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 transdermal and oral oestrogen replacement therapy on C-reactive protein levels in postmenopausal women: a randomised, placebo-controlled trial.
To investigate the effect of  postmenopausal oral and transdermal hormone therapy  on plasma levels of C-reactive protein ( CRP ) , we performed a r and omised , double-blind , double-dummy , placebo-controlled , 15-month study . One hundred and fifty-two healthy hysterectomised postmenopausal women received daily either placebo ( n = 49 ) , or transdermal 17beta-oestradiol ( E(2 ) ) 50 micro g ( tE(2 ) group , n = 33 ) , or oral E(2 ) 1 mg ( oE(2 ) group , n = 37 ) , or oral E(2 ) 1 mg combined with gestodene 25 micro g ( oE(2 ) + G group , n = 33 ) for thirteen 28-day treatment cycles , followed by four cycles placebo for each group . Data were collected at baseline and in cycles 4 , 13 and 17 . In cycle 13 , CRP was significantly increased in the oE(2 ) group compared to placebo ( P = 0.004 ) . The median percentage change from baseline versus placebo was + 75 % ( P < 0.001 ) . In cycle 17 , significantly lower values were observed in the oE(2 ) group compared to cycle 13 and to the placebo group ( -49 % , P < 0.001 ) . There were no significant changes versus placebo in the other groups . In conclusion , oral E(2 ) significantly increased CRP levels . This change was larger than the increase found during oral E(2 ) + G. Transdermal E(2 ) did not affect CRP levels
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 .