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At least 397 records · Page 22Linked to original sources
PubMed1996

Beneficial effect of treatment with transdermal estradiol-17-beta on exercise-induced angina and ST segment depression in syndrome X.

We investigated the acute effect of transdermal estradiol-17-beta on exercise-induced ischemia in 15 postmenopausal women (mean age 58 +/- 6 years) with syndrome X (angina pectoris, positive exercise test and normal coronary angiogram) and eight healthy women (mean age 58 +/- 5 years) in a placebo-controlled, double-blind crossover trial. Two exercise tests were performed on separate days, separated by at least 1 week, after application of placebo or 100 micrograms/24 h estradiol-17-beta. In the control group there was no difference between estradiol and placebo. Patients with syndrome X, on the other hand, showed an increased time to angina (323 +/- 99 versus 233 +/- 67 s, P = 0.0044), time to 1 mm ST depression (257 +/- 142 versus 187 +/- 122 s, P = 0.039), total exercise time (363 +/- 104 versus 323 +/- 85 s, P = 0.038), and working capacity (93 +/- 17 versus 89 +/- 15 W, P = 0.0086) during active treatment. In conclusion, estradiol-17-beta has a beneficial effect on myocardial ischemia in postmenopausal women with syndrome X and may be a useful therapeutic agent in this disease.

Administration, Cutaneous↗
PubMed1983

Sequential clomiphene citrate-menotropin therapy for induction or enhancement of ovulation.

Either to induce ovulation in anovulatory infertility patients or to enhance ovulation in patients with mild endometriosis or luteal phase inadequacy, we utilized a sequential regimen of low-dose clomiphene citrate (CC) followed by human menopausal gonadotropin (hMG) injections on alternate days; duration and dosage of menotropin therapy was individualized by using serum estradiol levels for monitoring until the time of administration of human chorionic gonadotropins. Previous therapeutic efforts without menotropins had been unsuccessful in all patients. One third of 70 treated patients conceived during 156 treatment cycles. The pregnancy rate was 44% in anovulatory patients (n = 34), and 26% in patients with ovulation dysfunction (n = 23). Pregnancy rates declined with patient's age. Four of the 23 patients that conceived had a spontaneous abortion (17%). The multiple gestation rate was 10.5%. A relative inhibition of cervical mucus development was noted and shown to be caused by CC. Hyperstimulation occurred in three patients. The discussed CC-hMG regimen approaches the effectiveness of standard hMG therapy; but compared with standard hMG therapy, it has significant economic advantages and seems to have a markedly lower rate of multiple gestation. However, like standard hMG therapy, CC-hMG therapy requires careful monitoring specifically, because hyperstimulation may occur.

Adult↗
PubMed1980

Ethinylestradiol and diethylstilbestrol induced antibodies and vascular thrombosis.

Antiethinylestradiol antibodies were demonstrated in several oral contraceptive users. The antibodies could be precipitated from serum immune complexes by 25% saturated ammonium sulfate. This test of serum precipitation was applied to a comparative study of 116 women on O.C and 65 men treated with diethylstilbestrol for a prostatic cancer. Controls without hormones were included in each group. The test was shown to discriminate among the estrogen users reactive and unreactive persons. 34% of women and 41% of men had high levels of precipitated immunoglobulins in 25% saturated ammonium sulphate. Study of the specificity of the Igs purified from the precipitates in reactive cases, showed that they were binding ethinylestradiol with an affinity constant consistent with an antigen antibody reaction. It is concluded that the oral ingestion of two different synthetic estrogen compounds may induce antiestrogen antibodies. The relation of these antibodies with the increased incidence of vascular thrombosis is considered.

Adolescent↗
PubMed2005

Impact of clinically relevant progestins on the neural effects of estradiol and the signaling pathways involved.

The natural ovarian hormone progesterone functions as an effective neuroprotective agent. However, in its native state it is not an efficient therapeutic compound because of its poor bioavailability. Thus, for practical therapeutic usage it became necessary to develop orally active progestogens for use in hormone therapy. We have shown that not all progestogens are equal in their ability to modulate neuronal survival and markers of neuronal plasticity. Thus, one cannot assume that all hormone therapies will perform the same, and it is crucial to determine the neural effects and interactions with estradiol of synthetic progestins used in place of natural progesterone. We have analyzed a number of clinically relevant progestins for neuroprotective efficacy. These in vitro analyses of neuroprotective efficacy could serve as a predictive index of clinical efficacy for progestins to protect against degenerative insults that lead to Alzheimer's disease. To aid in such therapeutic development, we determined the chemical structural features that predict progestin efficacy in the brain and showed that binding affinity does not predict neuroprotective efficacy or the direction of effect and thus cannot be used as an indicator of neurological benefit. In contrast, there was a set of common features of ligand-receptor interactions that are correlative and hopefully predictive of neuroprotective efficacy. Elucidation of the sites and targets of progestogen action should have a clear impact on both the use of hormone therapy for the prevention of neurodegenerative disease and the future design of target-specific hormone therapy formulations.

Animals↗
PubMed1985

Steroid receptors in human uterine carcinoma. Their biological importance and therapeutic implications.

