SEARCH · PubMed Health

Results for “ETHINYL ESTRADIOL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources

PubMed2003

Urinary 6-sulfatoxymelatonin excretion in hyperandrogenic women with polycystic ovary syndrome: the effect of ethinyl estradiol-cyproterone acetate treatment.

The role of melatonin in human reproduction is still unknown. Data obtained in patients with hypogonadism and precocious puberty suggest that melatonin and the reproductive hormones are interrelated. The aim of this study was to determine melatonin production in hyperandrogenic women. We studied 12 women with polycystic ovary syndrome (PCOS) and 10 women with idiopathic hirsutism (IH). Patients were treated with cyproterone acetate-ethinyl estradiol (Diane 35) for 4 months. Fasting blood samples for the determination of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone and dehydroepiandrosterone sulfate (DHEAS) and 24-h urine collections for the determination of 6-sulfatoxymelatonin (alpha MT6s) excretion were obtained from all patients at baseline and after 4 months of treatment. The results were compared with those obtained in 15 control women. At baseline, women with PCOS had significantly higher LH and testosterone levels than those with IH and controls. Their alpha MT6s values (52.6 +/- 20.3 micrograms/24 h) were significantly higher than the values in women with IH (34.3 +/- 7.1) and controls (30.5 +/- 6.5) (p < 0.001). Diane 35 treatment significantly decreased LH, FSH, testosterone and alpha MT6a values in PCOS (28.0 +/- 13.9 micrograms/24 h) (p < 0.0001). These results indicate that women with PCOS have increased melatonin production. The normalization of alpha MT6s and testosterone values during Diane 35 treatment suggests that sex steroids modulate melatonin secretion in these patients either directly or through the suppression of gonadotropin.

Adolescent↗

PubMed1990

Synthetic estrogens suppress granulosa cell progesterone production in vitro.

We evaluated the effect of commonly used pharmaceutical estrogens and zeranol, an estrogenic growth-promoting agent used in livestock, on progesterone (P) production by cultures of highly differentiated porcine granulosa cells (GC). The compounds were added to GC cultures over a dose range of 10(-8) to 10(-5) M with P and cell protein measured after 24 h. P production was suppressed by estradiol (minimal suppressive dose: 10(-7) M; maximal suppression to 11% of control), ethinyl estradiol (10(-7) M, 15%), diethylstilbestrol (10(-5) M, 72%), clomiphene citrate (10(-6) M, 30%), nafoxidine (10(-7) M, 33%), tamoxifen (10(-6) M, 37%), and zeranol (10(-5) M, 83%). P production was not suppressed by mestranol. GC protein was suppressed by estradiol, ethinyl estradiol, nafoxidine, and zeranol. These data suggest that synthetic estrogens have the potential to suppress luteal P production by a mechanism unrelated to the usual measures of estrogenicity.

Animals↗

PubMed2005

Myelotoxicity in genistein-, nonylphenol-, methoxychlor-, vinclozolin- or ethinyl estradiol-exposed F1 generations of Sprague-Dawley rats following developmental and adult exposures.

The myelotoxicity of five endocrine active chemicals was evaluated in F1 generation of Sprague-Dawley rats following developmental and adult exposures at three concentration levels. Rats were exposed to genistein (GEN: 25, 250 and 1250 ppm), nonylphenol (NPH: 25, 500 and 2000 ppm), methoxychlor (MXC: 10, 100 and 1000 ppm), vinclozolin (VCZ: 10, 150 and 750 ppm) and ethinyl estradiol (EE2: 5, 25 and 200 ppb) gestationally and lactationally through dams from day 7 of gestation and through feed after weaning on postnatal day (PND) 22 to PND 64. The parameters examined included the number of recovered bone marrow cells, DNA synthesis, and colony forming units (CFU) in the presence of granulocyte macrophage-colony stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF) and erythropoietin. Except for the EE2, the concentrations of other individual chemicals in the diet were in an approximate range that allowed for a comparison to be made in terms of myelotoxic potency. Decreases in the DNA synthesis, CFU-GM and CFU-M seemed to be the common findings among the alterations induced by these compounds. Using the numbers of alterations induced by each chemical in the parameters examined as criteria for comparison, the order of myelotoxic potency in F(1) males was: GEN>MXC>NPH>VCZ; the order in females: GEN>NPH>VCZ. Additionally, some of the functional changes induced by these compounds were gender-specific or dimorphic. Overall, the results demonstrated that developmental and adult exposures of F1 rats to these endocrine active chemicals at the concentrations tested had varied degrees of myelotoxicity with GEN being the most potent. Furthermore, the sex-specific effects of these chemicals in F1 male and female rats suggest that there may be interactions between these compounds and sex hormone in modulating these responses.

