Key result
Coexistent hyperhomocysteinemia and factor V Leiden linked to ~22-fold higher risk of idiopathic VTE.
Why the study?
Patients with rare familial homocystinuria who also carry factor V Leiden have increased VTE incidence, suggesting a possible interrelation of moderate hyperhomocyst(e)inemia, factor V Leiden, and VTE risk in the general population.
Does the coexistence of hyperhomocyst(e)inemia and factor V Leiden mutation increase the risk of future venous thromboembolism in initially healthy men?
Comparison
Men with hyperhomocyst(e)inemia and/or factor V Leiden mutation vs men without these abnormalities
Design
Large prospective cohort study
Follow-up
10-year
Authors
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May identify high-risk men for VTE surveillance; leaves open whether screening or intervention improves outcomes.
Cohort (n=791)
Does the coexistence of hyperhomocyst(e)inemia and factor V Leiden mutation increase the risk of future venous thromboembolism in initially healthy men?
Relative Risk: 21.8
p-value: p=.0004
The coexistence of hyperhomocyst(e)inemia and factor V Leiden mutation synergistically increases the risk of future venous thromboembolism in apparently healthy men.
Ridker et al. (1997) conducted a cohort in Venous Thromboembolism (n=791). Coexistent hyperhomocyst(e)inemia and factor V Leiden mutation vs. Men with neither abnormality was evaluated on Idiopathic VTE (RR 21.8, p=.0004). Coexistent hyperhomocyst(e)inemia and factor V Leiden mutation in healthy men was associated with a 20-fold increased risk of idiopathic VTE compared to neither abnormality (RR 21.8, P=0.0004).
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