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 .
Effects of oral and transdermal estrogen replacement therapy on markers of coagulation, fibrinolysis, inflammation and serum lipids and lipoproteins in postmenopausal women.
We compared the effects of oral estradiol ( 2 mg ) , transdermal estradiol ( 50 microg ) , and placebo on measures of coagulation , fibrinolysis , inflammation and serum lipids and lipoproteins in 27 postmenopausal women at baseline and after 2 and 12 weeks of treatment . Oral and transdermal estradiol induced similar increases in serum free estradiol concentrations . Oral therapy increased the plasma concentrations of factor VII antigen ( FVIIag ) and activated factor VII ( FVIIa ) , and the plasma concentration of the prothrombin activation marker prothrombin fragment 1 + 2 ( F1 + 2 ) . Oral but not transdermal estradiol therapy significantly lowered plasma plasminogen activator inhibitor-1 ( PAI-1 ) antigen and tissue-type plasminogen activator ( tPA ) antigen concentrations and PAI-1 activity , and increased D-dimer concentrations , suggesting increased fibrinolysis . The concentration of soluble E-selectin decreased and serum C-reactive protein ( CRP ) increased significantly in the oral but not in the transdermal or placebo groups . In the oral but not in the transdermal or placebo estradiol groups low-density-lipoprotein ( LDL ) cholesterol , apolipoprotein B and lipoprotein ( a ) concentrations decreased while high-density-lipoprotein ( HDL ) cholesterol , apolipoprotein AI and apolipoprotein All concentrations increased significantly . LDL particle size remained unchanged . In summary , oral estradiol increased markers of fibrinolytic activity , decreased serum soluble E-selectin levels and induced potentially antiatherogenic changes in lipids and lipoproteins . In contrast to these beneficial effects , oral estradiol changed markers of coagulation towards hypercoagulability , and increased serum CRP concentrations .  Transdermal estradiol or placebo had no effects on any of these parameters . These data demonstrate that oral estradiol does not have uniformly beneficial effects on cardiovascular risk markers and that the oral route of estradiol administration rather than the circulating free estradiol concentration is critical for any changes to be observed
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 .