Animals↗

PubMed2003

Cyproterone acetate for hirsutism.

BACKGROUND: Hirsutism is a distressing and relatively common endocrine problem in women which may prove difficult to manage. Cyproterone acetate, an anti-androgen, is frequently used to treat hirsutism, usually in combination with ethinyl estradiol. OBJECTIVES: The objective of this review was to investigate the effectiveness of cyproterone acetate alone, or in combination with ethinyl estradiol, in reducing hair growth in women with hirsutism secondary to ovarian hyperandrogenism. SEARCH STRATEGY: The Cochrane Menstrual Disorders and Subfertility Group trials register was searched (last search - 4 June 2002). The Cochrane Menstrual Disorders and Subfertility Group register is based on regular searches of MEDLINE (1966 to 2002), EMBASE (1980 to 2002), CINAHL (1982 to 2002), PsycINFO (1987 to 2002) and CENTRAL (Issue 2, 2002 of the Cochrane Library) the handsearching of several journals and conference proceedings, and searches of several key grey literature sources. All publications of randomised controlled trials of cyproterone acetate with or without estrogen versus placebo or other drug therapies for hirsutism were identified. SELECTION CRITERIA: All randomised controlled studies comparing:- cyproterone acetate to placebo- cyproterone acetate with ethinyl estradiol to placebo- cyproterone acetate with ethinyl estradiol to cyproterone acetate alone- cyproterone acetate (with or without estradiol) to other medical therapies for treatment of hirsutism. DATA COLLECTION AND ANALYSIS: Eleven studies were identified which fulfilled the inclusion criteria. Nine randomised studies were included in the review, and two were excluded because of insufficient information. Only one study had more than 100 women included in the analysis. The major outcomes included: subjective improvement in hirsutism, changes in Ferriman Gallwey scores, changes in linear hair growth and hair shaft diameter, alterations in endocrine parameters, side effects to treatment, withdrawals during therapy MAIN RESULTS: There were no clinical trials comparing cyproterone acetate alone with placebo. There was one small study comparing cyproterone acetate in combination with ethinyl estradiol to placebo. In this study there was a significant subjective reduction in hair growth with cyproterone acetate therapy, although the confidence limits were large. There were no studies comparing cyproterone acetate alone with cyproterone acetate in combination with ethinyl estradiol to treat hirsutism. In studies where cyproterone acetate was compared to other drug modalities (ketoconazole, spironolactone, flutamide, finasteride, GnRH analogues) no difference in clinical outcome was noted. There were, however, endocrinological differences in androgen and estrogen levels between different drug therapies. There were insufficient data to assess differences in side effects between women treated with cyproterone acetate and other medical therapy. REVIEWER'S CONCLUSIONS: Cyproterone acetate combined with estradiol results in a subjective improvement in hirsutism compared to placebo. Clinical differences in outcome between cyproterone acetate and other medical therapies were not demonstrated in the studies included in this review. This may be because of the small size of the studies, lack of standardized assessment and lack of objective determinants of improvement in hirsutism. The endocrinological effects of the different drug therapies reflect the mode of action. Larger carefully designed studies are needed to compare efficacy and safety profiles between drug therapies for hirsutism.

Androgen Antagonists↗

PubMed1981

Further studies on pituitary and ovarian function in women receiving hormonal contraception.

