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At least 883 records · Page 49Linked to original sources
PubMed2003

Estrogen altered oral tolerance induction in type II collagen-induced murine arthritis.

BACKGROUND: Estrogen plays an important modulatory role in the immune system, and is concerned with the pathophysiology of autoimmune diseases such as rheumatoid arthritis (RA), although the mechanism has not yet been clarified. Oral tolerance, a form of specific peripheral tolerance, which is recognized as a new therapeutic strategy, is related to the function of gut-associated lymphoid tissue. METHODS: In this study, using collagen-induced arthritis as an animal model of RA, the effects of 17beta-estradiol (E2) on oral tolerance induction were investigated. For induction of oral tolerance, mice were fed 60 microg type II collagen (CII) for 10 consecutive days prior to each CII immunization. Mice in the E2 treatment groups were injected with 5 microg (low dose) or 500 microg (high dose) E2 three times during the induction of oral tolerance. RESULTS: Oral tolerance induction suppressed the occurrence of arthritis, the proliferative response of splenocytes to CII and the specific DTH response. However, E2 treatment abrogated the suppression, which might be connected with a change in function of Peyer's patch (PP) lymphocytes. CONCLUSION: These results suggest that oral tolerance induction might be affected by estrogen treatment through alteration of intestinal immune responses.

Animals↗
PubMedDate not supplied

Therapeutic and endocrine effects of Decapeptyl, synthetic LH-RH agonistic analogue in premenopausal women with metastatic breast cancer. A pilot phase II study.

Twelve premenopausal patients with advanced breast cancer were entered into pilot phase II study to assess efficacy, toxicity and influence of the synthetic LH-RH agonistic analogue D-Trp6-LH-RH (Decapeptyl) on the patients' hormonal status. The patients, aged 33-50, with newly diagnosed stage IV or recurrent breast cancer were not previously treated by any kind of endocrine therapy. Steroid receptor status was known in 9 patients. Decapeptyl was applied monthly at a dose of 3.75 mg i.m. until progression. The therapeutic response was evaluated in 11/12 patients. Partial remission was achieved in 5, stabilization in 3, and 3 consecutive patients failed to respond. The best therapeutic response was obtained in patients with pleuropulmonal and soft-tissue involvement, aged 41-45, including those with incomplete ovarian suppression, and regardless of steroid receptor status. The mean serum gonadotropins and estradiol levels were suppressed. The treatment was free of any side effects, except hot flushes in 7 patients.

Adult↗
PubMed2002

Gonadal function in adolescents and young women with juvenile systemic lupus erythematosus.

The authors analysed the gonadal function and age of menarche of 23 female adolescents and young women with SLE, and correlated these with clinical, SLEDAI and therapeutic parameters. The presence of one or more clinical and laboratory parameters defined normal gonadal function: normal menstrual cycles with or without dysmenorrhea; elevated cervical mucus length; normal levels of plasma FSH, LH, estradiol, progesterone, prolactin and testosterone; normal urinary hormonal cytology; serial pelvic ultrasound compatible with ovulatory pattern; and present or previous pregnancy. The mean age of menarche (13.5 +/- 1.4 years) was greater than that found among 2578 healthy Brazilian adolescents (12.5 +/- 1.3 years; P = 0.0002). The delay in menarche correlated with an increase in the duration of the disease (P = 0.0085) and the cumulative dose of prednisone (P = 0.0013) used until the appearance of the menarche. The mean phase length in SLE was 31.5 +/- 10.3. Sixteen female (70%) patients showed normal and seven (30%) abnormal gonadal function. Gonadal function was not correlated with parameters of SLE. These results suggest that the patients of this study reach adulthood with a high chance of fertility.

Adolescent↗
PubMed1991

[Clinical and immunohistological findings of juvenile nasopharyngeal angiofibroma experienced in the last six years].

Five patients with juvenile nasopharyngeal angiofibroma were found between 1984 and 1990 in our department. Clinical findings, treatment, and postoperative follow-up were reported. Two patients belonged to stage III and remnant 3 patients belonged to stage I. In cases of stage I, a surgical approach through the suprahyoid pharyngotomy was a worthy procedure to try, because angiofibroma was observed under direct vision and hemostasis was easy. In therapeutic planning, the authors emphasized the need of a preoperative staging classification based on CT scanning and selective angiography. In immunohistochemical studies, Langerhans cells with S-100 protein positive were found. Fibroblasts revealed estradiol positive but testosterone showed negative in all cases. Thus, juvenile nasopharyngeal angiofibroma was considered to be neoplasm related estradiol.

