| Research Abstract |
(Objectives) Postmenopausal hormorie replacement therapy(HRT) decreases the incidence of coronary heart disease(CHD). According to the recent studies, however, HRT increased the risk of CHD in postmenopausal women. We previously demonstrated that oral HRT increases vascular inflammatory markers such as C-reactive protein(CRP) concentrations. In the present study, we evaluated whether oral HRT have a pro-inflammatory effect and investigated the effects of transdermal HRT on vascular inflammatory markers.
(Methods and Results) Postmenopausal women received no treatment or were treated with 0.625mg oral conjugated equine estrogen daily or with transdermal estradiol(25μg/day,n=15) for 3 months. Oral ERT significantly increased plasma concentrations of CRP, serum amyloid A protein(SAA), and matrix metalloproteinase(MMP)-3, but significantly decreased tissue inhibitor of MMP(TIMP)-1 concentrations by 8.6%. In contrast, transdermal ERT significantly decreased CRP concentrations and tended to increase TIMP-1 concentrations. Oral ERT significantly, decreased p-selectin concentrations, but the concentrations of intercellular adhesion molecule(ICAM-1) and vascular cell adhesion molecule(VCAM-1) did not change significantly. Transdermal ERT, however, significantly decreased all cell adhesion molecule concentrations.
(Conclusion) Oral HRT may have a pro-inflammatory effect by increasing vascular inflammatory markers. Oral HRT-induced increases in inflammatory markers and imbalances between MMP and TIMP-1 might be reversed by transdermal administration of estrogen. Because transdermally administered estrogen decreased cell adhesion molecule concentrations, the anti-inflammatory effect of transdermal HRT may actually be responsible for the favorable effect of estrogen on cell adhesion molecule, concentrations in postmenopausal women.
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