Pituitary and ovarian function was evaluated in women receiving 3 combined oral contraceptive preparations. Basal levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) and gonadotropic responses to gonadotropic releasing hormone (GnRH) were studied in 36 healthy, regularly ovulating women in the early follicular and mid-luteal phases of their menstrual cycle (non-treatment, control). These same women were then divided into 3 groups with 12 volunteers in each. Each group received an oral contraceptive preparation cyclically for 3 months. The preparations were: Nordette (30 microgram ethinyl estradiol and 150 microgram d-norgestrel), Nordiol (50 microgram ethinyl estradiol and 250 microgram d-norgestrel) and Biphasil (50 microgram ethinyl estradiol and 50 microgram d-norgestrel X 11 days and 125 microgram d-norgestrel X 10 days). In the third month of treatment, the tests were repeated on day 21, i.e. after 21 active pills, and on day 28, i.e. after 21 active and 7 inactive tablets. On active therapy, basal FSH and LH were similarly suppressed in the 3 groups. LH had varied responses to a bolus of GnRH, whilst the FSH responses were similar in the 3 groups. After 7 days of inactive tablets, basal FSH and LH had returned to pre-treatment, early follicular phase levels. However, the LH responses to a bolus of GnRH varied in the 3 groups, but again, no differences were noted in the FSH responses. Basal FSH, LH and E2 recovered earlier in the Nordette group during the 7 days of inactive tablets.

Contraceptives, Oral↗

PubMed1994

Comitogenic effects of estrogens on DNA synthesis induced by various growth factors in cultured female rat hepatocytes.

Ethinyl estradiol is a weak complete carcinogen and potent tumor promoter. In vivo, ethinyl estradiol causes a rapid but transient increase in liver growth, whereas in cultured female hepatocytes it enhances DNA synthesis induced by epidermal growth factor and is thus classified as a comitogen. The objectives of this study were to determine: (a) whether estradiol also has comitogenic activity; (b) whether the comitogenic effects of estrogen extend to complete hepatic mitogens other than epidermal growth factor and (c) whether inhibition of hepatocyte DNA synthesis by transforming growth factor-beta can be blocked by estradiol. Female rat hepatocytes in primary culture were exposed to estradiol with and without various growth factors, and we determined DNA synthesis by measuring [3H]thymidine incorporation into extracted DNA or by determining the nuclear labeling index by means of autoradiography. The results show that estradiol, like ethinyl estradiol, has comitogenic activity for epidermal growth factor, although it is somewhat less potent. Four complete hepatic mitogens showed different abilities to stimulate DNA synthesis, with hepatocyte growth factor > transforming growth factor-alpha > epidermal growth factor > acidic fibroblast growth factor. Estradiol enhanced DNA synthesis occurring in response to all four of these complete hepatic mitogens. This finding suggests that the mechanism of estrogen comitogenesis may involve effects at a point where the different signal-transduction pathways leading from the growth factors converge. The level of estrogen-mediated enhancement of DNA synthesis was similar for all four mitogens, ranging from 1.5 to 2.2-fold, depending on the experiment. Furthermore, determination of the nuclear labeling index showed that estrogen enhancement of DNA synthesis was associated with an increase in the percentage of hepatocytes that responded to the growth factors. Finally, estradiol did not specifically block the growth-inhibitory effects of transforming growth factor-beta.

Animals↗

PubMed1984

Influence of administration route and treatment duration on the glucoregulatory effects of sex steroids in female mice.

Glucose tolerance and plasma insulin concentrations were determined in intact female mice treated orally, subcutaneously and intramuscularly for 4 and 24 days with estradiol-17 beta (5 micrograms/kg/day), ethinyl estradiol (5 micrograms/kg/day) and progesterone (1 mg/kg/day). Estradiol-17 beta improved glucose tolerance and raised plasma insulin concentrations. These effects were generally greater after the longer treatment period and the s.c. administration route produced the greatest improvement in glucose tolerance with the smallest increase in plasma insulin. Ethinyl estradiol produced qualitatively similar effects to estradiol-17 beta, but quantitatively smaller. Progesterone raised plasma insulin concentrations after the longer treatment period, notably with oral and intramuscular administration, although glucose tolerance was not significantly altered. The results demonstrate the important influence of administration route and treatment duration on the changes in glucose homeostasis induced by sex steroids.

Administration, Oral↗

PubMed1985

Selectively reduced biliary excretion of cholyldiglycylhistamine but not of cholyltetraglycylhistamine in ethinyl estradiol-treated rats. A possible indicator of increased bile canalicular permeability.

