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PubMed1985

Use of a modified test system to determine early pregnancy factor (EPF) levels in patients with normal first trimester pregnancy and after therapeutic abortion.

Human pregnancy can be recognized as early as 48 hours after conception using the rosette inhibition test (RIT) to detect early pregnancy factor (EPF). A modification of the test as originally described by Morton et al. is demonstrated using a monoclonal pan T-cell antibody. Studies were performed to investigate the relationship between EPF levels during normal first trimester intact pregnancies and therapeutic abortions. The change in EPF levels is compared with those of hormones after interrupted pregnancy.

Abortion, Therapeutic↗
PubMed2002

An evaluation of bioequivalence of two 7-day 17beta-estradiol transdermal delivery systems by anatomical site.

An open-label, randomized, crossover study was conducted to assess the bioequivalence of two 7-day transdermal 17beta-estradiol delivery systems following application to the buttock in 42 postmenopausal women. The systems tested were a generic Estradiol Transdermal System (Mylan Pharmaceuticals, Inc.) and Climara (Berlex Laboratories, Inc.), the reference product. Each system was labeled to deliver 17beta-estradiol 0.1 mg/day and was applied for 7 days. Serial serum samples were assayed for estradiol, estrone, and estrone sulfate using validated assays. The bioequivalence confidence intervals for the ratio of log-transformed 17beta-estradiol Cmax values for the Estradiol Transdermal System and Climara were outside the interval of 0.80 to 1.25, indicating that the products were not bioequivalent. Application site reactions and skin irritation were more common with the Estradiol Transdermal System than with Climara. The odds of patch lifting or detachment were 6.95 times higher with the Estradiol Transdermal System than with Climara. Because these two transdermal delivery systems had been previously shown to be bioequivalent after application to the abdomen, the findings of this study suggest that bioequivalence at one anatomical site is not indicative of bioequivalence at another.

Administration, Cutaneous↗
PubMed1998

Pharmacokinetic comparison between Conpremin (Premarin) and a generic preparation of conjugated estrogens.

OBJECTIVES: To determine the relative bioavailability of the estrogenic components of a generic brand of conjugated estrogens marketed in Chile in comparison to that of Conpremin (Premarin in the United States). METHODS: A randomized cross-over study was conducted on 16 healthy postmenopausal women receiving single oral doses of either two Conpremin 0.625-mg tablets or two 0.625-mg tablets of the generic brand, with a 14-day wash-out interval between doses. A gas chromatography tandem mass spectrometry assay was used to determine estrogen components. RESULTS: The peak plasma concentrations of unconjugated and total estrone and equilin, unconjugated 17 beta-dihydroequilin and 17 beta-estradiol were higher and occurred earlier with the generic conjugated estrogens than with Conpremin. The 90% confidence limits for both variables lay outside the accepted bioequivalence limits of 80-125%. Additionally, no measurable plasma concentration of unconjugated delta 8,9-dehydroestrone or 17 beta-delta 8,9-dehydroestradiol was seen after administration of the generic conjugated estrogens. CONCLUSIONS: These pharmacokinetic results indicate that the generic tablets do not have the modified-release characteristics of Conpremin tablets. In addition, the absence of delta 8,9-dehydroestrone and 17 beta-delta 8,9-dehydroestradiol in the plasma indicates that the generic form is not compositionally equivalent to Conpremin.

Adult↗
PubMed2001

Bioequivalence and relative bioavailability of three estradiol and norethisterone acetate-containing hormone replacement therapy tablets.

