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PubMed1997

Inhibition of biliary bicarbonate secretion in ethinyl estradiol-induced cholestasis is not associated with impaired activity of the Cl-/HCO-3 exchanger in the rat.

BACKGROUND/AIMS: Bicarbonate is a major component of bile salt independent bile flow, which is impaired in ethinyl estradiol (EE)-cholestasis. To examine this subject in EE-cholestasis, we studied: 1) basal and glucagon-stimulated biliary bicarbonate secretion both in vivo and in the isolated perfused rat liver (IPRL); 2) H+/HCO-3 transport processes in isolated rat hepatocyte couplets. METHODS: Rats received EE (5 mg.kg b.w.-1) for 5 days. Intracellular pH (pHi) was measured (BCECF-AM) using a single-cell microfluorimetric setup. RESULTS: Bile flow was markedly (p < 0.01) decreased in EE-treated rats. Bicarbonate concentration in bile was decreased (p < 0.01) and bicarbonate secretion was 2.5-fold lower in EE-treated animals than in controls, both in bile-fistula rats [19.5 +/- 5.1 (n = 23) vs 54.2 +/- 5.7 (n = 20) nmol.min-1g liver-1; p < 0.01] and in the IPRL [11 +/- 2 (n = 8) vs 24 +/- 3 (n = 8) nmol.min-1.g liver-1; p < 0.01]. In control IPRL, a bile/perfusate gradient for bicarbonate is maintained, while it is lost in EE-treated IPRL because of the lower bicarbonate concentration in bile. Glucagon stimulated bile flow and bicarbonate secretion to a similar extent in EE-treated and control IPRL (+25% vs +23%). Resting pHi of EE-treated hepatocyte couplets was higher in comparison with controls in KRB [7.25 +/- 0.07 (n = 35) vs 7.20 +/- 0.05 (n = 33); p < 0.02] but similar in Hepes [7.08 +/- 0.07 (n = 24) vs 7.05 +/- 0.06 (n = 26)]. Basal activity of the Cl-/HCO-3 exchanger was similar in EE-treated and control hepatocyte couplets [H+ flux = 2.87 +/- 1.12 (n = 18) vs 3.01 +/- 1.23 mM/min (n = 15)] and was stimulated to a similar extent by glucagon. Na+/HCO3-symport activity was increased in EE-treated hepatocyte couplets (p < 0.05) while the Na+/H+ exchanger was unchanged. CONCLUSIONS: Bicarbonate biliary secretion is markedly impaired during EE-cholestasis in association with a marked decrease of bile salt independent bile flow. However, the Cl-/HCO-3 exchanger and its hormonal regulation are normal, indicating that the lower bicarbonate excretion in EE-cholestasis is not due to a compromised activity of this anion exchanger. Since the bile/perfusate gradient for bicarbonate is dissipated in EE-treated IPRL, the impaired bicarbonate excretion could be caused by a reflux of biliary bicarbonate via leaky tight junctions.

Animals↗

PubMed1985

Biliary permeability during ethinyl estradiol-induced cholestasis studied by segmented retrograde intrabiliary injections in rats.

The influence of ethinyl estradiol (EE) treatment on the permeability of the biliary tree in rats has been assessed by the segmented retrograde intrabiliary injection (SRII) technique. Three pairs of compounds were studied, inert [14C]sucrose and [3H]inulin; [14C]taurocholic acid (TC) and [14C]glycocholic acid (GC) and the non-ionic bile acid derivatives [125I]cholyldiglycylhistamine (CG2H) and [131I]cholyltetraglycylhistamine (CG4H). In control rats recovery in bile after SRII was always greater for the larger of any pair of compounds, confirming that the biliary tree acts as a filter, and that decreased recovery from bile during this technique is an index of greater biliary permeability. After EE treatment recovery of all compounds was significantly reduced, thus confirming that EE increases biliary permeability. Recovery of sucrose and inulin fell from 55-65% of the administered dose in controls to 8-9% in EE rats. Recoveries of TC, GC, CG2H and CG4H was also reduced, but their biliary recovery profiles were consistent with marked re-excretion into bile of that portion which had initially passed out of the biliary system by filtration. During the later phase of the experiment excretion of the negatively charged bile acids TC and GC was greater than that of the non-ionic bile acid derivatives CG2H and CG4H. Although the site at which these permeability changes have occurred is unknown, our results are compatible with previous data implicating increased tight junction permeability as a mechanism of EE-induced cholestasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1981

Steroidal actions and voluntary drinking of ethanol by male and female rats.

