Key result
Heterozygous factor V Leiden mutation is linked to ~394% higher DVT risk versus non-carriers.
Why the study?
The risk of developing deep venous thrombosis associated with factor V Leiden mutation in the Vojvodina population was not well established.
Does Factor V Leiden mutation increase the risk of deep venous thrombosis in the Vojvodina population?
Case-Control (n=150)
Does Factor V Leiden mutation increase the risk of deep venous thrombosis in the Vojvodina population?
Odds Ratio: 4.94 (95% CI 1.58–15.42)
Absolute Event Rate: 22.79% vs 5.63%
p-value: p=0.025
Factor V Leiden mutation is associated with a significantly increased risk of deep venous thrombosis, with heterozygous carriers having a 4- to 5-fold higher risk and homozygous carriers a 45- to 48-fold higher risk.
May inform selective thrombophilia testing in Vojvodina DVT patients; extends association to this population but leaves generalizability open.
FV Leiden Mutation and Deep Venous Thrombosis in Vojvodina: A Case-Control Study Between September 2007 and February 2010, the occurrence of symptomatic deep venous thrombosis (DVT) was investigated in a cohort of 79 consecutive patients. A case-control study inclu ded 71 healthy controls matched with cases for sex and age. The prevalence of factor V G1691A mutation genotype was analyzed. Eighteen cases (22.79%; 95% confidence interval (CI) 13.53% to 32.03%) and four controls (5.63%; 95% CI 0.27% to 10.99%) were heterozygous carriers of FV Leiden (p= 0.025). The odds ratio for DVT was 4.94 (95% CI 1.58 to 15.42) and the relative risk 4.04 (95% CI 1.44-11.38) compared with FV 1691G carriers. Four cases were homozygous carriers of FV Leiden, giving a prevalence of 5.06% (95% CI 0.23 to 9.89%) and no controls, therefore OR and RR calculation was based on the prevalence of homozygotes in the general Caucasian population. The OR for DVT was 47.28 (95% CI 0.04 - 52167.3) and the RR 45.57 (95% CI 0.04 to 49540.77; p=0.025) compared with FV 1691 G carriers. Our study confirms that factor V Leiden carriers in Vojvodina, as in similar studies previously carried out in other populations, have an increased risk of developing DVT. The evaluated risk of DVT in heterozygous carriers of the mutation is four- to five-fold higher, whereas for homozygous carriers it is 45- to 48-fold higher than in non-carriers. These results confirm that patients with DVT and their relatives should undergo screening for FV Leiden mutation.
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Salatić et al. (2010) conducted a case-control in Deep venous thrombosis (n=150). Factor V Leiden mutation vs. Non-carriers (FV 1691 G carriers) was evaluated on Deep venous thrombosis (OR 4.94, 95% CI 1.58-15.42, p=0.025). Heterozygous factor V Leiden mutation was associated with a significantly increased risk of deep venous thrombosis compared to non-carriers (OR 4.94).
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