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PubMed1996

[Cholesterol and its fractions in women after ovariectomy treated with estraderm TTS].

25 ovariectomized women mean age 47 +/- 5 years were treated with transdermal 17 beta Estradiol in the shape of Estraderm TTS 100 plasters. Drugs were administrated in 28 days cycles during 24 weeks. Chlormadinon in daily dose 2 mg was added from 16 to 28th day of the fourth therapeutic cycle. Total cholesterol, triglycerides, HDL and LDL fractions were checked using enzymatic method. First measurement was done before the treatment, the next in the last day of every cycle. Results were statistically analysed. After treatment there were significant increase in the mean values of HDL, significant decrease of triglycerides. Changes in mean level of LDL and total cholesterol were not statistically significant. Our results seem to confirm the previous observations concerned with transdermal estrogen replacement therapy and its efficacy in atherosclerosis prophylaxis.

Administration, Cutaneous↗

PubMed1980

Induction of ovulation with chronic intermittent (pulsatile) administration of LH-RH in women with hypothalamic and hyperprolactinemic amenorrhea.

Five women with hypothalamic amenorrhea were treated with LH-RH (10-15 microg i.v. at 90 min intervals for 17-20 days). In all women this chronic intermittent LH-RH administration resulted in a normalization of serum gonadotropin levels. Four women exhibited preovulatory estradiol serum levels with subsequent LH peaks. In three women the LH peaks were followed by normal luteal phase serum progesterone levels. One woman with hyperprolactinemic amenorrhea was also treated with the same therapeutic regimen which induced ovulation as judged from normal luteal phase serum progesterone levels. The results indicate that normal pituitary-ovarian function can be established in hypothalamic amenorrhea by chronic intermittent administration of LH-RH. They also suggest that in the human female hypothalamic LH-RH function may be only permissive in that the cyclicity of endocrine events during the menstrual cycle is regulated on pituitary and ovarian levels. Hyperproactinemic amenorrhea appears to be associated with insufficient endogenous LH-RH secretion which can be substituted by exogenous chronic intermittent administration of LH-RH. Elevated prolactin levels per se do not interfere with the pituitary positive feedback mechanisms nor with the gonadotropin action on the ovarian level.

Adult↗

PubMed2001

Antiatherogenic effects of 17 beta-estradiol and 17 alpha-estradiol and its derivative J811 in cholesterol-fed rabbits with thyroid inhibition.

OBJECTIVE: The aim of this study was to investigate the antiatherogenic effects of 17 beta-estradiol and 17 alpha-estradiol and its derivative J811 (estra-1,3,5(10),8-tetraene-3, 17 alpha-diol), having a non-feminizing effect and high antioxidant potential, in male rabbits. EXPERIMENTAL DESIGN: Male White-Russian rabbits weighing 2.1-2.6 kg were fed either a standard or a high-cholesterol (200 mg/kg) diet, with thyroid function-inhibiting thiouracil (20 mg/kg) combined with cholic acid (40 mg/kg) administered daily in sunflower oil for 3 months. During the last month of the study, estrogens were administered by gavage at a dose of 0.02 or 0.1 mg/kg. RESULTS AND CONCLUSIONS: All three estrogens exerted remarkable antiatherosclerotic effects. Decreases in serum and aortic-wall lipid parameters and the index of atherogenicity were dependent on estrogen dose. Morphological evaluation of the aortic wall (height of plaques, size of plaque relative to aortic half-circumference) showed only weak therapeutic effects with all three estrogens. It is an open question whether the treatment period was too short to reverse the above changes. On the other hand, the data clearly suggest that 17 alpha-estradiol and J811 offer new perspectives for the prevention of atherosclerosis in men, which is similar to that found with 17 beta-estradiol in women.

Animals↗

PubMed1990

[Treatment with low-dose vaginal estradiol in post-menopausal women. A double-blind controlled trial].

Twenty-three postmenopausal women with recurrent cystitis were allorted at random to treatment for five months with local oestrogen in the vagina or placebo treatment with the object of assessing the local effect on the vaginal epithelium and on the tendency to recurrent cystitis. The therapeutic group and the placebo group were entirely comparable prior to treatment. In the therapeutic group, the oestrogen index in vaginal scrapings was significantly higher after treatment than in the placebo group (p less than 0.01). The number of positive urine cultures and the patients/satisfaction with treatment wee not significantly different in the two groups.