Adolescent↗
PubMed2006

Activation of estrogen receptor alpha increases and estrogen receptor beta decreases apolipoprotein E expression in hippocampus in vitro and in vivo.

Previous evidence indicates that, in carriers of apolipoprotein E4 (ApoE4), estrogen therapy increased the risk of late-onset Alzheimer's disease (AD), whereas in individuals carrying ApoE2/3, estrogen therapy reduced the risk of AD [Cauley JA, Zmuda JM, Yaffe K, Kuller LH, Ferrell RE, Wisniewski SR, Cummings SR (1999) J Bone Miner Res 14:1175-1181; Yaffe K, Haan M, Byers A, Tangen C, Kuller L (2000) Neurology 54:1949-1954]. Estrogen mechanisms of action are mediated by two estrogen receptors (ERs), ERalpha and ERbeta. In this study, we determined the relationship between ER subtype and estrogen regulation of ApoE expression in HT-22 cells ectopically transfected with ERalpha or ERbeta, in primary cultured rat hippocampal neurons in vitro and in rat hippocampus in vivo by both molecular biological and pharmacological analyses. Results of these analyses demonstrated that activation of ERalpha either by 17beta-estradiol or a specific-agonist, propylpyrazole triol, up-regulated ApoE mRNA and protein expression. In contrast, the ERbeta-selective agonist, diarylpropionitrile, down-regulated ApoE mRNA and protein expression. These results demonstrate that, in vitro and in vivo, ApoE expression can be differentially regulated depending on activation of ER subtypes. These data suggest that use of ER-selective ligands could provide therapeutic benefit to reduce the risk of AD by increasing ApoE expression in ApoE2/3 allele carriers and decreasing ApoE expression in ApoE4 allele carriers.

Alzheimer Disease↗
PubMed1990

Sex steroids in human brain tumors and breast cancer.

The concentrations of three sex steroids, estradiol, progesterone and testosterone, were analyzed by radioimmunoassay after celite chromatography in brain tumor and breast cancer tissues. The concentrations in malignant gliomas and breast cancers showed interindividual variations, especially evident with regard to estradiol. High estradiol concentrations were recorded in two patients with malignant astrocytoma. The concentrations of 1.00 pg/mg and 3.32 pg/mg were 10 to 30 times as high as in normal female brain. In five of ten astrocytomas the estradiol concentration was higher than the lowest breast cancer value. The distribution of progesterone seemed more even, and the level was significantly lower in brain tumors and breast cancers as compared with female brain, perhaps indicating an increased metabolism. Testosterone levels were somewhat higher in brain tumors, as compared with breast cancers, but not different from values in brain tissue. There were no significant age or sex correlation or differences in the concentrations of steroids in the brain tumors. The results suggest that manipulation of sex steroid metabolism in malignant brain tumors can be of beneficial therapeutic value as has been shown for breast cancer and prostatic carcinoma.

Adolescent↗
PubMed2000

Neuroprotective effects of estrogens on hippocampal cells in adult female rats after status epilepticus.

PURPOSE: Estrogens have neuroprotective effects in ischemia, stroke, and other conditions leading to neuronal cell death (e.g., Alzheimer's disease). The present study examined whether estrogens may have neuroprotective effects after seizures. METHODS: The kainic acid model was used to determine if estrogens protect hippocampal cells after status epilepticus in adult female rats. Rats were ovariectomized 1 week before hormone replacement. beta-Estradiol benzoate (EB; 2 microg in 0.1 mL of oil) was injected subcutaneously 48 and 24 hours before seizure testing. We administered kainic acid (16 mg/kg intraperitoneally) and behaviorally monitored the rats for 5 hours. After this time, all rats were injected with pentobarbital (50 mg/kg intraperitoneally) irrespective of seizure severity. Some rats received two additional doses of EB, one immediately and one 24 hours after the seizures. Another group of rats received only these two doses of EB after the seizures, and yet another group of rats received pretreatment with the intracellular EB receptor antagonist tamoxifen before each of four EB injections. Control rats received oil instead of EB. Rats were killed 48 hours after seizures. Neuronal damage was evaluated in silver-impregnated and Nissl-stained sections. RESULTS: Estrogen treatment before kainic acid administration significantly delayed the onset of kainic acid-induced clonic seizures, whereas it did not change the onset of status epilepticus compared with oil-treated controls. Furthermore, estrogen treatment significantly protected against kainic acid-induced seizure-related mortality. In control rats, examination of Nissl-stained and silver-impregnated slides revealed severe neuronal damage in the vulnerable pyramidal neurons of the hippocampal CA3 subfield and in the hilus of the dentate gyrus. Estrogen pretreatment, as well as the combination of pretreatment and posttreatment, significantly reduced the number of argyrophilic neurons in both the CA3 and the dentate gyrus. Posttreatment only had no protective effects. The data indicate that intracellular EB receptors mediate this type of neuroprotective effect, because the tamoxifen pretreatment abolished EB neuroprotection. CONCLUSIONS: Our results suggest that estrogens can be beneficial in protecting against status epilepticus-induced hippocampal damage. Hormonal conditions may have differential effects on underlying epileptic state in some patients. Therefore, more studies are necessary to determine the prospective therapeutic advantage of hormonal treatment in seizure-related damage.