The effect of certain steroidal compounds with estrogenic and antiestrogenic properties on voluntary intake of ET by rats with preference to ET of both sexes was studied. The effect of a nonsteroidal antiandrogenic compound and its biologically active metabolite (SCH-16423) on these parameters was also evaluated. The observed behavioral drinking profile of ET was studied in conjunction with determination of L-ADH and L-ALDH as a function of drug treatment in both sexes. Acute administration of estrogenic compounds, estradiol and ethinyl estradiol, decreased voluntary drinking of ET by male and female rats, respectively. Short-term administration of the antiestrogenic compound TMX resulted in aversion to ET consumption in the male but not in the female rat. Acute administration of the SCH-16423 but not its parent nonsteroidal antiandrogen compound FL decreased ET drinking from predrug treatment. The biochemical results show an inhibitory action by the steroidal compound on hepatic L-M-ALDH with a lack of biochemical effect of FL and SCH-16423 on these enzymes. The results are discussed in conjunction with those available in literature to propose a hepatic-gonadal link in the preference to ET drinking and indicate that the underlying mechanism is probably related to the inhibitory action of estrogenic compounds used on L-M-ALDH.

Alcohol Dehydrogenase↗

PubMed1990

Pharmacokinetics and pharmacodynamics of oral contraceptive steroids: factors influencing steroid metabolism.

The time-dependent alterations in the serum concentrations of ethinyl estradiol, gestodene, and 3-keto-desogestrel during treatment with 30 micrograms of ethinyl estradiol + 75 micrograms of gestodene or 30 micrograms of ethinyl estradiol + 150 micrograms of desogestrel were investigated during 12 months. The levels of gestodene and 3-keto-desogestrel increased between days 1 and 21 of each cycle, reaching maximal levels during the third and sixth cycles. The serum concentrations of gestodene were fourfold to fivefold higher than those of 3-keto-desogestrel. The ethinyl estradiol levels increased significantly between days 1 and 10 during each cycle and were significantly higher by 70% during intake of ethinyl estradiol/gestodene compared with ethinyl estradiol/desogestrel, although the dose was identical. Intake of gestodene, in addition to 35 micrograms of ethinyl estradiol + 2 mg of cyproterone acetate, caused a rise in ethinyl estradiol levels. During treatment with ethinyl estradiol/gestodene and an additional 150 micrograms of levonorgestrel, there was a continuous increase in gestodene levels, although sex hormone-binding globulin level did not change. During treatment with 30 or 35 micrograms of ethinyl estradiol and 75 micrograms of gestodene, 150 micrograms of desogestrel, or 2 mg of cyproterone acetate, there were large intraindividual and interindividual variations in the steroid levels and ratios of estrogen: progestogen levels. There was no correlation with the occurrence of intermenstrual bleedings. It is concluded that ethinyl estradiol and nortestosterone derivatives may inhibit steroid-metabolizing enzymes in the liver, which results in a rise in the serum levels of contraceptive steroids. The cause of the large intraindividual variations is as yet unknown, but it is probably from changes in steroid metabolism.

Adolescent↗

PubMed1988

A multicentre comparative study of serum lipids and lipoproteins in four groups of oral combined contraceptive users and a control group of IUD users. World Health Organization. Task Force on Oral Contraceptives.