Administration, Intravaginal↗

PubMed2005

Aromatase inhibitors and cyclooxygenase-2 (COX-2) inhibitors in endometriosis: new questions--old answers?

The medical treatment of endometriosis needs to be optimized. Therapeutic management strategies for endometriosis-associated pain or recurrent disease are primarily aimed at downregulating ovarian function or antagonizing the effect of estrogen in ectopic endometrial implants. In this context, basic research is providing important results for the development of new, specific treatment modalities. Aromatase overexpression has recently been detected in endometriotic tissue. Aromatase (p450arom) is responsible for converting C19 androgens into estrogen in several types of human tissue. Aromatase activity causes local estrogen biosynthesis, which, in turn, stimulates prostaglandin E2 production by upregulating cyclooxygenase-2 (COX-2). Thus, a positive feedback cycle develops between the two systems. Another abnormality in endometriosis, the deficient 17beta-hydroxysteroiddehydrogenase type II (17beta-HSD-Type-II) expression, impairs the inactivation of estradiol to estrone. In contrast to the eutopic endometrium, these molecular aberrations increase the amount of local estradiol and prostaglandin E2 in endometriosis. In several human cell lines, prostaglandin and estrogen concentrations are associated with proliferation, migration, angiogenesis, apoptosis resistance and even invasiveness. Consequently, aromatase and COX-2 are thought to be promising new therapeutic targets. Thus, specific aromatase inhibitors (e.g. Letrozol/Femara, Anastrozol/Arimidex or Exemestan/Aromasin) or selective COX-2 inhibitors (e.g. Celecoxib/Celebrex, Rofecoxib/Vioxx, Valdecoxib/Bextra) are of great interest and should be studied in clinical trials in premenopausal woman with endometriosis to expand the spectrum of currently available treatment options.

Aromatase Inhibitors↗

PubMed2000

Steroid hormone activity of flavonoids and related compounds.

Soy isoflavones have been studied extensively for estrogenic and antiestrogenic properties. Other flavonoids, found in fruits, vegetables, tea and wine, have been much less tested for steroid hormone activity. We therefore assessed the estrogenic, androgenic and progestational activities of 72 flavonoids and structurally-related compounds. These compounds were tested on BT-474 human breast cancer cells at concentrations of 10(8)-10(-5) M, with estradiol (estrogen), norgestrel (progestin) and dihydrotestosterone (androgen) used as positive controls, and ethanol (solvent) as a negative control. pS2, an estrogen-regulated protein, and prostate-specific antigen (PSA), regulated by androgens and progestins, were quantified in tissue culture supernatants using ELISA-type immunofluorometric assays developed in-house. Of the 72 compounds tested, 18 showed estrogenic activity at 10(-5) M. Of this subset, seven also showed progestational activity at this concentration. The soy isoflavones, biochanin A and genistein, showed the most potent estrogenic activity, with a dose-response effect up to 10(-7) M. Of all other flavonoids, luteolin and naringenin displayed the strongest estrogenicity, while apigenin had a relatively strong progestational activity. Based on our data, we have formulated a set of structure/function relationships between the tested compounds. Flavonoids, therefore, exhibit significant steroid hormone activity, and may have an effect in the modification of cancer risk by diet, or in cancer therapeutics and prevention.

Breast Neoplasms↗

PubMed1999

Testosterone and its metabolites affect afterdischarge thresholds and the development of amygdala kindled seizures.

