COAGULOPATHY AND THROMBOSIS IN THE CONSUMPTION OF CONTRACEPTIVES

Hormonal contraceptives exert prothrombotic effects, related to estrogen (intensification of gene expression of coagulation factors II, VII, VIII, X, XII, fibrinogen, von Willebrand factor, heparanase, TAFI, induction of PCa resistance, decrease in expression of antithrombin, factor V, activation inflammation, vasodilatation in non-optimal conditions) as well as antithrombotic effects (activation of PS and TFPI, increase in PAI-1 gene expression and decrease in T-PA gene expression). Progestins activate heparanase, and induce vasodilation. Therefore, contraceptives have diametrically opposite effects, and the pro- or anti-thrombotic result largely depends on the pre-existing coagulant background. Different methods of hormonal contraception have distinct thrombotic risks. The thrombotic effect of estrogen is dose-dependent, diminishing at low doses. But even at doses of 10 µg, the prothrombotic effect persists. There is a difference between the types of estrogens. Thus, the use of estradiol valerate and estradiol decreases the thrombotic risk compared to ethinyl estradiol