A series of bile acid derivatives were synthesized, purified and radiolabelled. These were [125I]cholylglycylhistamine [( 125I]CGH), [125I] cholyldiglycylhistamine [( 125I]CG2H), [125I]cholyltriglycylhistamine [( 125I]CG3H), and [125I]cholyltetraglycylhistamine [( 125I]CG4H). These derivatives were rapidly excreted unchanged into the bile of bile-fistula rats. In normal rats the 30-min cumulative excretion following intravenous administration was only 39.0 +/- 0.7% for [125I]CGH but greater than 80% for the three larger compounds. This marked difference in biliary recovery between CGH and the other larger compounds could be due to a threshold biliary permeability, and we postulated that the critical molecular weight threshold for effective biliary retention of such compounds falls between [125I]CGH (MW 683) and [125I]CG2H (MW 740). Increased permeability, involving a shift to a higher molecular weight threshold would then be anticipated to diminish biliary excretion of [125I]CG2H (MW 740) before exerting a major influence on the biliary excretion of [125I]CG4H (MW 854). We previously reported functional and morphological studies which suggest that ethinyl estradiol (EE) may alter the permeability of bile canalicular tight junctions. In this study we have looked for further evidence of a progressive permeability change in EE-induced cholestasis by observing the biliary excretion of CG2H and CG4H in rats. Treatment with EE (5 mg/kg/day) for 3 days (EE3) or with the injection vehicle propylene glycol for 7 days (C7) reduced biliary excretion to a significant extent when compared to 3-day controls (C3) but had no differential effect on the 30-min recoveries from bile of CG2H and CG4H, respectively: C3 (81.2 +/- 1.8% and 81.7 +/- 2.1%, P = CN): C7 (72.3 +/- 3.0% and 73.5 +/- 3.6%, P = NS): EE3 61.8 +/- 2.5% and 61.9 +/- 2.7%, P = NS). However, treatment with EE for 7 days significantly reduced the biliary recovery of CG2H (46.8 +/- 9%) compared to EE3 rats (P less than 0.0025) but there was no significant change of biliary CG4H recovery (61.0 +/- 2.5%, P = NS) compared with EE3 rats. These results are compatible with our hypothesis that EE-induced cholestasis is associated with a change of biliary permeability which, as it progresses, affects successively larger molecules.

Animals↗

PubMed1984

In vivo characteristics of a specific recognition site for LDL on non-parenchymal rat liver cells which differs from the 17 alpha-ethinyl estradiol-induced LDL receptor on parenchymal liver cells.

Chemical modification of lysine or arginine residues of apolipoprotein B-100 in human low-density lipoprotein (LDL) with respectively reductive methylation (Me-LDL) or cyclohexanedione treatment (CHD-LDL) was applied to determine the role of these amino acids in LDL recognition by the various liver cell types. The cell association of native human LDL, Me-LDL and CHD-LDL to parenchymal and non-parenchymal cells was determined in vivo by isolating the various cell types 30 min after intravenous injection of the lipoproteins. In order to prevent degradation or release of cell-bound apolipoproteins during cell dissociation and purification, a low-temperature (8 degrees C) liver perfusion and cell isolation procedure was performed. It was found that reductive methylation of LDL inhibits the association of LDL to both parenchymal and non-parenchymal cells, indicating that lysine residues are important for recognition of LDL by both these cell types. In contrast, cyclohexanedione treatment of LDL did not influence the cell association of LDL to non-parenchymal cells. 17 alpha-Ethinyl estradiol treatment selectively increases the cell association of LDL by parenchymal cells (16-fold), leaving the non-parenchymal cell association uninfluenced. The increased cell-association of LDL to parenchymal cells is almost completely blocked by cyclohexanedione treatment of LDL (by 81%) or by methylation of LDL (by 97%). These data indicate that the arginine residues in LDL are not important for the recognition of LDL by non-parenchymal cells, whereas for the cell association of LDL to the estrogen-stimulated binding site on parenchymal cells both arginine and lysine residues are essential. The in vivo cell association of CHD-LDL or native LDL to non-parenchymal cells was lowered to the level of Me-LDL by ethyl oleate treatment of the rats, while no effect of ethyl oleate on parenchymal cells was noticed. These data suggest that the specific site for LDL on non-parenchymal cells, which need lysine residues on LDL for recognition, can be down-regulated by ethyl oleate treatment. The LDL, internalized by non-parenchymal cells, is effectively degraded. This degradation occurs at least partly in the lysosomes. It is suggested that the unique recognition site for LDL on non-parenchymal cells may be quantitatively important for serum LDL catabolism.

Animals↗

PubMed1996

Risk for ovulation in women taking a low-dose oral contraceptive (Microgynon) when receiving antibacterial treatment with a fluoroquinolone (ofloxacin).