Animals↗
PubMed2002

An unusual steroid-producing ovarian tumour: case report.

The rapid onset of virilization in a post-menopausal woman is usually the result of androgen secretion from a tumour of adrenal or ovarian origin. Androgen secreting neoplasms of the ovary are rare and usually show autonomous secretion. Rarely, these may be driven by the high levels of gonadotrophins seen in the post-menopausal state. We describe the case of a 67-year-old woman with high serum testosterone and estradiol in association with the high gonadotrophin levels usually associated with the post-menopausal state. All hormonal parameters showed a significant suppression over 12 h with administration of the GnRH antagonist, cetrorelix. This observation implies that excess hormone synthesis was of ovarian origin and was gonadotrophin driven. Localization of the tumour was not possible by conventional ultrasound or computerized tomography scanning, but was achieved by venous sampling. Complete cure was achieved by total abdominal hysterectomy and bilateral salpingo-oophorectomy, with restoration of the endocrine profile to that expected for a post-menopausal woman. Rapidly acting GnRH antagonists, such as cetrorelix, offer a safe and useful diagnostic and therapeutic option in the management of ovarian steroid-secreting tumours, which show gonadotrophin dependency.

Aged↗
PubMed1988

Comparison of in vivo and in vitro activity of estrogen-linked nitrosoureas in methylnitrosourea-induced rat mammary carcinoma.

The anticancer activity of estradiol-linked 2-chloroethylnitrosoureas in methylnitrosourea-induced rat mammary carcinoma was investigated using the short-term assay and the bilayer soft agar system after in vitro exposure as well as the monolayer methylcellulose assay following in vivo treatment. The aim was to evaluate to what extent previous in vivo findings are paralleled by the results of two in vitro test systems and the monolayer culture technique ex vivo. From the test systems investigated and under the conditions used, the results of the short-term test and the monolayer methylcellulose assay did not show a correlation with previous in vivo findings. Only the results of the bilayer clonogenic assay paralleled therapeutic parameters in vivo, although the degree of activity obtained in vivo was not reflected in vitro.

Animals↗
PubMed1989

Oestrogen induced suppression of collagen arthritis. IV: Progesterone alone does not affect the course of arthritis but enhances the oestrogen-mediated therapeutic effect.

The effects of 17 beta-oestradiol and progesterone on the development of type II collagen-induced arthritis (CIA) and the anti-type II collagen (CII) autoantibody response were investigated. Treatment with physiological doses of 17 beta-oestradiol, inducing serum levels below the estradiol peak at the end of pregnancy, abrogated the development of arthritis and suppressed the anti-CII autoantibody response. Treatment with progesterone alone did not have significant effects on the development of arthritis or on the anti-CII autoantibody response. However, a combined treatment with both progesterone and oestrogen in physiological doses induced a more pronounced suppression of CIA than the suppression induced with oestrogen treatment alone. These findings suggest that oestrogen, but not progesterone, may be the critical factor to explain the pregnancy-related down-regulation of CIA.

Animals↗
PubMed2006

Estrogen receptor positive breast cancer metastasis: altered hormonal sensitivity and tumor aggressiveness in lymphatic vessels and lymph nodes.

Breast cancers commonly spread to lymph nodes (LNs). If the primary tumors are estrogen receptor (ER) and/or progesterone receptor (PR) positive, then the likelihood that LN metastases express receptors exceeds 80%. However, due to lack of ER+ models, little is known about the role of hormones in breast cancer spread or the effects of the LN microenvironment on hormone responsiveness. We have developed metastasis models using ZsGreen labeled MCF-7 and T47D human breast cancer cells. Tumors are tracked in living mice by whole-body imaging, and macrometastases or micrometastases are detected by intravital imaging or fluorescence microscopy. Tumor growth is estrogen dependent and required for intratumoral lymphangiogenesis. Seventy-five percent of all tumors and >95% of larger tumors generate LN metastases. Occasionally more distant metastases are also observed. "Triads" of primary tumors, tumor-filled draining lymphatic vessels, and tumor-filled LNs from the same mouse show that (a) proliferation, as measured by 5-bromo-2'-deoxyuridine uptake, is higher in the LN than in the primary tumor. (b) High ER levels are extensively down-regulated by estradiol in primary tumors. However, there is partial failure of ER down-regulation in LNs associated with (c) reduced PR expression. This suggests that ER are dysfunctional in the LN microenvironment and perhaps hormone resistant. (d) CD44 is sparsely expressed in primary tumor cells but homogeneously overexpressed in cells transiting the lymphatics and populating LNs. We hypothesize that CD44 expression targets tumor cells for transport to, and uptake in, LNs. If so, the CD44 pathway could be targeted therapeutically to slow or prevent LN metastases.