OBJECTIVE: The primary objective was to demonstrate bioequivalence between the estrogen components ofActivelle (1 mg estradiol (E2) + 0.5 mg norethisterone acetate (NETA)) and the combined phase of Novofem (1 mg E2 + 1 mg NETA) and between the NETA components of the combined phase of Novofem (1 mg E2 + 1 mg NETA) and Trisequens (2 mg E2 + 1 mg NETA). SUBJECTS, MATERIALS AND METHODS: The study design was double-blind, randomized, three-way, balanced six-sequence cross-over. The washout period was 14 days between treatments. Single doses of the above-described tablets were administered in the morning following an overnight fast to 24 healthy postmenopausal or bilaterally oophorectomized women. Plasma concentration profiles of E2, estrone (E1; pharmacologically active metabolite of E2) and norethindrone (NET: NET was determined since NETA is very rapidly metabolized to NET) were measured over 72 h, and 36 h, respectively. For the two former substances a baseline correction was performed by subtracting the mean of two predose measurements from the concentrations measured after dosing. RESULTS: One subject dropped out of the study, completing only one treatment sequence; therefore, the results are based on 23 subjects. The baseline-corrected E2 and E1 AUC0-t (Novofem)/AUC0-t (Activelle) ratios were 105% and 100%, respectively; and the Cmax ratios 100% and 105%, respectively. Identical median tmax was observed for E2 (6 h) and for E1 (5 h). The NET AUC0-t (Novofem)/AUC0-t (Trisequens) ratio was 95%, and the corresponding Cmax ratio 98%. The median tmax for Novofem was 0.75 h and for Trisequens 1.0 h. CONCLUSION: Bioequivalence was demonstrated for E2, E1 and NET in accordance with the study objectives.

Administration, Oral↗
PubMed1982

[The antiestrogen effect].

The effects of estradiol, which are requisite for the normal occurrence of events related to reproduction, are not restricted to that field. They play a part in the overall trophicity of the female organism. On the other hand, relative or absolute estrogen hyperactivity results in harmful clinical effects and in disastrous cellular consequences, i.e. initiation or promotion of genital carcinomas. After a review of the different steps of the synthesis and action of estradiol, the various compounds that are active on these steps are considered: antigonadotropes (norsteroid progestogens, androgens, danazol, prolactin, corticosteroids, LHRH), inhibitors of estrogen synthesis (aminogluthetimide and testolactone), compounds that increase catabolism (progestogens), and antagonists of the cellular effect of estradiol (tamoxifen, nafoxidin, clomifen, progesterone, progestogens and androgens). The putative or established site of action and the main aspects of therapeutic use are given for each substance.

Aminoglutethimide↗
PubMed1992

Hormone treatment of endometriosis: the estrogen threshold hypothesis.

In women with recurrent pelvic pain caused by endometriosis, hormonal therapy with a gonadotropin-releasing hormone agonist is an effective alternative to surgical therapy. The basis for medical treatment of endometriosis is that endometriosis lesions are dependent on estradiol for continued growth. Further, end organ tissue varies in its sensitivity to estradiol. This forms the basis of the estrogen threshold hypothesis, that is, that a concentration of estradiol that will partially prevent bone loss may not stimulate endometrial growth. Thus there is a hierarchy of organ response to estradiol such that calcium metabolism is most sensitive followed by gonadotropin secretion, vaginal epithelial growth, lipid metabolism, and liver protein production. Similarly, breast cancer is most sensitive and endometriosis is least sensitive to estrogen. These differences may allow the design of regimens with a gonadotropin-releasing hormone agonist that maintain a therapeutic response and ameliorate potential adverse effects.

Bone Density↗
PubMed1990

Severe ovarian hyperstimulation syndrome using agonists of gonadotropin-releasing hormone for in vitro fertilization: a European series and a proposal for prevention.

Severe ovarian hyperstimulation syndrome (OHSS) was recorded in 8 of 413 patients after the use of gonadotropin-releasing hormone agonists (GnRH-a) associated with gonadotropins for in vitro fertilization. Seven of the 8 patients were pregnant. Common factors associated with the development of OHSS were high serum estradiol values on the day of ovulation induction and many follicles greater than or equal to 12 mm. Based on this experience, a new therapeutic schedule was used in a group of 10 patients who, after GnRH-a and gonadotropin stimulation, were judged to be at high risk of OHSS on the day of human chorionic gonadotropin (hCG). No hCG was administered and gonadotropins were stopped. The administration of GnRH-a was continued and, after a further period of pituitary desensitization, follicular stimulation was recommended with a lower dose of gonadotropins. No cases of OHSS occurred and 3 patients became pregnant.

Buserelin↗
PubMed1986

Enzyme-linked immunochemical measurement of estrogen receptor in gynecologic tumors, and an overview of steroid receptors in ovarian carcinoma.