UNLABELLED: In boys with epilepsy, pubertal increases in seizure frequency may be associated with rising androgen levels. The present study tested the hypothesis that testosterone (T) and/or its metabolites might affect amygdala seizure thresholds and the development of secondary generalization from amygdala foci (kindling). Afterdischarge thresholds and kindling rate were measured in gonadectomized (GDX) male rats, with or without T replacement therapy. Drugs that block either androgen or estradiol (E(2)) receptor-mediated responses were also tested. METHODS: Kindling electrodes were implanted in the basolateral amygdala of adult male Wistar rats. In Experiment 1, subjects were GDX and implanted with a silastic capsule containing either: cholesterol (control); T; 5% E(2) in cholesterol; or 5alpha-dihydrotestosterone (DHT). In Experiment 2, intact subjects were treated with daily injections of vehicle (control); daily injections of flutamide (an androgen receptor antagonist); or Silastic implants containing 1,4,9-androstatriene 3,17-dione (ATD; an aromatase inhibitor). RESULTS: In Experiment 1, initial afterdischarge (AD) thresholds were significantly lowered by E(2) treatment, as compared to cholesterol controls, and remained low throughout the kindling paradigm. In T replaced males, AD threshold significantly decreased over the kindling period, a response that was not observed in DHT treated rats. Rates of kindling were significantly faster as a result of T, E(2) and DHT treatment, as compared to cholesterol controls. E(2) treated males kindled the fastest of all 3 groups. In Experiment 2, initial AD thresholds were significantly lowered by flutamide treatment, as compared to cholesterol controls, and remained low throughout the kindling paradigm. AD threshold significantly decreased over the kindling period in intact males, a response that was blocked by ATD treatment. Both flutamide and ATD significantly slowed the rate of kindling, as compared to intact controls. ATD had the most dramatic inhibitory effect on kindling rate. CONCLUSIONS: In males, T and its two metabolites, E(2) and DHT, all appear to enhance the development of amygdala-kindled seizures. E(2) has the most potent epileptogenic effect. Antagonism of E(2) mediated effects in the brain may have potential therapeutic value for males with epilepsy.

Amygdala↗

PubMed1977

Significance of quantitative assessment of estrogen receptors for endocrine therapy in advanced breast cancer.

The predictive significance of quantitative assessment of estrogen receptors in tumor tissue was analyzed in women with advanced breast carcinoma. Receptor concentration was measured by the 3H-estradiol binding capacity of the cytosol fraction of biopsies taken before initiation of the treatment. The E. O. R. T. C. criteria for the assessment of the patients' response were used. In a total of 34 assessments, 25 biopsies contained receptors; the remaining ones were negative. Objective remission to various endocrine therapies was recorded in only eight of the receptor-positive patients. Responses occurred along the whole scale of receptor concentrations with an apparent crowding in the region of the higher values. Linear logistic regression analysis revealed that among 12 variables of known prognostic value, receptor concentration was the most significant in relation to therapeutic response. Other significant variables were bone involvement and age. Computations yielded formulas that are presented in graph form and provide an estimate of the probability of a given patient to respond to endocrine treatments. On the other hand, the results suggest that all patients are possibly hormone dependent, although to variable degrees. The latter concept has very definite therapeutic implications.

Adrenalectomy↗

PubMed2001

Novel antitumor effect of estradiol in athymic mice injected with a T47D breast cancer cell line overexpressing protein kinase Calpha.

PURPOSE: Resistance to tamoxifen (TAM) represents a significant challenge to the management of breast cancer. We previously reported that the estrogen receptor (ER)-negative hormone-independent T47D:C42 cell line has both elevated protein kinase Calpha (PKCalpha) protein expression and basal activator protein-1 activity compared with the parental ER+ (hormone-dependent) T47D:A18 cell line. Stable transfection of PKCalpha to the T47D:A18 breast cancer cell line results in increased basal activator protein-1 activity, reduced ER function, increased proliferation rate, and hormone-independent growth (Tonetti et al., Br. J. Cancer, 83: 782-791, 2000). In this report, we further characterize the role of PKCalpha overexpression in vivo to elucidate a possible molecular mechanism of tamoxifen resistance. EXPERIMENTAL DESIGN: To determine whether the T47D:A18/PKCalpha cell line would produce hormone-independent tumors in athymic mice, we injected T47D:A18, T47D:A18/neo, or the T47D:A18/PKCalpha20 cell clones bilaterally into the mammary fat pads of athymic mice. Tumor growth was evaluated following treatment with estradiol (E2), TAM, and the pure antiestrogen, ICI 182,780. RESULTS: Mice receiving either T47D:A18 or T47D:A18/neo cells produced tumors that grew in response to E2 treatment, whereas the untreated control and TAM-treated groups showed no tumor growth. Interestingly, mice receiving the T47D:A18/PKCalpha20 clone produced tumors in both the control and TAM groups, whereas tumor growth was inhibited in mice treated with E2. PKCalpha was also overexpressed in an MCF-7 tumor model that also exhibited TAM-stimulated and E2-induced regression. CONCLUSIONS: These results suggest that overexpression of PKCalpha in breast tumors results in hormone-independent tumor growth that cannot be inhibited by TAM treatment. Furthermore, the finding that E2 has an antitumor effect on breast tumors overexpressing PKCalpha is a novel observation that may have important therapeutic implications.

