Resistance - drug therapy
Activated Protein C Resistance - genetics
Adolescent
Adult
Aged
Aged, 80 and over
Anticoagulants
Anticoagulants - therapeutic use
APC resistance
Arginine
Biological and medical sciences
Blood. Blood coagulation. Reticuloendothelial system
Case-Control Studies
Factor V
Factor V - genetics
Female
Glycine
Humans
Immunoenzyme Techniques
Linear Models
Male
Medical sciences
Middle Aged
Pharmacology. Drug treatments
Phenprocoumon - therapeutic use
Point Mutation
Polymerase Chain Reaction
Statistics, Nonparametric
Warfarin - therapeutic use
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Summary:Resistance to activated protein C, caused by a single point mutation in the factor V gene (Arg506Gln or FV Leiden), is the most prevalent single risk factor associated with venous thromboembolic disease. The aim of this study was to investigate the effectiveness of standard oral anticoagulant therapy (OAT) in patients with the Arg506Gln mutation compared with a matched control group. The study compared selected variables in 27 patients carrying the Arg506Gln mutation with 27 sex- and age-matched controls in steady state oral anticoagulant treatment (OAT). The study showed that similar doses of vitamin K antagonists in carriers and noncarriers suppress and generate a uniform distribution of coagulation markers in steady state OAT. Thus, it seems that OAT with standard treatment doses is just as effective in patients with the Arg506Gln mutation as in comparable controls without the mutation.
ISSN:0049-3848
1879-2472
DOI:10.1016/S0049-3848(98)00123-6