Short- and Long-Term Effects on Lipid Metabolism of Oral Contraceptives Containing 30 μg Ethinylestradiol and 150 μg Desogestrel or 3-Keto-Desogestrel

Abstract

During a cross-over study with young female volunteers, the effects of a combination of 30 µg ethinylestradiol (EE) and 150 µg desogestrel (DG) or 3-keto-desogestrel (KDG) upon lipid metabolism were investigated on day 3 of the first cycle (day 3/1) and on day 21 of the third cycle of treatment (day 21/III). As compared to the control cycle, total cholesterol (CH), low-density lipoprotein CH (LDL-CH), and the apolipoproteins A-II and B were reduced already on day 3/1, the effects being more pronounced with the DG-containing formulation. On day 21/III of treatment with EE/DG, the levels of total CH, LDL-CH and apolipoprotein B did not differ from controls, while apolipoprotein A-II was significantly increased. The effects of EE/KDG were similar, except that on LDL-CH which was still reduced on day 21/III. The serum concentrations of total triglycerides (TG), very low-density lipoprotein CH (VLDL-CH), VLDL-TG, LD-TG, high-density lipoprotein CH (HDL-CH), HDL-TG, and apolipoprotein A-I were not significantly affected on day 3/1, but elevated on day 21/III. As during treatment with EE/KDG the peak level of KDG was higher than with EE/DG, the results indicate a more pronounced antagonistic effect of EE/KDG on some EE-induced changes on lipoproteins during the first days of intake. These short-term changes possibly reflect a rapid enhancement of hepatic uptake of remnants and LDL by EE. During long-term treatment, the other effects of EE, e.g. the stimulation of hepatic synthesis of TG, VLDL, and HDL and the inhibition of hepatic lipoprotein lipase, become apparent.

Oral Progestogen Combined with Testosterone as a Potential Male Contraceptive: Additive Effects between Desogestrel and Testosterone Enanthate in Suppression of Spermatogenesis, Pituitary-Testicular Axis, and Lipid Metabolism1

“…As 100 mg T enanthate (and, by inference, 50 mg also) weekly did not alter lipids when administered in men rendered hypogonadal experimentally (37), but 200 mg T enanthate weekly decreased HDL-C only with no change in total cholesterol or LDL-C (16,41,42), the observed overall changes in lipid metabolism during weeks 4 -24 (DSG plus T) were probably predominantly due to the effects of DSG rather than T. The magnitude of the fall of 22.6% in HDL-C during combined DSG and T enanthate treatment was greater than that observed with 200 mg T enanthate weekly alone (16,41,42) [it was typically 13-18%], similar to the 23% fall observed in men treated with 500 g levonorgestrel daily plus 100 mg T enanthate weekly (19) and was much greater than that when DSG was coadministered with estrogen in the female pill (43). As 100 mg T enanthate (and, by inference, 50 mg also) weekly did not alter lipids when administered in men rendered hypogonadal experimentally (37), but 200 mg T enanthate weekly decreased HDL-C only with no change in total cholesterol or LDL-C (16,41,42), the observed overall changes in lipid metabolism during weeks 4 -24 (DSG plus T) were probably predominantly due to the effects of DSG rather than T. The magnitude of the fall of 22.6% in HDL-C during combined DSG and T enanthate treatment was greater than that observed with 200 mg T enanthate weekly alone (16,41,42) [it was typically 13-18%], similar to the 23% fall observed in men treated with 500 g levonorgestrel daily plus 100 mg T enanthate weekly (19) and was much greater than that when DSG was coadministered with estrogen in the female pill (43).…”