Animals↗

PubMed1978

Subpopulations of breast carcinoma defined by S-phase fraction, morphology, and estrogen receptor content.

The S-phase fraction (SPF), defined as the number of cells per hundred that showed evidence of nuclear DNA synthesis detectable by autoradiography after in vitro incubation with tritiated thymidine, was measured in 170 primary, invasive carcinomas of the breast. Assay for estrogen receptor was performed on tissue from 129 carcinomas, and 34 were also assayed for progesterone receptor. The concentration of estradiol-17 beta was measured in the serum of 69 patients. All carcinomas were analyzed for a variety of histologic features and were classified into morphologic types. SPF were lognormally distributed and were negatively correlated with the patient's age and presence of estrogen receptor, but not with presence of progesterone receptor, size of the carcinoma, number of axillary nodal metastases, or concentration of estradiol-17 beta in serum. The SPFs of lobular, mucinous, and tubular carcinomas were consistently low (geometric mean 1.2, range 0.05 to 3.55), and the SPFs of medullary and atypical medullary carcinomas were consistently high (geometric mean 14.0, range 7.77 to 20.2), whereas carcinomas of other types (not otherwise specified) had an intermediate geometric mean (4.7) and a broad range (0.09 to 25.4). The carcinomas that were not otherwise specified could be divided into three groups with different geometric mean SPFs by nuclear morphologic criteria (1.2 for minimal atypicality, 3.5 for moderate, and 7.9 for severe). Therefore it is possible to sort breast carcinomas histologically into groups with low, intermediate, and high SPF. Correlations between SPF, estrogen receptor content, and microscopic morphology indicate the existence of distinctive subpopulations of breast carcinoma that may have epidemiologic and therapeutic importance.

Adenocarcinoma, Mucinous↗

PubMed2001

Assessment of endocrine status in patients undergoing in-vitro fertilization treatment. Is it necessary?

Endocrine evaluation as a prerequisite for every patient undergoing routine in-vitro fertilization (IVF) and embryo transfer for tubal or male factor infertility is still a matter of debate. The aim of this study was to determine if a full endocrine work-up, including the measurement of androgens, gonadotropins, prolactin and TSH, is conclusive for the subsequent success in IVF/ET. 71 infertile women without known endocrinopathies (e.g., polycystic ovarian disease), who were scheduled to enter the IVF/ET program were studied under strictly standardized conditions during the follicular phase of a natural cycle. Fasting serum concentrations of follicle stimulating hormone, luteinizing hormone, oestradiol, progesterone, prolactin, testosterone (T), dehydroepiandrosterone, 17-OH-progesterone, androstenedione and thyroid stimulating hormone (TSH) were measured using commercially available radioimmunoassays. Ovarian stimulation was performed by a long gonadotrophin-releasing hormone agonist/human menopausal gonadotrophin protocol. The overall clinical pregnancy rate was 15.5% in the first started IVF cycle. While patients who conceived in the first treatment cycle had significantly lower T levels (368 +/- 49 pg/ml) than those who did not (518 +/- 27 pg/ml, p=0.042, Kruskal & Wallis H-test), but the percentage of women with elevated T concentrations was not different. Similarly, TSH concentrations were significantly higher in women with a clinical pregnancy (1.9 +/- 0.2 mU/ml) than in non-pregnant women (1.4 +/- 0.3 mU/ml, p=0.046), but levels were still within the normal range. There were no further significant differences in hormone levels between pregnant and non-pregnant patients. These results do not suggest the measurement of a full hormonal profile in all infertile women before IVF/ET in non-endocrine infertility, taking into account the low likelihood to identify endocrinological disturbances, the considerable cost of endocrine testing and the paucity of therapeutic consequences.

17-alpha-Hydroxyprogesterone↗

PubMed2003

The menopausal mouse: a new neural paradigm of a distressing human condition.