We tested whether a newly available enzyme-linked immunoassay (EIA) validly measures estrogen receptor (ER) in gynecologic tumors. We first documented that ER so measured agreed with results by established radioligand-based assays [dextran-coated charcoal (DCC) and hydroxylapatite (HAP)] for in-house breast carcinomas and for proficiency testing specimens. Then, for gynecologic tumors, we found strong correlations between results for ER as measured by the two methods; e.g., for 27 ovarian carcinomas, r greater than or equal to 0.86. The same was true for ER measured in nine specimens of ovarian carcinoma from women who had undergone chemotherapy: r greater than or equal to 0.94. Radioinert estradiol or serum had no discernible effect on EIA measurements of ER, whereas our DCC assay was rendered uninterpretable. Evidently the EIA validly measures ER in steroidogenic tissues, including ovarian, and also in breast and uterine carcinomas. Clinical management of the latter is now based in part on results of steroid receptor assays. For ovarian carcinomas, ER assay can be helpful for determining the probable primary site of adenocarcinomas of unknown origin, and it is providing a rational basis for development of new diagnostic and therapeutic strategies.

Blood↗
PubMed2006

A double-blind randomized controlled trial of toremifen therapy for mastalgia.

HYPOTHESIS: Toremifen is effective in reducing breast pain and does not increase the incidence of adverse events as a therapy for moderate to severe mastalgia. DESIGN AND PATIENTS: In a double-blind randomized controlled trial, patients with moderate to severe mastalgia received toremifen citrate, 30 mg daily, or a placebo tablet for 3 menstrual cycles and were followed up for breast pain score and adverse events. The serum levels of estradiol, progesterone, and prolactin were examined before treatment and correlated with the response rate to toremifen treatment. RESULTS: Seventy-two (69.2%) of 104 patients receiving toremifen and 29 (31.9%) of 91 receiving placebo responded to the treatment, with reduction in breast pain score of more than 50% (P<.001). Among the patients with cyclical mastalgia, the response rate for toremifen was 76.7% (59/77), whereas the response rate for placebo was 34.8% (23/66; P<.001). In contrast, the response rate of patients with noncyclical mastalgia was 48.1% (13/27) for toremifen and 24.0% (6/25) for placebo (P = .09). Adverse events were observed in 44 (42.9%) of 104 patients receiving placebo and 46 (50.5%) of 91 patients receiving toremifen (P = .45). A positive correlation between baseline breast pain score and serum estradiol level was observed in patients with cyclical mastalgia (r = 0.35, P = .003). CONCLUSIONS: Toremifen effectively relieves moderate and severe cyclical mastalgia and tends to exert a positive therapeutic effect on noncyclical mastalgia. In addition, toremifen therapy does not increase the incidence of intolerable adverse event. Therefore, it is a feasible therapy for mastalgia, especially cyclical mastalgia.

Breast Diseases↗
PubMed2006

Estrogenic agonist activity of ICI 182,780 (Faslodex) in hippocampal neurons: implications for basic science understanding of estrogen signaling and development of estrogen modulators with a dual therapeutic profile.

The present study sought to determine the characteristics of ICI 182,780 (Faslodex) action in rat primary hippocampal neurons. We first investigated the neuroprotective efficacy of ICI 182,780 against neurodegenerative insults associated with Alzheimer's disease and related disorders. Dose-response analyses revealed that ICI 182,780, in a concentration-dependent manner, significantly promoted neuron survival following exposure to either excitotoxic glutamate (200 muM)- or beta-amyloid(1-42) (1.5 muM)-induced neurodegeneration of hippocampal neurons. At a clinically relevant concentration of 50 ng/ml, ICI 182,780 exerted nearly maximal neuroprotection against both insults with efficacy comparable with that induced by the endogenous estrogen 17beta-estradiol. Thereafter, we investigated the impact of 50 ng/ml ICI 182,780 on mechanisms of 17beta-estradiol-inducible neuronal plasticity and neuroprotection. Results of these analyses demonstrated that ICI 182,780 directly induced a series of rapid intracellular Ca(2+) concentration ([Ca(2+)](i)) oscillations in a pattern comparable with that of 17beta-estradiol. In addition, ICI 182,780 exerted dual regulation of the glutamate-induced rise in [Ca(2+)](i) identical to that induced by 17beta-estradiol. Further analyses demonstrated that ICI 182,780 induced significant activation of extracellular signal-regulated kinase 1/2 and Akt (protein kinase B) and significantly increased expression of spinophilin and Bcl-2, with efficacy comparable with neurons treated with 17beta-estradiol. Taken together, results of these in vitro analyses of ICI 182,780 provide direct evidence of an estrogenic agonist profile of ICI 182,780 action in rat hippocampal neurons. Therapeutic development of neuroselective estrogen receptor modulators that mimic ICI 182,780 is discussed with respect to the potential of safe and efficacious alternatives to estrogen therapy for the prevention of postmenopausal cognitive decline and late-onset Alzheimer's disease.

