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At least 613 records · Page 34Linked to original sources
PubMed1995

Contraceptive efficacy and safety of a monophasic oral contraceptive containing 150 micrograms desogestrel and 30 micrograms ethinyl estradiol: United States clinical experience using a "Sunday start" approach.

OBJECTIVE: To report on experience in the United States with a monophasic oral contraceptive (OC) containing 150 micrograms desogestrel and 30 micrograms ethinyl E2 (EE). The results of a multicenter evaluation of efficacy, cycle control, and safety over 6 months of exposure using a "Sunday start" regimen is evaluated. SETTING: Multicenter. DESIGN: Open noncomparative study. PARTICIPANTS: Study subjects were a mean age of 25 years, and the majority were educated, nonobese, white, nulliparous, and previously had used OCs. INTERVENTIONS: A total of 809 women were exposed to study medication for a total of 4,096 cycles (equivalent to 341.3 women-years of use). RESULTS: Efficacy was excellent. One user-failure pregnancy occurred (Pearl index 0.32); there were no method-failure pregnancies. Study medication was well tolerated; 6.6% of the subjects discontinued treatment because of drug-related adverse events. The study medication exhibited no adverse effects on blood pressure, body weight, or laboratory variables. Cycle control was evaluated in 697 subjects. In a total of 3,640 cycles, the incidences of intermenstrual bleeding, breakthrough bleeding, breakthrough spotting, and absence of withdrawal bleeding were 9.8%, 1.7%, 8.1%, and 1.4%, respectively, indicating appropriate cycle control. Patient acceptability was high; seven subjects (1%) discontinued the study because of menstrual irregularity (metrorrhagia). CONCLUSION: The results of this study, comparable to those demonstrated in a recent European multicenter study, add further documentation to the published data on the safety, efficacy, cycle control, and acceptability of this monophasic desogestrel-containing combined OC using a "Sunday start" approach.

Adolescent↗
PubMed1976

[Liver function tests under the influence of sequential treatment using ethinyl estradiol-norethisterone acetate and ethinyl estradiol-chlormadinone acetate].

30 young healthy women were investigated during the first therapy cycle with ethinyl-estradiol-norethisterone acetate and ethinyl-estradiol-chlormadinone acetate as a sequential regime. The following laboratory data were achieved by each of the investigated group of young women: serum aminotransferase (GOT and GPT), serum alkaline phosphatase and alpha-amylase-activity in serum, serum proteins, serum cholesterol, serum bilirubin, serum ZST, serum TTT and the indocyaningreen-clearance of the liver. The serum protein pattern was determined by the paper electrophoretic method. A significant decrease of the aminotransferase GPT was viable during the sequential therapy with ethinyl-estradiol and norethisterone acetate. This viable decrease of the GPT was induced through the application of norethisterone acetate to estrogen. The alkaline phosphatase was significant lightly lower and the beta-globuline lightly elevated at the end of the therapy cycle. The sequential therapy with ethinyl-estradiol and chlormadinone acetate induced only a significant increase of the ZST in serum.

Adolescent↗
PubMed1998

Effect of oral contraceptives containing 20 and 35 µg ethinyl estradiol on urinary prostacyclin and thromboxane levels in smokers and non-smokers.

