Key result
Factor V Leiden is linked to ~260% greater venous thrombosis risk, while beta-fibrinogen -455G/A appears protective.
Why the study?
Genetic factors and gene-lifestyle interactions in arterial and venous thromboembolism and pulmonary embolism survivors were studied to understand causation and inform therapy, risk prevention, and prognosis.
Do genetic variations such as Factor V Leiden, MTHFR C677T, and beta-fibrinogen dimorphism correlate with the risk of arterial and venous thromboembolism?
Population
146 arterial thromboembolism, 199 venous thromboembolism patients, and 58 pulmonary embolism survivors from North Western Russia
Comparison
Patients with thromboembolism and pulmonary embolism survivors versus controls for genetic variations
Design
Case-control study with genetic and biochemical assays
Authors
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Should not change thrombosis management; hypothesis-generating for genetic risks in specific populations.
Case-Control (n=403)
Do genetic variations such as Factor V Leiden, MTHFR C677T, and beta-fibrinogen dimorphism correlate with the risk of arterial and venous thromboembolism?
Absolute Event Rate: 34.5% vs 56.7%
p-value: p=<0.02
Genetic variations including Factor V Leiden, MTHFR C677T, and beta-fibrinogen dimorphism are significantly associated with the risk of arterial and venous thromboembolism, highlighting potential targets for risk stratification and targeted vitamin supplementation.
Harrington et al. (2003) conducted a case-control in Arterial and venous thromboembolism, pulmonary embolism (n=403). Genetic variations (Factor V Leiden, MTHFR C677T, -455G/A beta-fibrinogen) vs. Controls / non-carriers was evaluated on Pulmonary embolism (carrier frequency of -455G/A beta-fibrinogen dimorphism) (p=<0.02). Factor V Leiden increased venous thrombosis risk (OR 3.6), while the -455G/A beta-fibrinogen allele was underrepresented in pulmonary embolism survivors vs controls (34.5% vs 56.7%, p<0.02).
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