A comparison of the effects of ethinyl estradiol and estradiol valerate on serum and lipoprotein lipids

Lindberg, Ulla-Beth; Enk, L.; Crona, N.; Silfverstolpe, G.

doi:10.1016/0378-5122(88)90069-2

Cited by 15 publications

(7 citation statements)

References 13 publications

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“…15 In addition, the binding affinity of EE to the estrogen receptors is about 2-fold higher than that of E2, which induces stronger intercellular signals. 21,26,27 Furthermore, sulfated ethinyl estrogens are highly soluble in the water, which is essential for effective drug distribution in tissues. 17,27,31 The rationale of DAI recovery by EE-3-SO 4 , however, is still not clear.…”

Section: Discussionmentioning

confidence: 99%

“…21,26,27 Furthermore, sulfated ethinyl estrogens are highly soluble in the water, which is essential for effective drug distribution in tissues. 17,27,31 The rationale of DAI recovery by EE-3-SO 4 , however, is still not clear. We presume that EE-3-SO 4 alleviates traumatic axonal injury via increasing glucose uptake to stabilize ion channels.…”

Section: Discussionmentioning

confidence: 99%

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Treatment of traumatic brain injury with 17α-ethinylestradiol-3-sulfate in a rat model

Kim¹,

Yu²,

Cam-Etoz

et al. 2017

Journal of Neurosurgery

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OBJECTIVE17α-ethynylestradiol-3-sulfate (EE-3-SO4) is a highly water-soluble synthetic estrogen that has an extended half-life (∼ 10 hours) over that of naturally occurring estrogen (∼ 10 minutes). In this study, EE-3-SO4 was evaluated in a lateral fluid percussion–induced traumatic brain injury (TBI) model in rats.METHODSA total of 9 groups of Sprague-Dawley rats underwent craniectomy. Twenty-four hours later, lateral fluid percussion was applied to 6 groups of animals to induce TBI; the remaining 3 groups served as sham control groups. EE-3-SO4 (1 mg/kg body weight in 0.4 ml/kg body weight) or saline (vehicle control) was injected intravenously 1 hour after TBI; saline was injected in all sham animals. One day after EE-3-SO4/saline injection, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and partial brain oxygen pressure (PbtO2) were measured in Groups 1–3 (2 TBI groups and 1 sham group), and brain edema, diffusion axonal injury, and cerebral glycolysis were assessed in Groups 4–6 using MRI T2 mapping, diffusion tensor imaging (DTI), and FDG-PET imaging, respectively. Four days after dosing, the open-field anxiety of animals was assessed in Groups 7–9 by measuring the duration that each animal spent in the center area of an open chamber during 4 minutes of monitoring.RESULTSEE-3-SO4 significantly lowered ICP while raising CPP and PbtO2, compared with vehicle treatment in TBI-induced animals (p < 0.05). The mean size of cerebral edema of TBI animals treated with EE-3-SO4 was 25 ± 3 mm3 (mean ± SE), which was significantly smaller than that of vehicle-treated animals (67 ± 6 mm3, p < 0.001). Also, EE-3-SO4 treatment significantly increased the fractional anisotropy of the white matter in the ipsilateral side (p = 0.003) and cerebral glycolysis (p = 0.014). The mean duration that EE-3-SO4-treated animals spent in the center area was 12 ± 2 seconds, which was significantly longer than that of vehicle-treated animals (4 ± 1 seconds; p = 0.008) but not different from that of sham animals (11 ± 3 seconds; p > 0.05).CONCLUSIONSThese data support the clinical use of EE-3-SO4 for early TBI treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Treatment of traumatic brain injury with 17α-ethinylestradiol-3-sulfate in a rat model

Kim¹,

Yu²,

Cam-Etoz

et al. 2017

Journal of Neurosurgery

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“…92 In general, an E 2 dose of 1-2 mg provides similar systemic exposure to estrogen as does an EE dose of 5-10 lg, based on a number of estrogenic parameters, including binding affinity. [92][93][94] ER a and ER b are distributed throughout the body. In humans, both ER subtypes are found in uterine tissues; however, ER a is expressed primarily in the uterus, liver, kidney, and heart, whereas ER b is expressed principally in the bladder and the central nervous system.…”

mentioning

confidence: 99%

Tailoring Combination Oral Contraceptives to the Individual Woman

Archer

Lasa

2011

Journal of Women's Health

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“…Aux posologies é valué es, la synthè se de ces proté ines, é tait selon leur type augmenté d'un facteur 100 à 1000 avec l'EE en comparaison au 17b-estradiol. Même à la posologie de 10 mg/j, l'EE augmente d'un facteur 1,5 à 2,5 fois, les sous-fractions du HDL-cholesté rol [18], ainsi que celle des triglycé rides [19] par rapport à la prise de 2 mg/j de valé rate d'estradiol chez la femme mé nopausé e. Cet effet sur le mé tabolisme des lipoproté ines est retrouvé avec l'EE même avec des doses aussi faibles que 1 mg/j pour l'augmentation des triglycé rides et de 2,5 mg/j pour la baisse du LDL-cholesté rol ou l'augmentation du HDL-cholesté rol [20]. L'EE à la posologie de 50 mg/j ou de 20 mg/j entraîne é galement une augmentation nettement plus marqué e que le valé rate d'estradiol (2 mg/j) de certains facteurs impliqué s dans l'hé mostase, comme le fragment 1 + 2 de la prothrombine [21].…”

Section: Activite´biologique In Vivo Chez L'humainunclassified

Contraception orale estro-progestative : quelle différence entre éthinylestradiol et estradiol ?

Trémollières

2012

Gynécologie Obstétrique & Fertilité

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A comparison of the effects of ethinyl estradiol and estradiol valerate on serum and lipoprotein lipids

Cited by 15 publications

References 13 publications

Treatment of traumatic brain injury with 17α-ethinylestradiol-3-sulfate in a rat model

Treatment of traumatic brain injury with 17α-ethinylestradiol-3-sulfate in a rat model

Tailoring Combination Oral Contraceptives to the Individual Woman

Contraception orale estro-progestative : quelle différence entre éthinylestradiol et estradiol ?

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