Progressive and long-term sex hormone imbalance in the FSH-R haploinsufficient menopausal mouse leads to degenerative changes in the CNS associated with increased anxiety. The brain region most affected by aging in these mice is the hippocampus. Choline acetyltransferase (ChAT) enzymatic activity and synapsin immunoreactivity are reduced at 20 months of age. Neurons in the dentate gyrus show signs of progressive degenerative changes, hypertrophy and glyosis, and subsequent cell shrinkage and death. These results suggest that the menopausal mouse mimics degenerative changes in the hippocampus of hormonally imbalanced aging humans. We propose using this animal model to test the effectiveness of potential therapeutics in paradigms of accelerated aging.

Aging↗

PubMed1987

Effects of subcutaneous oestradiol implants on ovarian activity.

The effects of subcutaneous oestradiol implants on ovarian activity were investigated in 14 ovulating premenopausal women. Treatment with either 100 mg or 150 mg oestradiol was combined with cyclical oral norethisterone from days 20 to 26 of the cycle to ensure regular withdrawal periods and prevent endometrial hyperplasia. Ovarian function was monitored by regular pelvic ultrasonography and urinalysis over a period of nine cycles. During the first three cycles after hormone implantation, follicular development continued in almost half the study group, but only one of the women in each treatment group showed signs of follicular rupture and luteinization. By the sixth cycle, over half the women given the lower dose of oestradiol were developing follicles, including a large functional cyst in one, but none of them ovulated. A further implant given early in the seventh cycle was associated with ovarian suppression in all cases. Both doses of implant elevated the excretion of oestrone-3-glucuronide compared to pretreatment. The contraceptive and therapeutic implications of these results are discussed.

Adult↗

PubMed1996

The corpus luteum insufficiency: a multifactorial disease.

The pulsatile release pattern of LH during the entire menstrual cycle is well defined; however, the response of corpora lutea to these LH pulses in patients suffering from corpus luteum insufficiencies (CLI) is largely unknown. Patients suffering from CLI were selected from infertile patients on the basis of low progesterone (P < 25 nmol/L) in a blood sample withdrawn during a monitoring cycle. During the next cycle, nine blood samples were collected during the follicular and luteal phase and follicular development was assessed by vaginal sonography. Of 109 patients who had a CLI in the monitoring cycle, 55 had a CLI again, and 38 women agreed to undergo assessment of pulsatile hormone secretion. These women again had P < 25 nmol/L at days 6 and 7 of the luteal phase and blood samples were withdrawn through antecubital vein catheters from 0900-1700 h at 10-min intervals on days 7, 8, or 9 following ovulation. From 38 patients with such defined CLI, 16 (42%) had no LH episode and significantly lower basal LH levels in comparison with 14 control subjects. Thirteen (34%) of the patients had normal appearing LH episodes despite too low P and E2 concentrations, but their CL did not react to the LH episodes. The remaining 9 patients (24%) had normal LH episodes; their CL reacted to these episodes, but their basal P levels were too low. In all blood samples LH was not only determined using an immunoassay but also by the mouse Leydig cell testosterone production bioassay. It could be established that no CLI exists, which is due to the release of bioinactive LH. It is anticipated that the differentiation of three different types of CLI, one of hypothalamic and two of ovarian origin, may allow the development of differential diagnostic and therapeutic tools in the future.

Adult↗

PubMed1982

[Therapy in estrogen deficiency of the vagina].

Oestro-Gynaedron or Kolpi-Gynaedron vaginal gel were applied by the authors to 53 patients for treatment of oestrogen deficit of differentiated aetiology. The patients were between 17 and 73 years old. The therapy resulted soon in mitigation of subjective complaints, that is perception of burning, stinging, and dryness. The majority of patients was entirely free of complaints, following treatment. The cytological condition of atrophic colpitis was visibly improved. The authors are in agreement with numerous data in the literature according to which colpitis vetularum complaints can be completely eliminated by application of Oestro-Gynaedron or Kolpi-Gynaedron, with the colpocytological pattern being improved. Oestro-Gynaedron and Kolpi-Gynaedron were found to be properly applicable. Both medicaments have added greatly to the therapeutic potential by which to get to grips with fluor vaginitis.

Adolescent↗

PubMed2004

T lymphocytes do not directly mediate the protective effect of estrogen on experimental autoimmune encephalomyelitis.

