As GSD is the most potent
progestogen used in
oral contraceptives, the doses of GSD can be lower than those of other
progestogen components. The monophasic (30 micrograms EE + 75 micrograms GSD) and the triphasic formulation (30 micrograms EE + 50 micrograms GSD/40 micrograms EE + 70 micrograms GSD/30 micrograms EE + 100 micrograms GSD) suppress
gonadotropin release and ovarian function profoundly and inhibit ovulation reliably. The strong anti-estrogenic and progestogenic effectiveness of GSD is based on the high GSD serum concentrations achieved during daily intake. Because of the weak androgenic properties of GSD, both formulations can be characterized as
estrogen-dominant with respect to their hepatic effects. Except for the first cycles, both formulations afford good cycle control, and the rate of side effects is similar to that with comparable
low-dose oral contraceptives. The levels of total and free
androgens and
androgen precursors, as well as of peripheral
androgen activity, are significantly reduced, resulting in a reduced incidence of
acne. The concentrations of SHBG and other serum-binding
globulins are elevated considerably, and thyroid function is almost unaffected. The
estrogen-dominant effect on hepatic metabolism of both formulations also is reflected by a significant increase in the levels of
triglycerides and VLDL, HDL, and some
apolipoproteins, while
LDL-CH and total CH remain unchanged. Similar to other
low-dose oral contraceptives, the GSD-containing preparations cause a slight impairment of
glucose tolerance that does not appear to be of clinical relevance. However, a significant increase exists in pro-coagulatory and fibrinolytic activity that leads to a considerable stimulation of
fibrin turnover. In predisposed women, this may contribute to an elevated risk of venous and arterial thromboembolic diseases.