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Walsh BW, Kuller LH, Wild RA, et al. Effects of Raloxifene on Serum Lipids and Coagulation Factors in Healthy Postmenopausal Women. JAMA. 1998;279(18):1445–1451. doi:10.1001/jama.279.18.1445
From the Brigham and Women's Hospital, Boston, Mass (Dr Walsh); University of Pittsburgh, Pittsburgh, Pa (Dr Kuller); University of Oklahoma Health Sciences Center, Oklahoma City (Dr Wild); Lilly Research Laboratories, Indianapolis, Ind (Drs Paul, Lawrence, Shah, and Anderson); and Clinical Studies, St Petersburg, Fla (Dr Farmer).
Context.— Raloxifene is a selective estrogen receptor modulator that has estrogen-agonistic
effects on bone and estrogen-antagonistic effects on breast and uterus.
Objective.— To identify the effects of raloxifene on markers of cardiovascular risk
in postmenopausal women, and to compare them with those induced by hormone
replacement therapy (HRT).
Design.— Double-blind, randomized, parallel trial.
Setting.— Eight sites in the United States.
Participants.— 390 healthy postmenopausal women recruited by advertisement.
Intervention.— Participants were randomized to receive 1 of 4 treatments: raloxifene,
60 mg/d; raloxifene, 120 mg/d; HRT (conjugated equine estrogen, 0.625 mg/d,
and medroxyprogesterone acetate, 2.5 mg/d); or placebo.
Main Outcome Measures.— Change and percent change from baseline of lipid levels and coagulation
parameters after 3 months and 6 months of treatment.
Results.— At the last visit completed, compared with placebo, both dosages of
raloxifene significantly lowered low-density lipoprotein cholesterol (LDL-C)
by 12% (P<.001), similar to the 14% reduction
with HRT (P<.001). Both dosages of raloxifene
significantly lowered lipoprotein(a) by 7% to 8% (P<.001),
less than the 19% decrease with HRT (P<.001).
Raloxifene increased high-density lipoprotein-2 cholesterol (HDL2-C)
by 15% to 17% (P<.05), less than the 33% increase
with HRT (P<.001). Raloxifene did not significantly
change high-density lipoprotein cholesterol (HDL-C), triglycerides, or plasminogen
activator inhibitor-1 (PAI-1); whereas HRT increased HDL-C by 11% and triglycerides
by 20%, and decreased PAI-1 by 29% (for all, P<
.001). Raloxifene significantly lowered fibrinogen by 12% to 14% (P<.001), unlike HRT, which had no effect. Neither treatment changed
fibrinopeptide A or prothrombin fragment 1 and 2.
Conclusions.— Raloxifene favorably alters biochemical markers of cardiovascular risk
by decreasing LDL-C, fibrinogen, and lipoprotein(a), and by increasing HDL2-C without raising triglycerides. In contrast to HRT, raloxifene had
no effect on HDL-C and PAI-1, and a lesser effect on HDL2-C and
lipoprotein(a). Further clinical trials are necessary to determine whether
these favorable biochemical effects are associated with protection against
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