Abstract
Selective estrogen receptor modulators (SERMs) constitute a group of chemical compounds that are distinct from estrogen. The ideal SERM would provide an estrogen-like effect at bone, preserving bone mass and reducing the risk of osteoporotic fracture. Additionally, it would lower the risk of coronary artery disease through improvements in lipoprotein profiles, improved vascular endothelial function, and possibly other mechanisms. Unlike estrogen, however, the ideal SERM would exert no proliferative effect at the uterine endometrium, so that there would be no regular or irregular uterine bleeding. This chapter discusses the current understanding of the mechanism of action of SERMs and reviews the effects on the skeleton of tamoxifen and raloxifene, the two SERMs for which there are both preclinical and clinical data. Additionaly, the clinical effects of these two drugs on lipids, uterus, and breast, as well as their overall clinical safety and tolerability, are considered.
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