Abstract
Prothrombotic effects of HRT are related to several actions. Low doses of oestradiol are associated with less activation of coagulation, including TFPI and APC Resistance, and inflammatory markers if compared with regular dose: low dose and conventional dose formulations had similar effects on C reactive protein [11, 12]; however also the increase synthesis of clotting factors as to the decreased synthesis of clotting inhibitors as to an acquired form of activated protein C resistance are involved in the hypercoagulable state of women ongoing HRT [1]. As confirm of this trend to hypercoagulable state, markers of thrombin generation are frequently increased in women taking HRT: increased levels of prothrombin fragments 1+2, TAT complexes and D-dimer have been found in several studies [13]. Furthermore the increase in these markers was higher in women who subsequently developed recurrent VTE.
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