Effects of estrogen and the selective estrogen receptor modulator raloxifene on markers of inflammation in postmenopausal women

Abstract

Despite the demonstration of multiple biologic effects of estrogen that may protect against atherosclerosis and its ischemic manifestations, many women are reluctant to take chronic estrogen therapy because of fear of endometrial and breast cancer, and because of adverse effects including resumption of periodic vaginal bleeding. Accordingly, identification of alternative therapies that might replicate the biologic effects of estrogen but are devoid of these unwanted side effects of prolonged estrogen therapy would be of a considerable interest to women at risk for atherosclerosis. Raloxifene hydrochloride is a compound derived from a benzothiophene series of antiestrogens and is classified as a selective estrogen receptor modulator.1 In postmenopausal women, raloxifene appears to exert an estrogen-like effect on lipoprotein metabolism with reduction in low-density lipoprotein cholesterol and lipoprotein(a) levels, but does not increase high-density lipoprotein cholesterol levels.2 Because raloxifene has estrogenic effects on atherogenic lipoproteins, this compound may reduce vascular inflammation with antiatherogenic consequences. Such demonstration would have considerable implications for cardioprotection of postmenopausal women, potentially preferable to estrogen therapy for chronic use because of the apparent absence of carcinogenic effects of raloxifene on the breast and uterus. This study examined whether raloxifene reduces serum levels of markers of inflammation in postmenopausal women compared with responses to conjugated equine estrogens (CEE) hormone therapy.