A prospective clinical trial was conducted in three centres to assess the effects of the type and dose of progestogen, the dose of estrogen and the progestogen-to-estrogen ratio of oral contraceptives on lipid metabolism. The preparations selected contained levonorgestrel 250 micrograms + ethinyl estradiol 50 micrograms (Neogynon), levonorgestrel 250 micrograms + ethinyl estradiol 30 micrograms (Eugynon 30), levonorgestrel 150 micrograms + ethinyl estradiol 30 micrograms (Microgynon) or norethisterone acetate 1 mg + ethinyl estradiol 50 micrograms (Minovlar). Four-hundred-and-seven premenopausal women were randomly assigned to one of the four pill groups and compared to a control group of 119 users of a CuT220c intrauterine device. Total cholesterol, HDL-cholesterol, LDL-cholesterol and total triglycerides were monitored and the analysis includes the data of those who were followed over 48 weeks, 241 OC users and 87 IUD users. 250 micrograms of levonorgestrel were found to induce more unfavourable lipid changes in terms of atherosclerotic risk than 1mg of norethisterone acetate. Levonorgestrel was found to have a dose-effect on HDL-cholesterol and LDL-cholesterol serum levels, while ethinyl estradiol had a dose-effect on serum triglycerides. HDL-cholesterol was related to the progestogen-to-estrogen ratio. Most of these findings were consistent across centres. Finally, some comments are made on the implications of the study results on the design of future lipid studies.

Adolescent↗

PubMed1990

Oral contraceptives, lipoproteins, and atherosclerosis.

A nonhuman primate model was developed to study the effects of oral contraceptives on lipoproteins and atherosclerosis. Cynomolgus macaques were selected because of their susceptibility to diet-induced atherosclerosis and because their reproductive physiology, menstrual cycle, and circulating sex hormone patterns are similar to those of human females. The first study compared a vaginal ring containing levonorgestrel and estradiol with an oral contraceptive containing norgestrel and ethinyl estradiol. A second study compared two oral combinations: norgestrel-ethinyl estradiol and ethynodiol diacetate-ethinyl estradiol. As predicted, use of all the contraceptives led to lowering of high-density lipoprotein cholesterol levels. However, contrary to what might be expected, use of the ethinyl estradiol-containing oral contraceptives did not lead to an increase in the prevalence or extent of atherosclerosis. We concluded that ethinyl estradiol neutralized the atherogenic influence of the progestin component of oral contraceptives.

Animals↗

PubMed1997

Short-term treatment with levonorgestrel does not antagonize the ethinyl estradiol-induced increase of uterine blood flow in postmenopausal women.

The aim of this study was to determine the effect of a short-term ethinyl estradiol/levonorgestrel medication on blood flow in the uterine arteries in postmenopausal women in a prospective placebo-controlled double-blind study. Twenty-one healthy postmenopausal woman at least 2 years after menopause received 60 micrograms ethinyl estradiol (EE) for 14 days followed by 40 micrograms EE plus 125 micrograms levonorgestrel (LNG) for 12 days (total treatment period 26 days). Sonographically, uterine volume, endometrial thickness, and blood flow in the uterine arteries [as reflected by pulsatility (PI) and resistance indices (RI)] were measured. Uterine size increased from 44 to 80 mL (day 14, p < 0.001) and 87 mL (day 26, p = NS). Endometrium grew from 3 to 8 mm (day 14, p < 0.001) and 11 mm (day 26, p = NS). Uterine arterial PI fell from 2.76 to 1.37 (day 14, p < 0.001) and 1.34 (day 26, p = NS), whereas RI fell from 0.9 to 0.68 (day 14 and day 26, p < 0.001). In conclusion, short-term treatment with LNG does not antagonize the vascular effect of EE on the uterine arteries as reflected by PI and RI. This result might have clinical significance in the selection of the progestin used in hormonal replacement therapy.

Aged↗

PubMed2000

Induction of uterine adenocarcinoma in CD-1 mice by catechol estrogens.

