BACKGROUND: Ethinyl estradiol (EE) and progestins have the ability to alter endothelial function. The type of progestin and the ratio of EE to progestin used in oral contraceptive pills (OCPs) may determine how they affect the arterial vasculature. STUDY DESIGN: In this study, we investigated endothelial function across a cycle in very low dose (VLD) and low dose (LD) combination EE and desogestrel (DSG) OCP users during two phases: active (VLD=20 mcg EE/150 mcg DSG; LD=30 mcg EE/150 mcg DSG) and pill-free. Endothelial function was also measured during an EE-only hormone phase (10 mcg EE) in group VLD. RESULTS: Endothelium-dependent vasodilation was greater during the active phase compared to the pill-free phase in group LD (9.02+/-0.72% vs. 7.33+/-0.84%; p=.029). This phase difference was not observed in group VLD (5.86+/-0.63% vs. 6.56+/-0.70%; p=.108). However, endothelium-dependent vasodilation was higher during the EE-only phase, compared to the active and pill-free phases (8.92+/-0.47% vs. 5.86+/-0.63%, and 6.56+/-0.70%; p<.001) in group VLD. CONCLUSIONS: These data suggest DSG may antagonize the vasodilatory activity of EE and that this effect is further modulated by the EE-to-DSG ratio.
BACKGROUND:Ethinyl estradiol (EE) and progestins have the ability to alter endothelial function. The type of progestin and the ratio of EE to progestin used in oral contraceptive pills (OCPs) may determine how they affect the arterial vasculature. STUDY DESIGN: In this study, we investigated endothelial function across a cycle in very low dose (VLD) and low dose (LD) combination EE and desogestrel (DSG) OCP users during two phases: active (VLD=20 mcg EE/150 mcg DSG; LD=30 mcg EE/150 mcg DSG) and pill-free. Endothelial function was also measured during an EE-only hormone phase (10 mcg EE) in group VLD. RESULTS: Endothelium-dependent vasodilation was greater during the active phase compared to the pill-free phase in group LD (9.02+/-0.72% vs. 7.33+/-0.84%; p=.029). This phase difference was not observed in group VLD (5.86+/-0.63% vs. 6.56+/-0.70%; p=.108). However, endothelium-dependent vasodilation was higher during the EE-only phase, compared to the active and pill-free phases (8.92+/-0.47% vs. 5.86+/-0.63%, and 6.56+/-0.70%; p<.001) in group VLD. CONCLUSIONS: These data suggest DSG may antagonize the vasodilatory activity of EE and that this effect is further modulated by the EE-to-DSG ratio.
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