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Combined Oral Contraceptive Treatment of Adolescent Girls with Polycystic Ovary Syndrome: Lipid Profile

Abstract: The clinical signs and neuroendocrine features of adolescents with polycystic ovary syndrome (PCOS) resemble those found in adult women with PCOS. These adolescent patients are candidates for long‐term treatment by one of the different therapeutic approaches that have been proposed. It is therefore essential that the treatment does not induce unfavorable metabolic effects. We investigated and compared the effects of cyproterone acetate (CA) and desogestrel (D), as part of combined oral contraceptives (COC), on lipid metabolism and hirsutism in adolescents with PCOS. Twenty‐four girls with clinical signs of PCOS were recruited. They were all hyperandrogenemic and euthyroid and had normal prolactin plasma levels. Nonclassic congenital adrenal hyperplasia was ruled out by the ACTH stimulation test. Blood samples were obtained for sex hormone binding globulin (SHBG), total cholesterol (TC), LDL cholesterol, HDL cholesterol, triglycerides (TGs), apolipoproteins A‐I, A‐II, B, and lipoprotein (a) (Lp(a)) measurements. After the initial exam‐ination, therapy was initiated in a randomly selected order (12 and 12 patients were treated daily by 2 mg CA and 0.150 mg D, respectively, plus 0.035 and 0.030 mg ethinylestradiol, respectively). The degree of hirsutism and the lipid profile were reevaluated every 3 months after initiation of therapy for 1 year. Our data show that after 12 months of treatment with the D or CA COC, the Ferriman‐Gallway hirsutism score decreased and TC and LDL‐C increased. TGs and HDL‐C were raised significantly in the CA COC group, whereas apolipoprotein A1 increased during D COC treatment. The atheromatic indices did not change. These data suggest that treatment of adolescent girls with PCOS is comparably effective with the two contraceptive formulations and that the desogestrel COC could be considered in the treatment of adolescent PCOS patients because it does not have side effects on lipid metabolism.