Catechol estrogens may mediate estrogen-induced carcinogenesis because 4-hydroxyestradiol induces DNA damage and renal tumors in hamsters, and this metabolite is formed in the kidney and estrogen target tissues by a specific estrogen 4-hydroxylase. We examined the carcinogenic potential of catechol estrogen in an experimental model previously reported to result in a high incidence of uterine adenocarcinoma after neonatal exposure to diethylstilbestrol. Outbred female CD-1 mice were treated with 2- or 4-hydroxyestradiol, 17beta-estradiol, or 17alpha-ethinyl estradiol on days 1-5 of neonatal life (2 microg/pup/day) and sacrificed at 12 or 18 months of age. Mice treated with 17beta-estradiol or 17a-ethinyl estradiol had a total uterine tumor incidence of 7% or 43%, respectively. 2-Hydroxyestradiol induced tumors in 12% of the mice, but 4-hydroxyestradiol was the most carcinogenic estrogen, with a 66% incidence of uterine adenocarcinoma. Both 2- and 4-hydroxylated catechols were estrogenic and increased uterine wet weights in these neonates. These data demonstrate that both 2- and 4-hydroxyestradiol are carcinogenic metabolites. The high tumor incidence induced by 4-hydroxyestradiol supports the postulated role of this metabolite in hormone-associated cancers.

Adenocarcinoma↗

PubMed2003

Metformin versus ethinyl estradiol-cyproterone acetate in the treatment of nonobese women with polycystic ovary syndrome: a randomized study.

Metformin, an insulin-sensitizing drug, has been shown to improve ovarian function and glucose metabolism in obese women with polycystic ovary syndrome (PCOS), but its effects and possible benefits in nonobese PCOS subjects are not well known. Seventeen nonobese (body mass index < 25 kg/m(2)) women with PCOS were randomized to receive either metformin (500 mg twice daily for 3 months, then 1000 mg twice daily for 3 months; n = 8) or ethinyl estradiol (EE, 35 microg)-cyproterone acetate (CA, 2 mg) oral contraceptive pills (EE-CA; n = 9). Waist to hip ratio; serum concentrations of sex steroids, glucose, and insulin during a 75-g oral glucose tolerance test; early phase insulin and C-peptide secretion; and insulin sensitivity using a euglycemic hyperinsulinemic clamp were assessed at baseline and at 3 and 6 months of treatment. Metformin did not have any effect on glucose tolerance or insulin sensitivity, but fasting insulin concentrations decreased from 44.4 +/- 5.1 (SE) to 29.8 +/- 4.3 pmol/liter (P = 0.03), the waist to hip ratio decreased from 0.78 +/- 0.01 to 0.75 +/- 0.01 (P = 0.01), and hepatic insulin clearance increased during the treatment. Furthermore, metformin decreased serum testosterone levels from 2.7 +/- 0.3 to 2.0 +/- 0.2 nmol/liter (P = 0.01) and improved menstrual cyclicity. EE-CA did not have any significant effect on glucose tolerance, serum insulin levels, or insulin sensitivity, but it increased slightly the body mass index (P = 0.09) and significantly serum leptin concentrations (P < 0.001) and decreased serum testosterone levels from 2.1 +/- 0.2 to 1.4 +/- 0.2 nmol/liter (P = 0.03). In conclusion, EE-CA seems to be an efficient mode of therapy for hyperandrogenic symptoms associated with PCOS, but its possible negative effects on insulin and glucose metabolism also have to be taken into consideration in nonobese subjects. Metformin improved hyperandrogenism, hyperinsulinemia, and menstrual cyclicity, most likely through its positive effect on insulin clearance and abdominal adiposity. Thus, similarly to obese PCOS women, nonobese PCOS subjects with anovulation may also benefit from metformin treatment.

Adult↗

PubMed2000

Endocrine and metabolic effects of metformin versus ethinyl estradiol-cyproterone acetate in obese women with polycystic ovary syndrome: a randomized study.

