Lp(a) and lipids in adult Turner's syndrome: impact of treatment with 17beta-estradiol and norethisterone.
Turner's syndrome is associated with a high incidence of cardiovascular disease and hypothyreosis; conditions which are associated with abnormal lipid metabolism. To test whether alterations of lipid metabolism is present in healthy Turner's women, we compared lipids in a group of adult women with Turner's syndrome with an age matched group of healthy women. In addition the impact of sex steroid replacement therapy was studied in the women with Turner's syndrome. Patients were studied before and during treatment with hormonal replacement therapy, consisting of either oral 17beta-estradiol or transdermal 17beta-estradiol, and oral norethisterone. Control subjects were studied once in the early follicular stage of the menstrual cycle. The study group consisted of 26 (33.2+/-7.9 years) patients with Turner's syndrome and an age matched control group of 24 (32.7+/-7.6 years) normal women. Body composition measures, apolipoprotein (apo) B and apo A-I, Lp(a), cholesterol, HDL, LDL, triglycerides, thyroxine (TT4), free thyroxine (FT4), triiodothyronine (TT3), free triiodothyronine (FT3), TSH, and leptin were determined. Apo A-I levels were higher in Turner's patients (P45 g/l) Lp(a), more women with Turner's syndrome had high levels of Lp(a) than controls (P=0.024), while all other measures of lipid metabolism were comparable to controls. The level of TSH, FT3, and FT4 were significantly higher in Turner's patients, while TT4, TT3 and adjusted 24h energy expenditure were comparable to controls. Lp(a) (P=0.005), HDL (P=0.045) and apo A-I (P=0.039) decreased significantly, while there was a tendency towards a decrease in apo B (P=0.063) during treatment with sex hormones. In conclusion more women with Turner's syndrome than controls have high levels of apolipoprotein A-I and Lp(a), but only after dichomitization, while other markers of lipid metabolism are normal. Replacement therapy with female sex hormones lowered Lp(a), HDL cholesterol and apolipoprotein A-I.
Gravholt
C H
CH
Medical Department M (Endocrinology and Diabetes) and Medical Research Laboratories, Aarhus University Hospital, DK-8000, Aarhus, Denmark. ch.gravholt@dadlnet.dk
Christian Klausen
I
I
Weeke
J
J
Sandahl Christiansen
J
J
D000328:Adult; D016632:Apolipoprotein A-I / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D001824:Body Constitution; D002784:Cholesterol / Q000097:blood; D004958:Estradiol / Q000627:therapeutic use*; D005260:Female; D020249:Hormone Replacement Therapy; D006801:Humans; D008055:Lipids / Q000097:blood*; D017270:Lipoprotein(a) / Q000097:blood*; D009640:Norethindrone / Q000627:therapeutic use*; D045167:Progesterone Congeners / Q000627:therapeutic use*; D013963:Thyroid Hormones / Q000097:blood; D014280:Triglycerides / Q000097:blood; D014424:Turner Syndrome / Q000097:blood* / Q000188:drug therapy
D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D008055:Lipids; D017270:Lipoprotein(a); D045167:Progesterone Congeners; D013963:Thyroid Hormones; D014280:Triglycerides; D004958:Estradiol; D002784:Cholesterol; D009640:Norethindrone