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Hum. Reprod. Advance Access originally published online on June 28, 2006
Human Reproduction 2006 21(10):2715-2720; doi:10.1093/humrep/del245
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© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Differential effects of oral conjugated equine estrogen and transdermal estrogen on atherosclerotic vascular disease risk markers and endothelial function in healthy postmenopausal women

Jason Yen-Ping Ho1,3,6, Ming-Jer Chen1,4, Wayne Huey-Herng Sheu2,3,5, Yu-Chiao Yi1,5, Andy Chi-Wei Tsai1, Hwa-Fen Guu1 and Esther Shih-Chu Ho1,5,7

1 Department of Obstetrics and Gynecology 2 Department of Internal Medicine, Taichung Veterans General Hospital 3 Institute of Biomedical Sciences, National Chung Hsing University, Taichung 4 School of Medicine, National Yang Ming University, Taipei 5 Chung Shan Medical University and 6 Central Taiwan University of Science and Technology, Taichung, Taiwan

7 To whom correspondence should be addressed at: Department of Obstetrics and Gynecology, Taichung Veterans General Hospital, 160, Chung-Kang Road Section 3, Taichung 407, Taiwan. E-mail: bamboo{at}vghtc.gov.tw

BACKGROUND: Recent studies have revealed that HRT may increase the risk for atherosclerotic vascular disease (ASVD). METHODS: We investigated the effects of HRT via different administration routes on the markers for ASVD and endothelial function in healthy postmenopausal women. The oral HRT group (n = 18) received conjugated equine estrogen 0.625 mg/day; the transdermal HRT group (n = 18) received 17beta-estradiol (E2) gel 0.6 mg/day for 6 months. The control group (n = 30) had no treatment for 6 months. RESULTS: The C-reactive protein (CRP) rose from 0.129 ± 0.116 to 0.752 ± 0.794 mg/dl (P < 0.01) in the oral HRT group but remained unchanged in the transdermal HRT and control groups. The flow-mediated vasodilation (FMD) in the brachial artery was increased significantly by HRT from 6.0% before oral HRT to 14.7% after oral HRT (P < 0.001) and from 5.9% before transdermal HRT to 13.9% after transdermal HRT (P = 0.001). CONCLUSIONS: These data suggest that oral estrogen induces ASVD risk by increasing acute inflammation; however, transdermal estrogen avoids this untoward effect. Additionally, transdermal estrogen exerts a positive effect on endothelial function similar to that of oral estrogen. Therefore, the transdermal route might be favourable in terms of ASVD risks.

Key words: atherosclerotic vascular disease/C-reactive protein/estrogen/homocysteine/vasodilation


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