title: Hormonal agents used in lowering lipoprotein(a).
abstract: Lipoprotein(a) (Lp(a)) plasma concentrations in Caucasian populations are classified as a quantitative genetic trait. Although the prevailing view has been that Lp(a) levels are affected by age and gender, recent data are beginning to indicate otherwise. Lp(a) levels change throughout life especially in females after menopause. Lp(a) levels decrease in women treated with anabolic steroids such as stanozolol and danazol. The Lp(a) plasma concentration is also profoundly affected by sex hormone variations during pregnancy. In men with prostatic cancer Lp(a) levels are reduced about 50% by estrogen therapy, and increased 20% by orchidectomy. We have evaluated the changes in Lp(a) and lipid levels in postmenopausal women following estrogen/progestogen replacement therapy. The mean level of Lp(a) in treated women was about 50% lower after 6 and 12 months of replacement therapy. A significant correlation between basal Lp(a) levels and the changes at either 6 or 12 months was observed, suggesting that therapy was particularly efficacious in those women with high basal Lp(a) levels. One year after therapy cessation, Lp(a) concentrations tended to return to pre-therapy values. In addition estrogen-progestogen treatment significantly lowered total-cholesterol (12%) and LDL-cholesterol (28%), and increased HDL-cholesterol (18%). From these studies it appears that sex hormones are actively involved in the modulation of plasma Lp(a) levels and that both female and male sex hormones possess a lowering effect. The results confirm a direct effect of sex hormones on Lp(a) metabolism and suggest that estrogen-progestogen treatment of postmenopausal women can improve the lipid profile not only by lowering total- and LDL-cholesterol and raising HDL cholesterol, but also by lowering plasma Lp(a).
authors.affiliation: Institute of Pharmacological Sciences, University of Milan, Italy.
authors.forename: M R
authors.initials: MR
authors.lastname: Soma
authors.forename: M
authors.initials: M
authors.lastname: Meschia
authors.forename: F
authors.initials: F
authors.lastname: Bruschi
authors.forename: J D
authors.initials: JD
authors.lastname: Morrisett
authors.forename: R
authors.initials: R
authors.lastname: Paoletti
authors.forename: R
authors.initials: R
authors.lastname: Fumagalli
authors.forename: P
authors.initials: P
authors.lastname: Crosignani
mesh_terms: D015914:Estrogen Replacement Therapy; D004966:Estrogens, Conjugated (USP) / Q000494:pharmacology; D005260:Female; D012739:Gonadal Steroid Hormones / Q000378:metabolism; D006801:Humans; D008055:Lipids / Q000097:blood; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D017258:Medroxyprogesterone Acetate / Q000494:pharmacology; D008593:Menopause; D008875:Middle Aged; D011973:Receptors, LDL / Q000378:metabolism; D012727:Sex Characteristics; D013997:Time Factors
chemical_list: D004966:Estrogens, Conjugated (USP); D012739:Gonadal Steroid Hormones; D008055:Lipids; D017270:Lipoprotein(a); D011973:Receptors, LDL; D017258:Medroxyprogesterone Acetate