Objective: Several observational epidemiological studies have shown an increased risk of myocardial infarction (MI) in oral contraceptive (OC) users who smoke cigarettes. Nearly a quarter of all OC users are smokers. The etiology of MI in OC users has been shown to be thrombotic, and the thrombogenic effect of OCs appears to be due to the estrogen component of the formulation. There are epidemiologic data that indicate that decreasing the estrogen dosage in OCs decreases the risk of thrombosis. Smoking may enhance thrombosis in OC users by decreasing prostacyclin levels. The objective of the present study was to investigate the interaction between smoking and OC use with respect to thrombogenesis by studying the effects of OCs and smoking on urinary levels of prostacyclin PGI and thromboxane A(2) TX in smokers and non-smokers.Study Design: A total of 60 healthy women, aged 19-32 years, who were not taking any hormonal treatment for at least 3 months prior to initiating the study were divided into three equal groups: A) OC users who smoked (N = 20), B) OC users who did not smoke (N = 20), and a control group of 10 smokers and 10 non-smokers. To be eligible to participate in the study, all smokers had to smoke at least one pack of cigarettes per day. Each OC treatment group was randomized to receive either norethindrone (NET) acetate (1 mg)/ethinyl estradiol (EE(2)) (0.035 mg) (N = 10) or NET acetate (1 mg)/EE(2) (0.02 mg) (N = 10) daily for 3 months. Overnight urine collections and fasting blood samples were obtained at baseline and at 3 months prior to taking the last OC. Serum levels of NET and EE(2), as well as urinary levels of cotinine and the stable metabolites of prostacyclin and thromboxane A(2) (6-keto-prostaglandin F(1alpha) and thromboxane B(2), respectively), were measured by specific immunoassays.Results: Study subjects showed compliance with respect to smoking and OC use as determined by the levels of serum NET, EE(2), and cotinine. Comparing mean levels of PGI metabolites in the two groups of OC smokers, those taking 35 µg EE(2) showed a significant decrease in PGI. Comparing the ratio of PGI/TX in all smokers, only the smokers on the 35 µg formulation showed a significant decrease in the ratio, while there was no change in the 20 µg group. No significant changes in the ratio PGI/TX during the same time interval in smoking and non-smoking controls and OC non-smokers were observed.Conclusions: Women smokers taking 20 µg EE(2) OC had no thrombophilic changes of PGI and TXA(2) metabolites. Women smokers taking 35µg EE(2) oral contraceptive had thrombophilic changes in PGI/TXA metabolite ratio. Women smokers who use oral contraceptives may have less thrombotic risk taking formulations with 20µg EE(2) than 35µg EE(2).

Journal Article↗
PubMed1992

Hormonal regulation of corticosteroid-binding globulin biosynthesis in the male rat.

Corticosteroid-binding globulin (CBG) is an acidic glycoprotein produced primarily by the liver and is the major glucocorticoid transport protein in rat blood. Various hormone treatments are known to modify plasma CBG levels and may thereby influence the bioavailability of glucocorticoids. We have, therefore, examined serum CBG and hepatic CBG mRNA levels in male rats after sc steroid (25 micrograms/100 g BW twice daily of dexamethasone, prednisolone, corticosterone, estrone, estradiol, ethinyl estradiol, progesterone, or 5 alpha-dihydrotestosterone) or T4 (10 micrograms/100 g BW twice daily) administration. After dexamethasone treatment, serum CBG levels decreased significantly (P less than 0.002) within 48 h and were 26% of those in vehicle-treated animals by 72 h. At this time, CBG mRNA was undetectable in liver RNA extracts by Northern blotting or solution hybridization, and nuclear run-off experiments indicated that dexamethasone reduces CBG gene transcription in the liver by at least 14-fold. Treatment with ethinyl estradiol also reduced serum CBG levels significantly (P less than 0.015) compared to pretreatment values. No other significant changes in serum CBG levels were observed after any other steroid hormone treatment, and alterations in hepatic CBG mRNA levels were only observed after dexamethasone treatment. T4 administration for 72 h increased serum CBG and hepatic CBG mRNA levels by 66% and 39%, respectively, but did not influence the rate of CBG gene transcription. Thus, increased CBG biosynthesis after thyroid hormone treatment appears to be due to an increase in CBG mRNA stability. No change in the Concanavalin-A-binding properties of CBG molecules was observed after treatment with either dexamethasone or T4, and this suggests that these hormones do not influence the type of oligosaccharide chains associated with this protein. We, therefore, conclude that dexamethasone and T4 regulate hepatic CBG biosynthesis in the rat by modulating CBG mRNA synthesis and stability, respectively.

Animals↗
PubMed1985

Testosterone-induced decrement of prostatic vascular resistance in rats is reversed by estrogens.

