92308470 Coagulation activation following estrogen administration to postmenopausal women

Effect of Estrogen-Progestin Hormonal Replacement Therapy on Blood Coagulation and Fibrinolysis in Postmenopausal Women

“…[27][28][29][30] Some authors observed AT-III reduction with ethinyl estradiol [31][32][33] and with estradiol valerate. 32,33 On the other hand, AT-III reduction during HT with oral CEE was not observed by others, but this may be due to methodology.…”

Postmenopausal Hormone Replacement Therapy Increases Coagulation Activity and Fibrinolysis

“…8,10,11 Thrombosis results from inappropriate initiation and propagation of the hemostatic response and may occur as a result of activation of coagulation or inhibition of fibrinolysis. 12 That estrogen has a complex effect on the mechanisms underlying thrombosis is suggested by clinical studies indicating that although it produces a dose-dependent increase in plasma markers of thrombin and fibrin generation, 13,14 it also decreases plasma fibrinolytic inhibitory activity 14 -18 by decreasing levels of plasminogen activator inhibitor-1 (PAI-1). 14,16 -18 However, there is considerable uncertainty regarding the effects of combined HRT with estrogen and progestin on coagulation and fibrinolytic processes.…”

Hormone replacement therapy and cardiovascular disease: does route of administration and formulation matter?

“…Variable -increased in one (Rabbani et al, 2002) and unchanged in another (Lip et al, 1997) No change in this study (Stevenson et al, 2004) Insulin-like growth factor 1 (IGF-1) Decreases (Vongpatanasin et al, 2003) No change (Vongpatanasin et al, 2003) Prothrombotic (Caine et al, 1992) May be neutral (Stevenson et al, 2004) Venous thromboembolism Increased risk (Scarabin et al, 2003) No effect (Scarabin et al, 2003) Correspondence ª 2004 Blackwell Publishing Ltd, British Journal of Haematology, 124, 836-844 tion that this marker was elevated by transdermal HRT (Stevenson et al, 2004) may potentially be less alarming given that there was no increase in thrombotic activity, and the observation that transdermal HRT did not appear to predispose to venous thromboembolism (Scarabin et al, 2003). The concept of matrix metalloproteinase (MMP) involvement in atherogenesis is more controversial.…”

“…In particular, HRT lowers total cholesterol, low-density lipoprotein (LDL)-cholesterol and systolic blood pressure and raises high density lipoprotein (HDL)-cholesterol (The Writing Group for the PEPI Trial, 1995). However, it also has other effects that may impact in a less favourable way on the progression of atherosclerosis and thrombosis (Lip & Felmeden, 2001); in particular, oral HRT has been associated with increased levels of hsCRP (Cushman et al, 1999) and increased haemostasis (Caine et al, 1992), possibly predisposing to venous throm-boembolism -the latter being increased with HRT in observational studies (Daly et al, 1996) or randomized trials (Beral et al, 2002). Nonetheless, a pilot study in type 2 diabetics (open, longitudinal follow-up study of 19 HRT users and nine controls) found that none of the measured markers of cardiovascular risk were adversely affected by transdermal HRT, contrasting with previous studies using oral preparations (Stojanovic et al, 2003).…”