ABOUT FACTOR V LEIDEN AND THROMBOPHILIA

A blood clot that seemed random. A family history of DVTs. A question about whether birth control or surgery carries extra risk for you — your genes hold the answer.

Whole genome sequencing identifies Factor V Leiden, prothrombin 20210G>A, and other thrombophilia variants — enabling targeted prevention and informed decisions about contraceptives, surgery, and pregnancy.

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About this condition

Factor V Leiden / Thrombophilia

Factor V Leiden is the most common inherited thrombophilia in individuals of European descent. It results from a single mutation in the F5 gene (c.1601G>A) that renders Factor V resistant to inactivation by activated protein C, shifting the hemostatic balance toward clot formation. Prothrombin thrombophilia, caused by a variant in the F2 gene (20210G>A), elevates prothrombin levels and similarly increases clotting risk. Both follow autosomal dominant inheritance with incomplete penetrance — many carriers never develop thrombosis without additional trigger factors.

Factor V Leiden affects 3–8% of individuals of European ancestry, with much lower prevalence in African and Asian populations. Heterozygotes have a 3–8-fold increased lifetime risk of deep vein thrombosis (DVT) or pulmonary embolism (PE); homozygotes have approximately 80-fold increased risk. Prothrombin 20210G>A occurs in 2–5% of European populations and confers a 2–5-fold increased VTE risk in heterozygotes. Risk is substantially amplified by additional factors: oral contraceptive use raises DVT risk to 35-fold in FVL heterozygotes, and combined heterozygosity for both F5 and F2 variants further compounds risk.

Identifying a thrombophilia variant has major clinical implications. For women, it informs contraceptive choice — combined hormonal contraceptives are contraindicated, while alternative options such as intrauterine devices or progestin-only methods are preferred. For surgery, it guides perioperative anticoagulation strategies. During pregnancy, heterozygous carriers have moderately increased VTE risk (1–2%), while homozygotes require pharmacological thromboprophylaxis. A finding in one family member triggers cascade testing of relatives, identifying at-risk individuals before a first thrombotic event.

Factor V Leiden and prothrombin 20210G>A represent distinct genetic mechanisms — APC resistance vs. elevated prothrombin — but confer similar clinical VTE risk; compound heterozygosity significantly increases risk.

Gene locus
F5 (1q24.2), F2 (11p11.2)

Standard thrombophilia panels test only two variants. They miss rare F5 variants causing APC resistance and fail to capture the full coagulation pathway.

Rare APC-resistant variants are hidden from standard testing

Conventional thrombophilia panels test only the single Factor V Leiden variant (c.1601G>A) and the single prothrombin 20210G>A variant — missing other rare F5 variants that produce APC resistance (such as Factor V Cambridge, Factor V Hong Kong) that also increase VTE risk. Additionally, standard panels do not systematically screen other coagulation and fibrinolysis genes where additional variants may modify thrombotic risk. Studies show that patients with clinical thrombophilia phenotypes sometimes have negative standard panel results despite a clear genetic basis.

A finding changes contraceptive strategy and pregnancy planning

When Factor V Leiden or prothrombin 20210G>A is confirmed, it enables several critical clinical decisions: avoidance of combined hormonal contraceptives (which raise VTE risk to unacceptable levels), adoption of alternative contraception (IUD, progestin-only methods), perioperative anticoagulation planning, pregnancy thromboprophylaxis if homozygous or if there is prior thrombosis, and cascade testing of first-degree relatives. For family members, identifying carrier status before a first thrombotic event enables proactive prevention.

One test. A lifetime of answers.

One kit, sent to your home. Your entire genome sequenced at the clinical standard used for diagnostic decisions. 200+ physician-ready reports delivered to your Genome Manager in 6–8 weeks — permanent and updated as science advances.

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