The possibility of escape ovulation in women using a fluoroquinolone ofloxacin for antibacterial treatment at a dose of 200 mg twice daily for 7 days when taking a combined oral contraceptive (Microgynon, 150 micrograms levonorgestrel and 30 micrograms ethinyl estradiol) was studied in 20 women. By using a placebo-controlled, randomized, cross-over design 6 contraceptive pill cycles were followed. Follicle-stimulating hormone and estradiol concentrations were measured on tablet days 5-8, 19-21; progesterone was assayed on days 19-21 during treatment with ofloxacin or placebo. Ultrasonographical investigations for measurements of the number and diameter of ovarian follicles were performed on one of days 5-10, 11-17, 18-24, 25-28. No indications of ovulation during ofloxacin medication were detected. It is concluded that alternative contraceptive precautions should not be needed when ofloxacin is prescribed for patients taking oral contraceptives.

Adult↗

PubMed1999

Hemostatic effects of smoking and oral contraceptive use.

This review addresses current knowledge of the effects of lower dose oral contraceptives (containing 35, 30, or 20 micrograms of ethinyl estradiol) on hemostasis in smoking and nonsmoking women. Evidence suggests that formulations containing 30 and 35 micrograms ethinyl estradiol induce a significant activation of coagulation, whereas oral contraceptive preparations with 20 micrograms ethinyl estradiol appear to have a negligible effect or no effect. In nonsmokers who take oral contraceptives any procoagulatory effects that may occur are counterbalanced by fibrinolytic effects. In smokers, however, compensatory fibrinolytic effects to offset the procoagulatory effects seen with 30-micrograms ethinyl estradiol oral contraceptive formulations are absent, shifting the hemostatic profile toward a hypercoagulable state. This suggests that a formulation with the lowest dose of ethinyl estradiol may be most suitable for smokers who wish to use this form of contraception.

Blood Coagulation↗

PubMed1986

Administration of low-dose estrogen rapidly and directly stimulates growth hormone production.

We tested the concept that estrogen directly stimulates growth hormone (GH) production by determining whether low-dose treatment with ethinyl estradiol increases the GH reserve, as assessed by levodopa administration, without inhibiting somatomedin-C (Sm-C) levels. Twenty-three prepubertal short normal children underwent levodopa tests before and after being treated with ethinyl estradiol. One bedtime dose of ethinyl estradiol (20 to 40 micrograms/sq m, n = 8) resulted in a significant increase in GH levels during levodopa testing, with no significant change in Sm-C levels (0.27 +/- 0.03 vs 0.36 +/- 0.1 units/mL). Two days of a comparable ethinyl estradiol dose (n = 12) raised the mean basal GH level (2.4 +/- 0.4 vs 9 +/- 3 ng/mL) and had a similar effect on peak GH response, without affecting the mean Sm-C level. Eighteen of the 23 patients responded (maximum GH level, greater than or equal to 7 ng/mL) to levodopa before estrogen; all 20 children who received ethinyl estradiol priming in a dose of 20 micrograms/sq m or more also responded. We conclude that low-dose estrogen therapy rapidly stimulates GH production without decreasing Sm-C plasma levels. These results support the concept that the estrogen effect is direct. This action may be important for the stimulation of growth by estrogen. This effect can be conveniently employed to enhance the specificity of the levodopa test for profound GH deficiency.

Adolescent↗

PubMed2006

Ontogeny of androgen receptor and disruption of its mRNA expression by exogenous estrogens during morphogenesis of the genital tubercle.