Surgical material of primary uterine carcinoma from postmenopausal patients was analyzed with regard to cytosol content of estradiol (ER) and progesterone (PR) receptors, as well as their binding sites in nuclear compartment. A dextrancoated charcoal technique was used and binding data were calculated from Scatchard plots. In all examined specimens intracellular high-affinity, low-capacity estrogen - and progesterone-binding proteins (which have the characteristics of steroid receptors), with equilibrium dissociation constants (Kd's) of 10(-10)M and 10(-9)M respectively, have been observed in detectable levels. DNA binding ability of steroid-receptor complexes was examined and clearly demonstrated even at 4 degrees C by using DNA-cellulose slurry. Preheating of complexes at 25 degrees cause increased DNA binding ability in some specimens, but significant loss of this ability in other tumors. The relationship between the nuclear retention of steroid-receptor complexes and their interaction with nuclear components (giving a response) is discussed on the basis of steroid-responsive and unresponsive systems. Present investigation indicate that described steroid analysis may become an important tool in predicting the value of endocrine therapy in human uterine carcinoma.

Cell Nucleus↗
PubMed1990

The pharmacokinetic model and distribution pattern of new sexual-steroid-hormone-linked anticancer agents.

Sexual-steroid-hormone-linked anticancer agents are a new group of cytotoxic drugs designed for a site-directed chemotherapy of tumors containing sexual steroid hormone receptors. The hormone (e.g. estradiol or testosterone) should act as a carrier that leads to a preferential receptor-mediated drug accumulation in hormone-receptor-positive tumors (such as mammary carcinomas and prostatic cancer). In several preclinical therapeutic studies of sexual-hormone-receptor-positive breast cancer, for instance, conjugates of 2-chloroethyl-carbamoyl-L-alanine linked to estradiol or dihydrotestosterone showed, in comparison to the unlinked single agent, a significantly higher antineoplastic activity and a clearly lower systemic toxicity. But there is still only limited knowledge about the pharmacokinetic properties and the mode of action of these new drugs. For this reason in the present article a more comprehensive pharmacokinetic model and the pattern of distribution of new sexual-steroid-hormone-linked anticancer agents have been described.

Antineoplastic Agents↗
PubMed1981

Effect of ethinyl estradiol on development of mouse fetuses.

Pregnant ICR/JCL mice were given orally 0.02, 0.3, or 2.0 mg/kg body weight/day of ethinyl estradiol in olive oil or vehicle alone on day 11 through day 17 of pregnancy. Pregnant mice of another group received a single oral dose of ethinyl estradiol on day 8 or day 11 of pregnancy. A lethal effect on fetuses of both groups with single and continuous exposure to ethinyl estradiol was observed in a dose-response relationship. Growth suppression of fetuses was only found at term in a dose-response relationship following continuous exposure to ethinyl estradiol. Hypertrophic nipples were seen in 42% of surviving female fetuses prenatally exposed to 2.0 mg/kg of ethinyl estradiol singly on day 11 of gestation. There was not an increase in other congenital malformations in any of the treated groups. These findings indicate that administered ethinyl estradiol can affect the developing mouse embryo but the embryotoxic doses in the mouse are substantially greater than the usual therapeutic or contraceptive doses in the human.

Abnormalities, Drug-Induced↗
PubMed2006

Dose and temporal pattern of estrogen exposure determines neuroprotective outcome in hippocampal neurons: therapeutic implications.

To address controversies of estrogen therapy, in vitro models of perimenopause and prevention vs. treatment modes of 17beta-estradiol (E(2)) exposure were developed and used to assess the neuroprotective efficacy of E(2) against beta-amyloid-1-42 (Abeta(1-42))-induced neurodegeneration in rat primary hippocampal neurons. Low E(2) (10 ng/ml) exposure exerted neuroprotection in each of the perimenopausal temporal patterns, acute, continuous, and intermittent. In contrast, high E(2) (200 ng/ml) was ineffective at inducing neuroprotection regardless of temporal pattern of exposure. Although high E(2) alone was not toxic, neurons treated with high-dose E(2) resulted in greater Abeta(1-42)-induced neurodegeneration. In prevention vs. treatment simulations, E(2) was most effective when present before and during Abeta(1-42) insult. In contrast, E(2) treatment after Abeta(1-42) exposure was ineffective in reversing Abeta-induced degeneration, and exacerbated Abeta(1-42)-induced cell death when administered after Abeta(1-42) insult. We sought to determine the mechanism by which high E(2) exacerbated Abeta(1-42)-induced neurodegeneration by investigating the impact of low vs. high E(2) on Abeta(1-42)-induced dysregulation of calcium homeostasis. Results of these analyses indicated that low E(2) significantly prevented Abeta(1-42)-induced rise in intracellular calcium, whereas high E(2) significantly increased intracellular calcium and did not prevent Abeta(1-42)-induced calcium dysregulation. Therapeutic benefit resulted only from low-dose E(2) exposure before, but not after, Abeta(1-42)-induced neurodegeneration. These data are relevant to impact of perimenopausal E(2) exposure on protection against neurodegenerative insults and the use of estrogen therapy to prevent vs. treat Alzheimer's disease. Furthermore, these data are consistent with a healthy cell bias of estrogen benefit.

Alzheimer Disease↗