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 .
Randomized Comparison of Intranasal and Transdermal Estradiol
Objective To compare the efficacy and patient acceptability of intranasal versus transdermal 17β-estradiol ( E2 ) delivery systems for postmenopausal symptoms . Methods Postmenopausal women were r and omly assigned to intranasal 17β-E2  , 300 μg daily ( n = 176 )  or transdermal 17β-E2 ( delivering 50 μg/day ) , two patches per week ( n = 185 ) for 12 weeks , followed by a 4-week period with the alternate treatment . Efficacy was compared between groups using the Kupperman Index and vasomotor symptoms at week 12 . Patient acceptability was compared by patient choice of administration route and by question naire at week 16 . Results Intranasal and transdermal therapy produced significant reductions in the Kupperman Index and in the occurrence of hot flushes and night sweats at week 12 . Alleviation of climacteric symptoms was statistically equivalent in the two treatment groups ( P < .001 ) . The difference between groups in the Kupperman Index score of −0.5 ± 0.9 ( 95 % confidence interval −2.3 , 1.3 ) was within the predetermined interval of equivalence . Both therapies were well tolerated with similar adverse event rates , except for moderate and severe mastalgia which was significantly less frequent with intranasal E2 ( 7.2 % ) than with the patch ( 15.5 % , P = .02 ) . Sixty-six percent of patients chose to continue the intranasal therapy and 34 % the transdermal therapy ( P < .001 ) . Satisfaction was greater with intranasal therapy at week 16 ( P < .001 ) . Conclusion Intranasal and transdermal estrogen delivery systems had equivalent efficacy and similar safety profiles . Intranasal therapy was the patients ' choice for long-term treatment
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 .