Animals↗
PubMed1984

Testosterone, 17 Ks, 17 beta E2 FSH-LH variations and hirsutism modifications during spironolactone therapy.

The research here reported concerns 9 hirsute women, four of them with PCO and five with idiopathic hirsutism, who underwent treatment with spironolactone. 4 non hirsute hypertensive cases served as control. For one year hair growth, testosterone, 17 Ks, estradiol and gonadotropins behaviours were studied in all of the patients. Results clearly show that the peripherical response (the hair) to the therapy is only just sufficient, and corresponds to a good reduction of the androgenic hormones in blood. However, there is also an LH gonadotropin secretion reduction which is statistically scarcely significant. If the therapeutic response of hair were good, fetal risk could be prevented with safe and contemporaneous contraception. However, since the response is scarcely sufficient, we do not think this therapy is more advisable than other ones.

17-Ketosteroids↗
PubMed2005

Regulation of endogenous gene expression in human non-small cell lung cancer cells by estrogen receptor ligands.

Estrogen receptor (ER) agonists and antagonists elicit distinct responses in non-small cell lung cancer (NSCLC) cells. To determine how such responses are generated, the expression of ERalpha, ERbeta, and ER coregulators in human lung fibroblasts and human NSCLC cell lines was evaluated by immunoblot. Ligand-dependent estrogenic responses in NSCLC cells are probably generated via ERbeta and the p160 coactivator GRIP1/TIF2, because expression of these proteins was detected, but not full-length ERalpha or the p160 coactivator SRC-1. ERbeta and GRIP1/TIF2 are shown to interact in vitro in a ligand-dependent manner and thus may form functional transcription complexes in NSCLC cells. Furthermore, the capacity of ER ligands to regulate gene expression in NSCLC cells was explored using gene miniarrays. Expression profiles were examined after treatment with ER agonist 17-beta-estradiol (E2), the pure ER antagonist ICI 182,780 (fulvestrant, Faslodex), or epidermal growth factor, which served as a positive control for an alternative growth stimulus. E-cadherin and inhibitor of differentiation 2 were differentially regulated by E2 versus ICI 182,780 in 201T and 273T NSCLC cell lines. Epidermal growth factor also stimulated proliferation of these cells but had no effect on expression of E-cadherin and inhibitor of differentiation 2, suggesting they are specific targets of ER signaling. These data show that NSCLC cells respond to estrogens/antiestrogens by altering endogenous gene expression and support a model in which ICI 182,780 reduces proliferation of NSCLC cells via its ability to disrupt ER signaling. ICI 182,780 may therefore have therapeutic benefit in NSCLC.

Carcinoma, Non-Small-Cell Lung↗
PubMed2006

17-beta-Estradiol decreases p38 MAPK-mediated myocardial inflammation and dysfunction following acute ischemia.

Understanding the inflammatory response to myocardial ischemia is an important part of achieving the elusive clinical goal of perfect myocardial protection. While it is established that estrogen affects the chronic inflammatory processes of coronary atherosclerosis, the effects of estrogen on acute myocardial proinflammatory signaling are unknown. To study this, myocardial ischemia and reperfusion was performed in rat hearts from normal adult males, normal adult females, ovariectomized (OVX) females, males supplemented with E2, and OVX females supplemented with E2. Following reperfusion, homogenized hearts were analyzed for TNF-alpha, IL-1beta, and IL-6 gene and protein expression, p38 MAPK activation, and the apoptosis-related proteins caspase-3 and Bcl-2. Hearts from proestrus females demonstrated significantly better post-ischemic functional recovery than males. E2 supplementation to males and OVX females improved post-ischemic myocardial functional recovery, reduced the production of TNF-alpha, IL-1beta and IL-6, and decreased the activation of p38 MAPK and caspase-3 when compared to their untreated counterparts. These results suggest that the effect of estrogen on cardioprotection against myocardial I/R may be attributed to its anti-inflammatory and anti-apoptotic properties. Further understanding of these mechanisms may allow therapeutic manipulation of sex hormones in the treatment of acute ischemic injury.

