Short-term effects of low-dose atorvastatin on inflammatory status and lipid profiles in perimenopausal hypercholesterolemic, hypertriglyceridemic women.
The short-term and small-dose pleiotropic effects of atorvastatin and influence on sex steroid production were investigated in 35 premenopausal and 71 postmenopausal hypercholesterolemic, hypertriglyceridemic women, as well as the temporal differences in these pleiotropic effects. Atorvastatin (10 mg daily) was given for 6 months and fasting lipid concentrations, high sensitive CRP, and coagulo-fibrinolytic parameters were measured at baseline and after 3 and 6 months of therapy. Atorvastatin reduced the low-density lipoprotein cholesterol, remnant-like particle lipoprotein cholesterol, and malondialdehyde-modified low-density lipoprotein cholesterol after 3 and 6 months in both pre- and postmenopausal women. Atorvastatin decreased significantly high-sensitivity C-reactive protein concentration (-47.6% and -58.0%, P<0.01) and tissue plasminogen activator/plasminogen activator inhibitor-1 ratio (-31.8% and -40.0%, P<0.001) after 6 months in pre- and postmenopausal women. There was no correlation between the pleiotropic effects and the improvement in the lipid profile. Furthermore, atorvastatin has no influence on sex steroid production in both pre- and postmenopausal period. The results indicate some short-term pleiotropic effects of small-dose atorvastatin therapy without influence of endocrinological status, which may be important with respect to the early benefits of statin therapy in the perimenopausal hyperlipidemic women.
Ushiroyama
Takahisa
T
Department of Obstetrics and Gynecology, Osaka Medical College, Takatsuki 569-8686, Osaka, Japan. gyn003@poh.osaka-med.ac.jp
Nosaka
Sakura
S
Ueki
Minoru
M
D000328:Adult; D000069059:Atorvastatin; D001777:Blood Coagulation / Q000187:drug effects; D002097:C-Reactive Protein / Q000037:antagonists & inhibitors; D002784:Cholesterol / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood / Q000378:metabolism; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects; D012739:Gonadal Steroid Hormones / Q000096:biosynthesis; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000097:blood / Q000188:drug therapy*; D015228:Hypertriglyceridemia / Q000097:blood / Q000188:drug therapy*; D007249:Inflammation / Q000378:metabolism*; D008055:Lipids / Q000097:blood*; D008074:Lipoproteins / Q000097:blood; D008315:Malondialdehyde / Q000378:metabolism; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D017698:Postmenopause / Q000378:metabolism; D017697:Premenopause / Q000378:metabolism; D011446:Prospective Studies; D011758:Pyrroles / Q000627:therapeutic use*; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000037:antagonists & inhibitors; D014280:Triglycerides / Q000097:blood
D008078:Cholesterol, LDL; D012739:Gonadal Steroid Hormones; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D008074:Lipoproteins; D017395:Plasminogen Activator Inhibitor 1; D011758:Pyrroles; D014280:Triglycerides; C112017:remnant-like particle cholesterol; D008315:Malondialdehyde; D002097:C-Reactive Protein; D002784:Cholesterol; D000069059:Atorvastatin; D010959:Tissue Plasminogen Activator