Abstract
Over 100 million women worldwide use hormone therapy (HT), that is, oral contraceptives (OCs) or hormone replacement therapy (HRT); however, the use of HT is associated with an increased risk of venous thromboembolism (VTE), including deep-vein thrombosis, pulmonary embolism and cerebral vein thrombosis [1–3]. While the risk is low in absolute terms, OCs are the major cause of thrombotic events in young women [1]. The increased risk of VTE is most probably due to the administration of exogenous estrogens, which leads to procoagulant changes [1,2]. The risk is still present with low-dose OCs (second and third generations; 20–30 mg of the estrogen ethinylestradiol) used currently, and with HRT preparations, which contain even lower dosages of estrogen and progestin compared with OC. HRT increases the risk of VTE by 2–3-fold compared with women without HT [4]. The risk is higher during the first year of HT use (up to 1/1000/year), with the use of a third-generation OC (desogestrel or gestodene instead of levonorgestrel or norgestrel) and among women with thrombophilic risk factors [1].
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