Background: The effects of an oral contraceptive pill containing cyproterone acetate on lipid metabolism in women with polycystic ovary syndrome (PCOS) was studied.
Materials and methods: Seventy-two women with PCOS were treated for 36 consecutive cycles with an oral contraceptive containing 0.035 mg of ethinylestradiol and 2 mg of cyproterone acetate. Hormonal, lipid and glucose profiles were studied before and after 12 and 36 cycles of treatment. Lipid, lipo-and apolipoprotein values were compared to a healthy control group. Statistical analysis was by one way analysis of variance and Bonferroni's t tests.
Results: The treatment suppressed gonadotropin and androgen values and increased the levels of sex hormone binding globulin. After 12 and 36 cycles a significant increase in triglycerides, high density lipoprotein (HDL) cholesterol system, and apoprotein B levels was seen. Low density lipoprotein (LDL) cholesterol and LDL cholesterol/HDL cholesterol ratio were reduced. Insulin and glucose plasma concentrations did not change. During treatment triglycerides, total cholesterol and apoprotein B values were higher than in the control group. There were no differences in plasma levels of LDL-C and HDL-C in PCOS and in the control group.
Conclusion: Lipid and lipoprotein changes observed after treatment could be due to the estrogen dominance of the treatment. The plasma concentration of triglycerides and total cholesterol during treatment does not change appreciably and the LDL-C/HDL-C ratio improved.
PIP: In Italy, endocrinologists at the University of Brescia compared the hormonal, lipid, and glucose profiles of 72 women with polycystic ovary syndrome (PCOS) and acne using an oral contraceptive (OC) (0.035 mg ethinyl estradiol and 2 mg cyproterone acetate) with those of 39 women who did not have PCOS. They examined their profiles before and after 12 and 36 cycles of treatment. After cycle 12, the OC reduced luteinizing hormone (LH), follicle stimulating hormone (FSH), and all androgen levels (p 0.01), while it increased the levels of sex hormone binding globulin (SHBG) (p 0.01). After 12 cycles, the levels of triglycerides, high density lipoprotein (HDL) cholesterols, apoprotein A1, apoprotein A2, and apoprotein B increased significantly [respectively, 52%, 19% (HDL), 15% (HDL2), and 8% (HDL3), 34%, 35%, and 11%; p 0.05]. The lipid profile after cycle 36 was not much different than it was after cycle 12. At baseline, the PCOS women had lower levels of HDL cholesterol and apoproteins A1 and A2 than did the controls (p 0.05). After 36 cycles of OC treatment, PCOS women had higher levels of triglycerides, total cholesterol, and apoprotein B than controls (p 0.05). Between baseline and cycle 36 of OC treatment, the low density lipoprotein (LDL) cholesterol/HDL cholesterol ratio fell from 1.99 to 1.58. The final ratio equalled that of the controls. The higher estrogenic activity of the OC was probably responsible for the lipid and lipoprotein changes affected by treatment. These findings show that the OC produced an anti-atherogenic lipo-apolipoprotein pattern which corrected the metabolic effects of hyperandrogenism.