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 .
Increased plasma concentrations of TGF-beta1 after hormone replacement therapy.
OBJECTIVES AND DESIGN Hormone replacement therapy ( HRT ) in postmenopausal women may reduce the cardiovascular risk . A dominant protective role of transforming growth factor beta ( TGF-beta1 ) on coronary arteries has been proposed . Lp(a ) lipoprotein may block the activation of latent TGF-beta1 . Given this background , we examined the effects of HRT on TGF-beta1 and Lp(a ) lipoprotein in 99 postmenopausal women . The women had angiographically documented coronary heart disease ( CHD ) and were r and omized to either sequential transdermal 17beta-oestradiol for 14 weeks and then medroxyprogesterone ( MPA ) for 14 days ( HRT ) or to a control group ( C ) . RESULTS Serum levels of TGF-beta1 were increased in the HRT group compared with the C group after 3 months ' treatment and this effect was sustained after 12 months . There was a significant reduction in Lp(a ) lipoprotein serum levels after 3 months ' treatment in the HRT group compared with the C group . However , after 12 months , no significant difference in changes in Lp(a ) lipoprotein serum levels was detected between the two groups . CONCLUSION The novel observation that transdermal 17beta-oestradiol in postmenopausal women increases levels of TGF-beta1 and lowers the concentration of Lp(a ) lipoprotein suggests yet another possible mechanism for the cardioprotective effect of HRT . Whereas combination therapy of oestradiol and MPA preserves the beneficial effect on TGF-beta1 , it reduces the unopposed oestradiol effects on Lp(a ) lipoprotein
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 .