Animals↗
PubMed1982

[Effect of bromocriptine on the endocrine profile during pregnancy].

In this paper, we revealed the changes in maternal plasma concentration of PRL, HCG, HPL, progesterone (P), estradiol-17 beta (E2), estriol (E3), estetrol (E4) and dehydroepiandrosterone-sulfate (DHEA-S) after the administration of bromocriptine during pregnancy. Blood samples were collected from 23 women with gestation ranging from 7 to 28 weeks. Sixteen patients had therapeutic abortion and other 7 patients had inevitable abortion. PRL, HCG, HPL, P, E2, E3, E4 and DHEA-S were measured by radioimmunoassay. The PRL decreased significantly at 120 and 180 minutes after the administration of bromocriptine in any case. In 4 cases out of 10 cases in early normal pregnancy, plasma E2 level decreased to 50% lower than the basal level, but no significant change of E2 occurred after bromocriptine in early and mid pregnancy. Bromocriptine made no change in HCG, HPL, P, E3, E4 and DHEA-S for any group. Our data suggested that bromocriptine had effect on only plasma PRL level, and this drug or the change of PRL level had no effect on P, estrogen, DHEA-S, HPL and HCG concentration during pregnancy.

Bromocriptine↗
PubMed1997

Estrogens attenuate neuronal injury due to hemoglobin, chemical hypoxia, and excitatory amino acids in murine cortical cultures.

A growing body of evidence supports the hypothesis that estrogens may be beneficial in Alzheimer's disease and other neurodegenerative processes. Less is known of their therapeutic potential in acute CNS insults. In this study, we assessed the effect of estrogens in three injury paradigms that may be relevant to CNS hemorrhage, trauma, and ischemia. Supraphysiologic concentrations of 17beta-estradiol, estrone, or equilin attenuated neuronal loss due to prolonged exposure to the pro-oxidant hemoglobin, with complete protection at 10 microM. Most of this effect persisted despite concomitant treatment with the antiestrogen ICI 182,780 or the protein synthesis inhibitor cycloheximide. In contrast, the non-estrogenic steroid methylprednisolone, which is currently in clinical use in spinal cord injury, reduced neuronal loss by only about 30%. High concentrations of equilin or estrone also attenuated the submaximal neuronal injury induced by 3.5-4.5 h exposure to the cytochrome oxidase inhibitor sodium azide, with near complete protection at 30 microM. Estrogens had a weaker and somewhat variable effect on pure excitotoxic injury, reducing neuronal loss due to 24 h kainate exposure by about half, and due to 24 h NMDA exposure by 15-65%; similar neuroprotection was provided by the antioxidant 21-aminosteroid U74500A. These results suggest that estrogens may be beneficial in acute CNS injuries associated with oxidative and excitotoxic stress. Investigation of high dose estrogen therapy in in vivo models of CNS hemorrhage, trauma, and ischemia is warranted.

Animals↗
PubMed1991

The Lupron screening test: tailoring the use of leuprolide acetate in ovarian stimulation for in vitro fertilization.

STUDY OBJECTIVE: To evaluate the prognostic and therapeutic value of a Lupron (leuprolide acetate; Tap Pharmaceuticals, North Chicago, IL) screening test before ovarian stimulation for in vitro fertilization (IVF). DESIGN: Prospective. SETTING: Outpatient IVF program. PATIENTS: Eighty patients exhibited four early estradiol (E2) patterns. Patients with pattern A and B remained on a flare-up ovarian stimulation protocol. Patients with pattern C were randomized to three ovarian stimulation protocols. Patients with pattern D were treated with the flare-up protocol using a high pure follicle-stimulating hormone (FSH) dose. RESULTS: Patterns, A, B, C, and D occurred in 44%, 16%, 25%, and 15% of the patients, respectively. The E2 pattern recurred in 77% of subsequent IVF cycles. Pattern A and B patients achieved a 41% (23/56) and 22% (5/23) ongoing pregnancy rate (PR) per stimulated cycle. An early luteal phase Lupron protocol had the best ongoing PR per stimulated cycle (10/27, 37%) in patients with a pattern C response. Pattern D patients had a 20% (5/25) ongoing PR per stimulated cycle. CONCLUSION: The Lupron screening test allows prospective selection of stimulation protocols in ovulatory patients undergoing IVF. Early E2 patterns A and B should be treated with the flare-up protocol. Pattern C patients benefit from the luteal phase Lupron protocol and pattern D patients benefit from a high pure FSH flare-up protocol.

Adult↗