Venous thromboembolism (VTE) remains an important cause of morbidity and mortality, with well-recognised inherited and acquired risk factors. Women are particularly at risk of this condition because of pregnancy, the use of combined oral contraceptive pills, and hormone replacement therapy. A number of long-term sequelae may occur following an episode of VTE in women, such as development of the post- thrombotic syndrome, restriction of future contraceptive choice, bleeding events related to anticoagulants, and recurrence of thrombosis. In recent years there has been a marked increase in our understanding of genetic risk factors important for the development of VTE, and of their interaction with acquired risks. In particular, the description of the factor V Leiden and (more recently) prothrombin 202 lOA mutations have highlighted common genetic variations that are associated with a modest increased risk of thromboembolism. These genetic mutations may also be associated with other conditions that are associated with coagulation activation, such as preeclampsia. Thrombophilia is a rapidly expanding and complex field, and undoubtedly new abnormalities will be described within the next few years