PURPOSE: The ontogeny of androgen receptor expression in male and female mouse genital tubercles, and the effects of in utero ethinyl estradiol exposure on androgen receptor mRNA expression in the hypospadias model were studied. MATERIALS AND METHODS: Androgen receptor mRNA expression was measured in mouse genital tubercles from fetuses and pups collected on gestational days 12, 14, 16 and 18, and from newborns using immunohistochemistry and real-time quantitative polymerase chain reaction. Pregnant dams were exposed to ethinyl estradiol or corn oil as controls from gestational days 12 to 17. Genital tubercles of gestational day 19 fetuses were then examined by further quantitative polymerase chain reaction analysis after identification of the seam area using a dissecting microscope to diagnose hypospadias in males. RESULTS: Androgen receptor protein was detected in genital tubercles by gestational day 14. Androgen receptor mRNA expression increased gradually in each sex during normal development. However, female genital tubercles expressed a higher level of androgen receptor mRNA throughout development compared to male genital tubercles (p <0.0001). In utero ethinyl estradiol exposure led to a 5.4 and 4.5-fold increase in androgen receptor mRNA in the genital tubercles of female and male embryos (p = 0.004 and 0.001, respectively). Hypospadiac male genital tubercles showed increased androgen receptor mRNA expression compared to control males (p = 0.006). Levels in hypospadiac males did not differ from those in control females but they were less than those in ethinyl estradiol treated females (p >0.05 and 0.01, respectively). CONCLUSIONS: Androgen receptor protein is expressed abundantly in male and female genital tubercles. Androgen receptor mRNA levels are higher in female than in male genital tubercles through development and they increase in response to in utero ethinyl estradiol exposure with ethinyl estradiol treated females having the highest levels of expression, followed by ethinyl estradiol treated hypospadiac males. We infer that higher estrogen in genital tubercles results in a physiological response of increased androgen receptor mRNA expression. We found no direct association between changes in androgen receptor mRNA expression and the presence or absence of hypospadias in males, suggesting that alterations in the expression of proteins other than or in addition to androgen receptor result in anomalous urethral development. This finding supports the idea that the etiology of hypospadias is multifactorial in origin.

Animals↗

PubMed1998

Estrogens increase transcription of the human endothelial NO synthase gene: analysis of the transcription factors involved.

Estrogens have been found to reduce the incidence of cardiovascular disease that has been ascribed in part to an increased expression and/or activity of the vasoprotective endothelial NO synthase (NOS III). Some reports have shown that the level of expression of this constitutive enzyme can be upregulated by estrogens. The current study investigates the molecular mechanism of the NOS III upregulation in human endothelial EA.hy 926 cells. Incubation of EA.hy 926 cells with 17beta-estradiol or the more stable 17alpha-ethinyl estradiol enhanced NOS III mRNA and protein expression up to 1.8-fold, without changing the stability of the NOS III mRNA. There was no enhancement of NOS III mRNA after incubation of EA.hy 926 cells with testosterone, progesterone, or dihydrocortisol or when 17alpha-ethinyl estradiol was added together with the estrogen antagonist RU58668, indicating a specific estrogenic response. Nuclear run-on assays indicated that the increase in NOS III mRNA is the result of an estrogen-induced enhancement of NOS III gene transcription. In transient transfection experiments using a 1.6 kb human NOS III promoter fragment (which contains no bona fide estrogen-responsive element, ERE), basal promoter activity was enhanced 1.7-fold by 17alpha-ethinyl estradiol. In electrophoretic mobility shift assays, nuclear extracts from estrogen-incubated EA.hy 926 cells showed no enhanced binding activity either for the ERE-like motif in the human NOS III promoter or for transcription factor GATA. However, binding of transcription factor Sp1 (which is essential for the activity of the human NOS III promoter) was significantly enhanced by estrogens. These data suggest that the estrogen stimulation of the NOS III promoter could be mediated in part by an increased activity of transcription factor Sp1.

Base Sequence↗

PubMed2004

Pregnancy despite imminent ovarian failure and extremely high endogenous gonadotropins and therapeutic strategies: case report and review.

PURPOSE: To attempt ovulation induction in a woman with premature ovarian failure who had very high serum follicle stimulating hormone (FSH) levels (e.g., 164 mIU/ml) by merely using ethinyl estradiol without gonadotropins. METHODS: Ethinyl estradiol (20-40 microg) was used to lower serum FSH. Monitoring of follicular maturation was performed using sonography to determine follicle size and serum estradiol. Progesterone vaginal suppositories (200 mg twice daily) were used following demonstration of oocyte release from the follicle. RESULTS: Follicle maturation and ovulation was achieved in six of ten treatment cycles. A clinical pregnancy occurred in the ninth treatment cycle and a live delivery of a healthy baby occurred. CONCLUSIONS: Despite small ovaries, amenorrhea, and failure to have withdrawal menses following progesterone, absence of antral follicles on initial ultrasound, and consistently extremely high serum FSH, ovulation and pregnancy is possible by merely lowering the serum FSH.

Adult↗

PubMed1999

Thalidomide does not alter estrogen-progesterone hormone single dose pharmacokinetics.

