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 transdermal estradiol and oral conjugated estrogens on haemostasis variables.
The effects of oral and transdermal administration of estrogen replacement therapy ( ERT ) have been fairly well investigated regarding lipoprotein and carbohydrate metabolism , while the effects of different modes of estrogen administration on the haemostatic system have been less well studied . To delineate and compare the effects of perorally administered conjugated estrogens ( CE ) and transdermally administered estradiol ( E2 ) in doses needed for hormone replacement therapy ( HRT ) on haemostasis parameters , 23 postmenopausal women were engaged in a study with an open cross-over design . The doses compared ( 0.625 mg CE and 50 micrograms E2/24h ) are the lowest which , with few exceptions , eliminate climacteric symptoms . Both CE and E2  increased factor VII : C , factor VII : Ag , and the prothrombin fragment1 + 2 . The increase in factor VII : Ag , however , was significantly higher after treatment with CE . These changes were all towards a state of hypercoagulability . Furthermore , CE decreased plasminogen activator inhibitor ( PAI ) and the thrombin-antithrombin complexes ( TAT ) , as well as antithrombin ( ATIII )
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 .