Hormonal contraceptives and venous thrombosis

Abstract

Oral contraceptive use is associated with venous thrombosis. However, the mechanism behind this remains unclear. The aim of this thesis was to evaluate genetic variation in the first-pass metabolism of contraceptives, to identify the clinical implications of hormonal contraceptive use after a thrombotic event and to provide an overview of the risk of venous thrombosis per combined oral contraceptive. We found that the UGT2B7 gene in the first-pass metabolism may at least in part explain the risk of venous thrombosis in oral contraceptive users. Furthermore, 20% of women continued or switched to a different contraceptive after a thrombotic event. Contraceptive use after an event was associated with a threefold increased risk of recurrent venous thrombosis, which depended on the ethinylestradiol dose, type of progestagen and whether the contraceptive was triphasic or not. All ten combined oral contraceptives commonly used and included in the analysis increased the risk of a first venous thrombosis. The highest risk of venous thrombosis was found among users of drospirenone with 30 _g ethinylestradiol, cyproterone acetate with 35 _g ethinylestradiol and levonorgestrel with 50 _g ethinylestradiol. Users of levonorgestrel with 20 _g ethinylestradiol had the lowest risk of venous thrombosis among combined oral contraceptive users.