Metformin, a biguanide antihyperglycemic drug, has been shown to improve ovarian function and glucose metabolism in women with polycystic ovary syndrome (PCOS), but results concerning its effects on insulin sensitivity are controversial. Oral contraceptive pills are commonly used in the treatment of PCOS; but, like metformin, their influence on insulin sensitivity is not well known. We randomized 32 obese (body mass index > 27 kg/m2) women with PCOS, either to metformin (500 mg x 2 daily for 3 months, then 1,000 mg x 2 daily for 3 months) or to ethinyl estradiol (35 microg)-cyproterone acetate (2 mg) oral contraceptive pills (Diane Nova) for 6 months. Metformin significantly decreased the waist-to-hip ratio, serum testosterone, fasting free fatty acid, and insulin concentrations and improved oxidative glucose utilization and menstrual cyclicity, with slight (but nonsignificant) improvements in insulin hepatic extraction and insulin sensitivity. Diane Nova significantly decreased serum testosterone and increased serum sex hormone-binding globulin concentrations and glucose area under the curve during oral glucose tolerance test. It is concluded that metformin, probably by way of its effect on adipose tissue, leads to reduction of hyperinsulinemia and concomitant improvement in the menstrual pattern; and therefore, it offers a useful alternative treatment for obese, anovulatory women with PCOS. Despite slight worsening of glucose tolerance, Diane Nova is an efficient treatment for women with hyperandrogenism and hirsutism.

Adult↗

PubMed1978

Pharmacologically induced hypolipidemia. The ethinyl estradiol-treated rat.

The aim of this study was to examine in detail the lipid and apoprotein concentrations in the serum of rats treated with pharmacologic doses (5 mg/kg/d for 5 d) of the synthetic estrogen derivative ethinyl estradiol. The results show that in rats, estrogen-induced hypolipidemia is associated with a nearly complete absence of the lipid and protein moieties normally found in d less than 1.21 fraction of serum. Quantitation of specific apolipoproteins by immunoelectrophoresis show that most apolipoproteins are decreased by more than 90% in the serum of estrogen-treated rats. In contrast to the changes in d less than 1.21 lipoproteins, estrogen treatment only slightly reduced serum phospholipid concentrations (by only 10%) and caused no change in the concentration of serum albumin. The results show that the ethinyl estradiol-treated rat is an excellent model of drug-induced hypolipidemia.

Animals↗

PubMed1996

Hormonal treatment for bleeding irregularities in Norplant implant users.

OBJECTIVE: Our purpose was to evaluate whether prolonged or irregular bleeding during Norplant implant use could be alleviated with the use of oral hormonal medication. STUDY DESIGN: One hundred fifty users of the Norplant levonorgestrel contraceptive implant with prolonged or frequent bleeding were enrolled in this prospective, randomized, comparative study and assigned to one of three treatment groups for 20 days: ethinyl estradiol 50 microg, an oral contraceptive (50 microg ethinyl estradiol and 250 microg levonogestrel), and placebo. Total days of bleeding during treatment and length of the bleeding-free interval were analyzed. RESULTS: Women treated with the levonorgestrel-ethinyl estradiol pill bled an average of 2.6 days during treatment compared with 5.4 and 12.3 days in the ethinyl estradiol and placebo groups, respectively. Differences between both hormonal groups and placebo were significant (p <0.00001); moreover, the combined pill was more effective than ethinyl estradiol along (p <0.0001). CONCLUSION: The combined pill proved to be an excellent palliative treatment and is a more practical approach because of availability at all clinic sites.

Adult↗

PubMed1998

Metabolic and endocrine effects of the desogestrel-containing oral contraceptive Mircette.

OBJECTIVE: The purpose was to evaluate the metabolic effects of Mircette (brand of desogestrel/ethinyl estradiol and ethinyl estradiol), a low-estrogen, desogestrel-containing oral contraceptive. STUDY DESIGN: Women taking Mircette were evaluated to determine its effects on lipid profiles (n = 74), carbohydrate metabolism (n = 25), and endocrine parameters (n = 53). RESULTS: During cycles 3 and 6 of Mircette treatment, changes from baseline included mean increases in serum triglycerides and very low-density lipoprotein cholesterol ranging between 50% and 60%. Smaller mean increases were observed at these time points in high-density lipoprotein cholesterol subfraction 2 (range between 17% and 25%), total cholesterol (<10%), high-density lipoprotein cholesterol (range between 10% and 15%), and high-density lipoprotein cholesterol subfraction 3 (range between 9% and 13%), with only nominal changes (<6%) in low-density lipoprotein cholesterol and lipoprotein. Patients receiving Mircette showed no mean changes in fasting plasma glucose or serum insulin levels but did have modest increases in glucose and insulin levels after a glucose challenge. Mircette treatment suppressed follicle-stimulating hormone, luteinizing hormone, 17beta-estradiol, and progesterone to levels consistent with inhibition of ovulation and increased concentrations of thyroid- and cortisol-binding globulins. CONCLUSIONS: Overall, Mircette treatment was associated with expected effects on the pituitary-ovarian axis, triglycerides, and serum binding proteins; a modest decline in glucose tolerance; and a favorable effect on lipid profiles as a result of increases in total high-density lipoprotein cholesterol and high-density lipoprotein cholesterol subfraction 2 in the absence of changes in total cholesterol or low-density lipoprotein cholesterol.