Amyloid beta-Peptides↗
PubMedDate not supplied

17 beta Estradiol-induced increase in brain dopamine D-2 receptor: antagonism by MIF-1.

Animal behavioral and neurochemical studies implicate dopaminergic systems in the neurological sequelae induced by estrogen. In the present study, we demonstrated for the first time that MIF-1, a neuropeptide unrelated to classical dopamine agonists, when given prior to, concurrently with, and after 17 beta-estradiol, antagonized significantly the estrogen-induced increase in the density of dopamine D-2 receptor both in the striatum and the mesolimbic area of male rat brain. The current findings have implications for the prophylactic and therapeutic potential for MIF-1 in extrapyramidal motor disorders caused by estrogen imbalance in humans.

Animals↗
PubMedDate not supplied

The effect of varying low-dose combinations of norethindrone acetate and ethinyl estradiol (femhrt) on the frequency and intensity of vasomotor symptoms.

OBJECTIVE: To determine whether there is a significant reduction in frequency and severity of hot flashes in symptomatic postmenopausal women who are administered continuously different dose combinations of norethindrone acetate and ethinyl estradiol. DESIGN: Two randomized clinical trials (Study 1 and Study 2) were conducted in which study participants recorded in daily diaries the frequency of their hot flashes. Study 2 participants also recorded the number of mild, moderate, or severe hot flashes they experienced. In Study 1, a total of 219 postmenopausal women reporting vasomotor symptoms were placed randomly into groups to receive either a placebo or 1 of 4 treatments (0.2 mg/1 microg; 0.5 mg/2.5 microg; 1 mg/5 microg; or 1 mg/10 microg norethindrone acetate/ethinyl estradiol). In Study 2, a total of 266 highly symptomatic postmenopausal women were placed randomly to receive either a placebo or 1 of 3 treatment groups [0.5 mg/2.5 microg; 1 mg/5 microg; or 1 mg/10 microg norethindrone acetate (NA)/ethinyl estradiol (EE)]. Total duration of treatment was 16 weeks in Study 1 and 12 weeks in Study 2. Study 1 subjects had to have at least 10 hot flashes during the week before randomization. Study 2 subjects had to have at least 56 moderate to severe hot flashes during the week before randomization. RESULTS: In both studies, there was a dose-related decrease in hot flash frequency with the highest dose (1 mg NA/10 microg EE) group that had the greatest response. Significant differences from placebo (p < 0.05, Dunnett's test) occurred within 4 weeks in Study 1 for hot flash frequency with a percent reduction in frequency ranging from 33% for placebo to 84% for both the 1 mg NA/10 microg EE and 1 mg NA/5 microg EE dose groups. Likewise, Study 2 significant reductions in hot flash frequency occurred by Week 2 for 1 mg NA/10 microg EE, Week 3 for 1 mg NA/5 microg EE, and Week 5 for 0.5 mg NA/2.5 microg EE (p < 0.05, Dunnett's test). This dose effect was also apparent with regard to severity. In addition, more subjects had clinically meaningful reductions in hot flash frequency or elimination as the dose combinations increased. CONCLUSION: There were significant reductions in hot flash frequency and severity with continuous treatment with norethindrone acetate and ethinyl estradiol combinations. The time at which significant reductions were observed, as well as the magnitude of the response, were dose dependent. The opportunity for lower-dose options of a new continuous-combined hormone replacement therapy provides therapeutic flexibility for women who are recently menopausal.

Adult↗
PubMed1976

Hormones and gynecologic cancer.

Available basic information about the regulation of rates of production, blood levels, intracellular metabolism, and action of steroid hormones and prolactin is reviewed and related to high-risk factors and therapeutic procedures applicable to gynecologic cancer.

Androgens↗