OBJECTIVES: To determine the single- and multiple-dose pharmacokinetics of oral thalidomide (200 mg/day, administered for 21 days) and to assess the effects of steady-state plasma concentrations of thalidomide on the single-dose pharmacokinetics of ethinyl estradiol (INN, ethinylestradiol) and norethindrone (INN, norethisterone). METHODS: A randomized, 2-period crossover study was performed in 10 healthy premenopausal female volunteers. The pharmacokinetic profiles of plasma concentrations of thalidomide were evaluated with both noncompartmental and compartmental methods, whereas those of ethinyl estradiol and norethindrone were calculated with noncompartmental methods. The effects of steady-state plasma thalidomide concentrations on the pharmacokinetics of ethinyl estradiol and norethindrone were determined with use of an ANOVA model that included treatment sequence, subject within sequence, period, and treatment as factors. RESULTS: Thalidomide plasma concentrations were best predicted by a 1-compartment model with first-order absorption and elimination and an absorption time-lag. There were no significant differences between pharmacokinetic parameters for thalidomide after 1 dose and those after 18 consecutive doses. Except for a minor decrease of the elimination rate constant (k(e)) for ethinyl estradiol, coadministration of thalidomide had no significant effects on the pharmacokinetic profiles for either ethinyl estradiol or norethindrone. The change in k(e) for ethinyl estradiol during thalidomide administration was not associated with any alteration in the clearance or elimination half-life for this hormone. CONCLUSIONS: Multiple-dose pharmacokinetics of thalidomide is similar to the single-dose profile. This study did not investigate the efficacy of the 21-day fixed ethinyl estradiol-norethindrone regimen, but the results suggest that thalidomide is unlikely to affect the pharmacokinetics of orally administered hormonal contraceptives.

Administration, Oral↗

PubMed1994

A comparison of the effects of two monophasic low dose oral contraceptives on the inhibition of ovulation.

Fifty-three women were randomly allocated to one of two combined low-dose monophasic oral contraceptives (20 micrograms ethinyl estradiol with 75 micrograms gestodene or 20 micrograms ethinyl estradiol with 150 micrograms desogestrel). The ability of these formulations to inhibit ovulation was compared using hormonal parameters and ovarian ultrasound. The effects on three treated cycles were compared with pre- and post-treatment cycles. No ovulations occurred in either group during therapy. Twenty-one percent of women were observed to show some follicle-like structures accompanied by raised serum estradiol in at least one treatment cycle. No significant differences between the two preparations were demonstrated on residual ovarian function. The secretion of estradiol and progesterone was significantly reduced throughout all three treatment cycles. Mean LH and FSH concentrations were comparable with both treatments. A secondary analysis of cycle control and tolerance was undertaken. Significantly less bleeding was seen in the gestodene group during cycle 2 (p = 0.02). There were no differences between the two treatments with respect to the other cycle control parameters. Approximately half the women recorded intracyclic bleeding during the first treatment cycle. This improved during cycles 2 and 3. Both formulations were tolerated well.

Adolescent↗

PubMed1991

The effect of tetracycline on levels of oral contraceptives.

Despite the widespread use of tetracycline for treatment of dermatologic disorders and sexually transmitted diseases, the pharmacodynamics of oral contraceptive use in the presence of tetracycline has not been studied. Seven normal women ingested an oral contraceptive containing ethinyl estradiol 35 micrograms and norethindrone 1 mg in the follicular phase of the menstrual cycle. On day 0 baseline ethinyl estradiol and norethindrone levels were obtained at 0, 1/2, 3/4, 1, 2, 4, 12, and 24 hours after oral contraceptive administration. On day 1 tetracycline 500 mg was given orally every 6 hours while the oral contraceptive was continued. Tetracycline, ethinyl estradiol, and norethindrone levels were determined at the same time intervals as on day 0. Oral contraceptive and tetracycline were continued for up to 10 days, and additional concentrations of ethinyl estradiol, norethindrone, and tetracycline were determined between days 5 and 10. Four additional normal women ingested tetracycline for 5 to 10 days. Tetracycline levels were determined at the time intervals noted above on day 1 and days 5 to 10. No significant decrease in plasma ethinyl estradiol or norethindrone concentration was seen with either short-term (24 hours) or long-term (5 to 10 days) ingestion of tetracycline. Similarly, levels of tetracycline do not significantly decrease with ingestion of a low-dose oral contraceptive.

Adolescent↗