Adolescent↗

PubMed1992

Impact of short-term estrogen administration on growth hormone secretion and action: distinct route-dependent effects on connective and bone tissue metabolism.

We recently reported that estrogen exerts distinct effects on the GH/IGF-1 axis that are dependent on the route of delivery, probably reflecting a first-pass effect on hepatic IGF-1 production. Oral administration reduces IGF-1 and increases GH levels; transdermal administration elevates IGF-1 without changing GH concentrations. Since mesenchymal tissue is a target for GH and IGF-1 action, we studied changes in the GH/IGF-1 axis following oral (ethinyl estradiol, 20 micrograms/day) versus transdermal (Estraderm 100 TTS, Ciba Geigy, 100 micrograms 17 beta-estradiol per day) estrogen delivery and compared corresponding effects on connective and bone tissue metabolism. Mean 24 h GH levels, IGF-1, markers of fibroblast (procollagen III) and osteoblast (procollagen I, osteocalcin) function, and indices of bone turnover (fasting urinary hydroxyproline and calcium to creatinine ratios, UOHPr/Cr and UCa/Cr) were measured before and after 2 months of either oral or transdermal therapy in two groups of postmenopausal women. Transdermal estrogen administration significantly (p less than 0.05) increased IGF-1, procollagen III, procollagen I, osteocalcin, and UOHPr/Cr. In contrast, oral estrogen administration had a suppressive effect; the levels of IGF-1 (p = 0.001), procollagen III (p = 0.018), procollagen I (p = 0.002), osteocalcin (p = 0.015), and UOHPr/Cr (p = 0.004) were significantly different from those measured during transdermal administration. Both treatments significantly reduced UCa/Cr (p less than 0.015). IGF-1 changes during estrogen therapy were significantly related (p less than 0.05) to changes in procollagen III, procollagen I, osteocalcin, and UOHPr/Cr. Transdermally delivered estrogen stimulates IGF-1 production, increases osteoblastic function, and stimulates bone and nonbone collagen synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗

PubMed1987

Drug-induced intrahepatic cholestasis: characterization of different pathomechanisms.

The pathogenesis of intrahepatic cholestasis in rats was studied using isolated perfused livers as an experimental model. Three basic mechanisms were differentiated: Permeabilization of the bilio-sinusoidal barrier associated with electron microscopic alterations of the tight junctional complexes was found in livers of rats treated with alpha-naphthylisothiocyanate (ANIT, 250 mg/kg body weight). Consequences of these alterations were: reflux of bile constituents such as taurocholate and sulfobromophthalein and increased access to the biliary space of paracellular markers such as inulin and sucrose. The clear-cut mechanism of ANIT cholestasis was used to distinguish other mechanisms of intrahepatic cholestasis. Inhibition of the basic process of fluid secretion was found to be the primary event in the development of cholestasis induced by estrogens. After 5 days of treating rats with ethinyl estradiol (5 mg/kg/day), bile flow was diminished in isolated livers while the permeability of the biliary tract to sucrose and inulin was not affected. Accordingly, the maximal concentration of taurocholate in bile was increased, indicating that its secretion was sustained. The same effect was observed after 1 week of treatment with the depot estrogen estradiol valerate (1 mg/kg/week). After 3 weeks of treatment, however, the taurocholate concentration in bile was lowered and the clearance of sucrose was increased. Bile flow remained at the same cholestatic level for 20 weeks. These results suggest that estrogens have the potency to increase tight junctional permeability only in a second step in the development of cholestasis, following the inhibition of bile flow. An additional mode of secretory inhibition was induced by lowering the concentration of Ca2+ in the perfusate of isolated liver.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Naphthylisothiocyanate↗

PubMed1980

The mechanism of action of a new low-dosed combined oral contraceptive.

