For non-oral HT , decreases in lipoprotein(a ) , cell adhesion molecules , and factor VII generally were significant , resistance to activated protein C ( APCr ) was slightly increased , and other markers including CRP and homocysteine did not change .
Compared with oral HT , changes in CRP and APCr were smaller , changes in cell adhesion molecules and some fibrinolytic parameters tended to be smaller , whereas changes in other factors including lipoprotein(a ) and homocysteine did not differ .
( S ) Potentially unfavorable changes seen with oral HT on two important markers , CRP and APCr , are substantially smaller with non-oral HT .
Non-oral HT has minor effects on the other cardiovascular risk markers studied .
Therefore , compared with oral HT , non-oral HT appears be safer with respect to atherosclerotic and venous thromboembolic disease risk
OBJECTIVE To review the effects of non-oral administration of postmenopausal hormone therapy ( HT ) on risk markers for atherosclerotic and venous thromboembolic disease .
Non-oral postmenopausal HT appears not to increase venous thromboembolic risk , whereas the effect on coronary heart disease risk is less clear .
The effects of hormone replacement therapy on hemostatic variables in women with angiographically verified coronary artery disease: results from the estrogen in women with atherosclerosis study.
Data on the effect of hormone replacement therapy on hemostasis are inconsistent , and there are few data in women with coronary artery disease . In a single-center , open , r and omized study , 118 postmenopausal women with angiographically verified coronary artery disease were r and omized to hormone replacement therapy , given as long-cycle transdermal 17-beta-estradiol ( 50 microg/24 hour ) for 3 months with sequential medroxy-progesterone acetate for 14 days , or to a control group receiving no therapy .  Hemostatic parameters were measured at baseline and after 3 and 12 months of therapy . The coagulation inhibitors antithrombin , protein C , and protein S , but not tissue factor pathway inhibitor , decreased significantly from baseline in the hormone replacement therapy group at both 3 and 12 months as compared with the control group . The absolute decreases within the hormone replacement therapy group were 3 to 10 % . No significant differences between the two treatment groups were observed for the coagulation products prothrombin fragment 1 + 2 or thrombin-antithrombin complex or for D-dimer , although there were significant decreases in the levels within the hormone replacement therapy group . Levels of fibrinogen , activated factor VII , and factor VII antigen were not significantly influenced by hormone replacement therapy treatment . Similarly , nonsignificant changes were detected for the fibrinolytic parameters tissue plasminogen activator activity , tissue plasminogen activator antigen , and global fibrinolytic activity , but plasminogen activator inhibitor type 1 was significantly lower in the hormone replacement therapy group due to a question able increase in the levels in the control group . In conclusion , treatment with transdermal estradiol combined with long-cycle progestins was associated with no net activation of coagulation despite reduced levels of coagulation inhibitors
For non-oral HT , decreases in lipoprotein(a ) , cell adhesion molecules , and factor VII generally were significant , resistance to activated protein C ( APCr ) was slightly increased , and other markers including CRP and homocysteine did not change .
Compared with oral HT , changes in CRP and APCr were smaller , changes in cell adhesion molecules and some fibrinolytic parameters tended to be smaller , whereas changes in other factors including lipoprotein(a ) and homocysteine did not differ .
( S ) Potentially unfavorable changes seen with oral HT on two important markers , CRP and APCr , are substantially smaller with non-oral HT .
Non-oral HT has minor effects on the other cardiovascular risk markers studied .
Therefore , compared with oral HT , non-oral HT appears be safer with respect to atherosclerotic and venous thromboembolic disease risk
OBJECTIVE To review the effects of non-oral administration of postmenopausal hormone therapy ( HT ) on risk markers for atherosclerotic and venous thromboembolic disease .
Non-oral postmenopausal HT appears not to increase venous thromboembolic risk , whereas the effect on coronary heart disease risk is less clear .