The function and growth of the rat prostate are stimulated by androgens and inhibited by estrogens. To study the influence of these hormones on the prostatic blood flow, prostatic vascular resistance was measured in castrated adult rats, which were testosterone supplemented and treated with different estrogenic substances. Prostatic blood flow was measured using the microsphere technique. Testosterone supplementation for 8-9 days after castration resulted in decreased vascular resistance in both the ventral and dorsolateral prostates. In testosterone-supplemented rats, treatment for the same period of time with estradiol benzoate, ethinyl estradiol, and diethylstilbestrol induced increased vascular resistance in both the ventral and dorsolateral prostates. However, treatment with estromustine or estramustine did not change prostatic vascular resistance significantly. It was concluded that the testosterone-induced decrease of prostatic vascular resistance was reversed by estradiol, ethinyl estradiol, and diethylstilbestrol, possibly by a direct effect on the prostate.

Animals↗
PubMed1986

Inhibition of androgen receptor binding by natural and synthetic steroids in cultured human genital skin fibroblasts.

The ability of various natural and synthetic steroids (some of which are widely used in clinical practice) to compete with dihydrotestosterone receptor binding in human genital skin fibroblasts was studied. Binding was assessed in fibroblast monolayers after incubation for 1 h at 37 degrees C with 2 nM 3H-dihydrotestosterone in the presence or absence of increasing concentrations of the steroid to be tested. Inhibition constants (Ki) were determined as the concentration of competitor-required for 50% inhibition of 3H-dihydrotestosterone binding. In addition, relative binding activity (RBA) of each test compound was calculated. Each competitor was tested in at least two different cell strains. The concentrations of unlabeled methyltrienolone (a synthetic nonmetabolizable androgen) and dihydrotestosterone for 50% inhibition of 3H-dihydrotestosterone binding were in the same order of magnitude, namely, 2 nM (2.2 respectively, 2.4 nM), whereas the affinity of testosterone was approximately one-fifth that of dihydrotestosterone. Other potent competitors for dihydrotestosterone binding were three progestins (norgestrel, gestoden, and medroxyprogesterone acetate) which have Ki values similar to testosterone. An order of magnitude lower Ki values (around 10(-7) M) were found for the androgen 17 alpha-propylmesterolone, the antiandrogen cyproterone acetate, and the progestin norethisterone acetate. Binding affinities of all other steroids to the androgen receptor were markedly lower and showed the following order of potency: estrogens (estradiol, ethinyl estradiol, diethylstilbestrol) greater than glucocorticoids as well as aromatase inhibitors and potassium canrenoate.(ABSTRACT TRUNCATED AT 250 WORDS)

Binding, Competitive↗
PubMed2006

Modeling effects of mixtures of endocrine disrupting chemicals at the river catchment scale.

For endocrine disrupting chemicals in the environment, concerns arise primarily from the effects that may be induced in wildlife. A well studied example is estrogenic chemicals in the aquatic environment and their effects on fish. Directly measuring effects, in fieldwork studies, is an expensive and time-consuming approach that is fraught with many difficulties, ranging from study design right through to data analysis and interpretation. An alternative approach would be to predict the scale of effect(s) using suitable modeling techniques. We have attempted to do this using estrogenic chemicals as an example. We chose this group of aquatic pollutants because of the current considerable interest in them and the wealth of biological data available on them. Using the established GREAT-ER hydrological model,we have first predicted the concentrations and then the estrogenic effects on fish, of estrone, estradiol, ethinyl estradiol, and nonylphenol individually throughout an entire river catchment. We then show that knowledge of the biological responses of fish to mixtures of these chemicals can be used to predict the effect of environmentally realistic mixtures of them. To determine the degree of risk posed by this group of chemicals, it was necessary to take into account mixture effects: assessment on a chemical by chemical basis led to underestimations of the risk. Finally, we show that the approach can be used to predict how the risk will be affected by changes in the concentration of one chemical in the mixture. Although we have used only one endpoint (vitellogenin induction as an estrogenic response) and one group of similarly acting chemicals, we suggest that this general approach could prove extremely useful to regulatory authorities and other parties charged with protecting aquatic wildlife from adverse effects caused by chemicals in their environment.