The effect of a new low-dosed combined oral contraceptive (OC) containing 37.5 microgram ethinyl estradiol and 0.75 mg lynestrenol (Ovoresta M) upon gonadotropin release and follicular activity was studied in two groups of normally cyclic women. When the administration of the OC was started on day 1 of the cycle, the normal pattern of gonadotropin secretion was disrupted, and the midcycle LH and FSH peak was abolished. The mean level of LH and FSH was somewhat lower than in normal cycles, but the difference was not significant. In one case, serum estradiol rose to the level of the normal cycle indicating follicular activity. Even though there was a rise in serum estradiol to normal values when the OC was started on day 10 of the cycle (in 4/5), both the midcycle LH and FSH surge and ovulation were suppressed (in 3/4). The pituitary response to 100 microgram LH-RH on day 21 was impaired. The LH-response correlated significantly with the serum estradiol concentration. In summary, the low-dosed OC exerts its effect by interfering with follicular ripening and inhibiting the preovulatory LH surge.

Adult↗

PubMed1990

Inhibition of ovulation by low-dose monophasic contraceptive containing gestodene.

Ovulation inhibition by the monophasic oral contraceptive containing 75 ug of gestodene and 30 ug of ethinyl estradiol was evaluated in 25 healthy volunteers for five cycles: a pretreatment cycle, three treatment cycles, and a posttreatment cycle. Serum luteinizing and follicle- stimulating hormones, estradiol, and progesterone levels were measured on days 8 through 17; progesterone was measured once, around day 21. Pelvic ultrasound examinations were performed on cycle days 8 to 17, luteinizing and follicle-stimulating hormone levels reached values on the lower limit of detection. Luteal activity was not detected in treated cycles. Follicular activity, which was reflected by estradiol levels, was mot strongly depressed during the first treated cycle. Pelvic ultrasound examinations confirmed excellent inhibition of follicular maturation. Restoration of ovarian function in the posttreatment cycle was excellent and showed a midcycle hormonal profile identical to the pretrial cycle.

Adult↗

PubMed1985

A randomized cross-over comparison of two low-dose oral contraceptives upon hormonal and metabolic parameters: I. Effects upon sexual hormone levels.

The effect of a low-dose triphasic oral contraceptive (OC) containing ethinyl estradiol and levonorgestrel (EE/NG) upon serum levels of endogenous sexual hormones was compared to that of a preparation containing EE and desogestrel (EE/DG). Blood samples were taken on Day 6, 11, 21, and 28 of a control cycle and of the third cycle of treatment with either the EE/NG or EE/DG preparation (11 volunteers each). After a washout period of 3 months, the contraceptives were changed in a cross-over fashion. Blood samples were again taken on Day 6, 11, 21, and 28 of the third washout cycle and the third treatment cycle. There was no significant suppression of serum LH and FSH during treatment with EE/NG and EE/DG except on Day 21, while estradiol levels were significantly lowered. Similar to the gonadotropin concentrations, the estrogen levels showed great individual variations; although they were depressed in the majority of the women, there was a considerable stimulation of follicular activity in 36% of the women under EE/NG and 18% under EE/DG. Both EE/NG and EE/DG suppressed significantly serum progesterone, testosterone, and DHEA-S, while prolactin was unaffected. In three cases an escape ovulation seemed to have occurred, but no pregnancy was observed. The spottings (8/22 women) and breakthrough bleedings (6/22 women) did not correlate with the serum levels of estradiol. The results indicate that the suppression of gonadotropin secretion during treatment with low-dose OC is a time-dependent process which in some women may be at or below the threshold of safe ovulation inhibition.

Adult↗