Gender influences mediated by 17 beta-estradiol (E2) have been associated with susceptibility to and severity of autoimmune diseases such as diabetes, arthritis, and multiple sclerosis. In this regard, we have shown that estrogen receptor-alpha (Esr1) is crucial for the protective effect of 17 beta-estradiol (E2) in murine experimental autoimmune encephalitis (EAE), an animal model of multiple sclerosis. The expression of estrogen receptors among various immune cells (eg, T and B lymphocytes, antigen-presenting cells) suggests that the therapeutic effect of E2 is likely mediated directly through specific receptor binding. However, the target immune cell populations responsive to E2 treatment have not been identified. In the current study, we induced EAE in T-cell-deficient, severe combined immunodeficient mice or in immunocompetent mice with encephalitogenic T cells from wild-type Esr1+/+ or Esr1 knockout (Esr1-/-) donors and compared the protective E2 responses. The results showed that E2-responsive, Esr1+/+ disease-inducing encephalitogenic T cells were neither necessary nor sufficient for E2-mediated protection from EAE. Instead, the therapeutic response appeared to be mediated through direct effects on nonlymphocytic, E2-responsive cells and down-regulation of the inflammatory response in the central nervous system. These results provide the first demonstration that the protective effect of E2 on EAE is not mediated directly through E2-responsive T cells and raise the alternative possibility that nonlymphocytic cells such as macrophages, dendritic cells, or other nonlymphocytic cells are primarily responsive to E2 treatment in EAE.

Animals↗

PubMed1989

Contrasting ability of antiestrogens to inhibit MCF-7 growth stimulated by estradiol or epidermal growth factor.

A potential mechanism is described by which a growth factor may prevent the action of antiestrogens or reactive the growth of hormone-responsive breast carcinoma in patients undergoing tamoxifen (TAM) treatment. Epidermal growth factor (EGF)-stimulated growth (10(-8) M EGF) was assayed in the MCF-7 breast cancer cell line in the presence of various concentrations (10(-10) to 10(-6) M) of three antiestrogens, 4-hydroxytamoxifen (OH TAM), TAM and ICI 164384. In each case, the EGF-stimulated increases in DNA were not inhibited by the antiestrogen. OH TAM and ICI 164384 inhibited estradiol (E2) stimulated cell proliferation in a dose-related fashion. However, in the presence of both E2 and EGF, these two antiestrogens inhibited E2 effects only; EGF promotion of growth was unaffected. Pretreatment of MCF-7 cells for 2 days with either OH TAM or ICI 164384 did not inhibit EGF-induced increases in cell proliferation. We propose that eventual antiestrogen therapeutic failure may be caused by the paracrine influences of growth factors from neighboring cells.

Breast Neoplasms↗

PubMed2002

Morphometric analyses of endometriotic tissues to determine their grade of activity.

The last revised classification of endometriosis of the American Fertility Society takes the extension of endometriotic lesions and the three macroscopic appearances of this disease into consideration. The aim of this study was to determine whether morphometric analyses are able to describe the grade of activity of endometriotic lesions according to their macroscopic-morphological appearances. Endometriotic samples of 45 patients were analyzed morphometrically using a semiautomatical planimeter. Six different parameters were investigated: the cytoplasmic surface of epithelial cells, the nucleus surface of epithelial cells, the nucleus surface of stromal cells, the gland surface, the gland circumference and the gland diameter. No statistically significant differences (p > 0.05) between the macroscopic appearances of the endometriotic lesions and the six analyzed morphometric parameters were found. The majority of the endometriotic lesions showed median values for the cytoplasmic surface of epithelial cells, the nucleus surface of epithelial cells and the gland surface that did not differ from the median values of all tissues, independently of the macroscopic appearances of these lesions and of the corresponding serum hormonal levels of 17 beta-estradiol and progesterone that were measured at the time of biopsy (p > 0.05). Our morphometric data showed that the red and so-called 'active' endometriotic lesions did not exhibit different morphometric characteristics from the so-called 'inactive' black or white lesions. We found that white and black lesions showed in some cases higher morphometric values than the mean values, so that these macroscopic appearances of endometriotic lesions cannot be considered as 'burned-out' endometriotic tissues. Therefore, black or white endometriotic lesions also have to be considered as therapeutically relevant, as they cannot be defined as 'inactive' endometriosis.

Adult↗