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Cardiovascular Research 2002 53(3):642-649; doi:10.1016/S0008-6363(01)00461-8
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

The effect of 17β-estradiol on MCP-1 serum levels in postmenopausal women

Stefan Störk*, Klaus Baumann, Clemens von Schacky and Peter Angerer

Medizinische Klinik, Klinikum der Universität München - Innenstadt, Ziemssenstr. 1, D-80336 München, Germany

* Corresponding author. Tel.: +49-931-201-7088, fax: +49-931-201-7124 s.stoerk{at}medizin.uni-wuerzburg.de

Objective: Monocyte chemoattractant protein-1 (MCP-1) is considered a propagator of atherosclerosis and a key modulator of monocyte activity. Hormone replacement therapy (HRT) is currently being investigated as a means towards prevention of atherosclerosis. We aimed to assess (1) the range of circulating MCP-1 levels in postmenopausal women, (2) the correlation between MCP-1 and atherosclerotic burden, and (3) the effects of commencement and discontinuation of HRT on MCP-1 serum levels. Methods: This clinical prospective trial investigated 51 postmenopausal women at increased risk for cardiovascular events who were randomized to receive either no HRT or 1 mg 17β-estradiol continuously plus sequential progestagen over 1 year. Intima-media thickness (IMT) of carotid and femoral arteries was measured by ultrasound. Serum levels of MCP-1 and cellular adhesion molecules were measured by ELISA. Results: At baseline, MCP-1 levels and overall mean maximum IMT correlated (r=0.589; P<0.0001, Pearson's coefficient). MCP-1 levels in serum gradually decreased after 3, 6, and 12 months of HRT by 16.8±15.7% at 12 months (P<0.0001, MANOVA). Similarly, all cellular adhesion molecules decreased significantly by 6–12%. After 12 months, women decided whether to continue or discontinue treatment. At 18 months, in women discontinuing HRT (n=17), MCP-1 levels rose by 21±20% (P=0.003), but remained lowered in women continuing HRT. Conclusion: Our observations indicate that 17β-estradiol may have an antiatherosclerotic effect by reducing MCP-1 serum levels and cell adhesion molecules.

KEYWORDS Arteries; Atherosclerosis; Cytokines; Hormones; Infection/inflammation


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