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 percutaneous estradiol and conjugated estrogens on the level of plasma proteins and triglycerides in postmenopausal women.
Percutaneous administration of estradiol ( E2 ) is a new substitutive treatment for postmenopausal women . In order to compare hepatic action of percutaneous E2 with that of conjugated estrogens , 18 postmenopausal women were allocated at r and om to receive one of these two types of natural estrogens for 21 days . Eight patients ( group I ) received conjugated estrogens orally , 1.25 mg daily . Ten patients ( group II ) were told to apply percutaneous E2 ointment , 5 gm ( i.e. , 3 mg of E2 ) , each evening on the abdominal skin .  E2 , estrone ( E1 ) , follicle-stimulating hormone ( FSH ) , and luteinizing hormone ( LH ) , and several markers of estrogen action were evaluated before and after treatment . Both types of treatment were biologically effective , as indicated by the decrease in plasma gonadotropins and the increase in estrogen levels . However , conjugated estrogens produced a greater increase in E1 than in E2 ; hence , the E2/E1 ratio was 0.57 in group I , whereas it was approximately 1 in group II . Plasma renin substrate increased significantly ( by 180 % ) in group I but not in group II . In the same way , conjugated estrogens produced a modest ( 12 % ) but significant decrease in antithrombin III , whereas there was no variation with percutaneous E2 . Sex steroid-binding protein was the most sensitive parameter for the hepatic action of estrogen , and increased by 18.66 % with percutaneous E2 and by 150 % with conjugated estrogens .  Plasma triglycerides tended to increase in group I and to decrease in group II , but not significantly . Therefore , percutaneous administration of of E2 , in contrast to conjugated estrogens , can produce plasma levels of estrogens closer to those observed in the follicular phase and less alterations in protein synthesis . This lesser toxicity may be explained partially by the route of administration , since with percutaneous administration of E2 , the steroid bypasses the liver
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 .