Raloxifene, Serum Lipids, and Coagulation Factors
Source: Walsh BW, et al. JAMA 1998;279:1445-1451.
Although use of hormone replacement therapy (HRT) is anticipated to extend cardiovascular and skeletal benefits to most recipients, the combination of adverse effects like breast tenderness and vaginal bleeding, coupled with fear of increased risk of breast cancer, dampen the enthusiasm of a large number of American women.
Raloxifene is not an estrogen. Rather, it is a benzothiophene derivative that binds to the estrogen receptor, producing estrogen antagonist effects in some tissues (breast, uterus) and estrogen-agonist effects in others (bone, lipids). Since it does not mimic the effects of estrogen in all tissues, it is known as a selective estrogen receptor modulator.
The authors studied 390 postmenopausal women receiving either raloxifene (60 or 120 mg qd), HRT (conjugated equine estrogen, 0.625 mg qd plus medroxyprogesterone acetate, 2.5 mg qd), or placebo for six months. Included in outcome measures were serum LDL, HDL, and triglycerides, and fibrinogen.
Both doses of raloxifene and HRT were approximately equally effective in reducing LDL (12-14%); HRT raised HDL 11% and triglycerides 20%, but raloxifene was neutral to both. HRT did not favorably affect fibrinogen, but raloxifene reduced it 12-14%. Whether these favorable cardiovascular marker effects will translate into reduced cardiovascular risk is yet to be determined. -lk
The Therapeutics and Drugs Briefs in this issue were written by Michael H. Crawford, MD, Robert S. Flinn Professor, Chief of Cardiology, University of New Mexico, Albuquerque and by Louis Kuritzky, MD, Courtesy Clinical Assistant Professor, University of Florida, Gainesville.
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