Venous thromboembolism (VTE) is a specific reproductive health risk for women. In pregnancy the relative risk of VTE is increased approximately 5-fold and in the puerperium it is increased by as much as 60-fold. Additionally, large numbers of women worldwide are exposed to an increased relative risk of VTE as a result of using combined hormonal contraception (CHC), in particular combined oral contraceptives (COCs). Even women undergoing infertility treatment may be exposed to situations of significantly increased risk of VTE [1]. Users of menopausal hormone therapy (MHT) have a two- to four-fold increased risk of VTE compared with non-users [2], comparable to the attributable risk of CHC. The risk for VTE induced by MHT is, however, higher in absolute figures because of the age factor per se, but is also dependent on the composition of the MHT used, since users of estrogen-only preparations have lower risk of VTE than women receiving combined estrogen-progestin preparations [3]. Also the dose and route of administration seems of importance, as women treated with transdermal MHT have lower risk of VTE than women receiving orally administered MHT, as consistently demonstrated in clinical studies [2]. Moreover, epidemiological and pharmacological factors may contribute to the precipitation of VTE among MHT users. The pharmacodynamics of MHT on the hemostatic system may be of particular interest [4], because MHT changes the inhibitory potential of coagulation significantly. Consequently, the choice of MHT may translate into clinical manifestations in thrombosis-prone individuals. Venous thrombosis mostly manifests in the deep veins of the leg, but may occur in other sites, such as the upper extremities, cerebral sinus, liver and portal veins or retinal veins. Major complications of VTE are a disabling postthrombotic syndrome or acute death from a pulmonary embolus (PE) occurring in 1–2 per cent of patients [5].