Estrogen/progesterone replacement versus pravastatin and their sequential association in hypercholesterolemic postmenopausal women.
OBJECTIVE
The objectives of this study were to assess serum lipid changes in response to an oral estrogen combined with progesterone (Group A) as compared with pravastatin (Group B) and to evaluate the additive effects of the sequential addition of statin to hormonal replacement therapy (HRT) and of HRT to statin.


METHODS
Thirty-seven of 63 hypercholesterolemic menopausal women initially submitted to a 4-month diet were randomised to oral conjugated estrogens (0.625 mg)/micronised progesterone (200 mg) or to pravastatin (40 mg). After 6 months, each group received both medications for another 6 months.


RESULTS
Nineteen percent of women corrected their lipids below decision levels with diet alone. Low density lipoprotein-cholesterol (LDL-C) decreased by 8+/-5% with HRT and by 26+/-3% (P<0.001) with the statin. These single medications increased high density lipoprotein-cholesterol (HDL-C) by 13+/-5% (P<0.01) and 11+/-7%, respectively. Combined interventions produced cumulative LDL-C reductions of 40+/-2 and 42+/-3% (P<0.001) and additive HDL-C augmentations of 16+/-4 and 23+/-5% (P<0.01) with proportional changes in apolipoprotein (Apo)B-100 and ApoA-1. These combined effects brought the atherogenic index (C/HDL-C) for Groups A and B, respectively, from a moderate (5.18+/-0.25 and 5.87+/-0.18) to a reduced (3.35+/-0.20 and 3.52+/-0.19) risk category. Triglycerides (TG) which were increased by HRT and decreased by the statin returned to baseline during combined treatments. No changes in diet, physical activity or anthropomorphometric measurements explained the lipid modifications.


CONCLUSIONS
In menopausal patients with elevated C not responding to diet, pravastatin was most effective to decrease LDL-C, and oral estrogen-micronised progesterone most effective to increase HDL-C. Marked reduction of the atherogenic index is achieved by sequential combinations of medications resulting from beneficial cumulative effects on both C-LDL and C-HDL.
Lemay
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A
Départements d'Obstétrique-Gynécologie et de Biologie Médicale, Endocrinologie de la reproduction, Centre de Recherche, Hôpital St-François d'Assise, CHUQ, Université Laval, 10 rue de l'espinay, Quebec P.Q., G1L-3L5, Canada. andre.lemay@ogy.ulaval.ca
Dodin
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Turcot
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Déchêne
F
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Forest
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JC
D000284:Administration, Oral; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D001053:Apolipoproteins / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004032:Diet; D004966:Estrogens, Conjugated (USP) / Q000008:administration & dosage; D015444:Exercise; D005260:Female; D020249:Hormone Replacement Therapy; D006801:Humans; D006937:Hypercholesterolemia / Q000517:prevention & control*; D008875:Middle Aged; D017698:Postmenopause; D017035:Pravastatin / Q000627:therapeutic use*; D011374:Progesterone / Q000008:administration & dosage; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood
D000924:Anticholesteremic Agents; D001053:Apolipoproteins; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004966:Estrogens, Conjugated (USP); D014280:Triglycerides; D011374:Progesterone; D017035:Pravastatin