Endocrine Disruptors↗
PubMed1983

Antagonistic action of estrogens, flutamide, and human growth hormone on androgen-induced changes in the activities of some enzymes of hepatic steroid metabolism in the rat.

The dose-dependent effects of daily estrogen (estradiol, ethinyl estradiol, diethylstilbestrol) administration on the activities of three hepatic androgen-dependent microsomal enzymes (3 alpha- and 3 beta-hydroxysteroid dehydrogenase and 5 alpha-reductase) in male rats were examined. Antiestrogens were then tested for their ability to block the feminizing action of 10 micrograms estradiol/day on these enzyme activities; nafoxidine and monohydroxytamoxifen were the most effective. The prevention of 5 alpha-dihydrotestosterone-induced changes in these activities in ovariectomized females was investigated. All three estrogens at a dose of 1 microgram blocked the action of 500 micrograms androgen. A similar androgenic blockade was achieved by daily administration of 5 mg flutamide or constant infusion of human GH (5 micrograms/h). Simultaneous administration of 200 micrograms monohydroxytamoxifen prevented the androgen-antagonizing action of estrogens, but not of flutamide nor of GH. Large doses of estrogens have the same repressive effect as androgens on 5 alpha-reductase activity in female castrates. Using the diethylstilbestrol-treated rat as a model, it is demonstrated that this effect can be prevented by antiestrogen, but not by GH. It is concluded that androgens and low doses of estrogens affect these enzyme activities by acting at different levels of central regulation, whereas large doses of estrogens act directly on the liver via hepatic estrogen receptors. These conclusions are corroborated by studies of hepatic estrogen receptor concentrations.

3-Hydroxysteroid Dehydrogenases↗
PubMed1976

Failure of estrogens and androgens to inhibit bone resorption in tissue culture.

The effects of estrogens, androgens, and glucocorticoids on bone resorption were compared in organ culture. At a concentration of 10(-5) M, corticosterone, testosterone, dihydrotestosterone, dehydroepiandosterone, estradiol, ethinyl estradiol and estrone did not inhibit the release of 45Ca from 19-day fetal rat long bone shafts in control or para-thyroid hormone (PTH)-treated cultures after 2 or 5 days. Cortisol inhibited both control and PTH-stimulated resorption at 10(-5) M and 10(-6) M. 17beta-Estradiol was inhibitory at 3 X 10(4) M. However, it was less effective than the estrogenically inactive epimer 17alpha-estradiol, in 8 day control cultures or in cultures containing low concentrations of PTH. At 10(-5) m, neither 17beta-estradiol nor 17alpha-estradiol inhibited resorption stimulated by prostaglandin E2 or by osteoclast activating factor.

Androgens↗
PubMed2004

Comparative analysis of estrogenic activity in sewage treatment plant effluents involving three in vitro assays and chemical analysis of steroids.

In this study, we assessed and compared the suitability of three in vitro screening tools for the measurement of estrogenic activity in sewage treatment plant effluents (STPEs). These assays were the yeast estrogen screen (YES), production of zona radiata proteins (ZRPs) in trout hepatocytes, and the induction of reporter gene expression in the transfected rainbow trout gonad cell line RTG-2. Data obtained with the YES were additionally compared with calculated estrogenicity, based on steroid analysis data of the effluents. For comparison purposes, the response of the in vitro systems toward the estrogenic chemicals beta-estradiol, ethinyl estradiol, bisphenol-A, nonylphenol, and octylphenol was assessed. All three assays showed sensitivities in the same order of magnitude in response to the steroid compounds tested, with ZRP production being the least sensitive. Regarding the estrogenic environmental chemicals tested, the RTG-2 assay was more than an order of magnitude more sensitive than the other two assays. Despite their different sensitivities toward selected test chemicals, the three in vitro systems indicated estrogenic activity in the same concentration range for the tested STPEs. Calculated estrogenicity (chemical analysis) and measured estrogenicity (YES) were of the same order of magnitude for the STPEs tested. The present study indicates that all three in vitro systems, with the yeast-based system being the easiest and most robust, are applicable for the screening of estrogenic activity in effluent samples.

Animals↗