Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Estrogen Receptor Modulators”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,441 records · Page 80Linked to original sources
PubMed2005

Sodium nitroprusside-induced osteoblast apoptosis is mediated by long chain ceramide and is decreased by raloxifene.

Release of high levels of nitric oxide (NO) is associated with osteoblastic cell death. The mechanisms of NO-induced cytotoxicity are not well documented and it is presently not known if estrogenic compounds prevent this effect. We studied the role of ceramides in cell death induced by the NO donor sodium nitroprusside (SNP) and we tested the possibility that 17beta-estradiol, the anti-estrogen ICI 182.780 and two selective estrogen receptor modulators raloxifene and tamoxifen modify osteoblastic cell apoptosis. SNP dose-dependently decreased MC3T3-E1 osteoblast viability, increased NO production in the culture media and enhanced the release of intracellular ceramides C22 and C24. Cell death induced by SNP was partially inhibited when MC3T3-E1 cells were pretreated with raloxifene and tamoxifen but was not modified when the cells were pretreated with 17beta-estradiol or ICI 182.780. Cell death induced by SNP resulted from apoptosis as demonstrated by Annexin-V and propidium iodide labeling and a reduction of SNP-induced MC3T3-E1 apoptosis was confirmed in the presence of raloxifene and tamoxifen. SNP induction of C22 and C24 production was inhibited by a pretreatment with raloxifene but not with 17beta-estradiol. Moreover, the synthetic ceramide C24 (0.75 and 1microM) decreased MC3T3-E1 cell viability and osteoblast cell death induced by C24 was partially decreased by raloxifene and to a lesser extent by 17beta-estradiol. These data demonstrate that SNP-induced cell death is mediated by the long chain ceramides C22 and C24 and that raloxifene protected osteoblast from apoptosis induced by SNP, an effect that might be relevant to its pharmacological properties on bone remodeling.

Animals↗
PubMed2004

Sex and gender issues and venous thromboembolism.

At least 250,000 episodes of VTE leading to hospitalization or death are estimated to occur in the United States each year. A number of clinical and demographic risk factors for VTE are recognized,with the latter including both age and race. Overall,the incidence of VTE does not appear to vary significantly by sex, as evidenced by a lack of consistency in the magnitude and even direction of effect of sex in a variety of epidemiologic studies of varying design. Several studies have shown a higher incidence among women than men during childbearing age. The issue of a gender effect on the natural history of VTE has not been well studied. The main influence of gender on VTE is the relationship between female gender and several well-recognized clinical risk factors for VTE:oral contraceptive use, hormone replacement therapy, estrogen receptor modulator therapy, and pregnancy. Hormonal therapies are associated with a twofold to threefold increase in VTE incidence. Risk is higher with some formulations than others, during initial use, and among women who are obese, smoke, or have one of several forms of heritable thrombophilia. The pregnant state is associated with a threefold to fivefold increase in VTE risk, and thromboembolism is a major cause of peripartum death. Heritable thrombophilias are also important co-determinants of VTE risk in pregnancy. The mechanisms through which pregnancy and hormonal therapies increase VTE risk have not been definitively established, but hormonal effects on levels of coagulation and anticoagulation factors likely play a role. Venous compression and venous injury also contribute to increased risk during pregnancy and the puerperium. Approaches to diagnosis of VTE in the pregnant woman are largely the same as in the nonpregnant patient, but special treatment considerations do apply. Warfarin is embryopathic, particularly between the 6th and 12th weeks of pregnancy, and should be avoided in favor or heparin or low-molecular weight heparin when treatment of the pregnant woman is necessary. Guidelines have been published to assist the clinician in decision making about prophylaxis of pregnant women at increased risk or pregnancy-related or post-partum VTE.

Contraceptives, Oral↗
PubMed2006

Old and new perspectives in the pharmacological treatment of advanced or recurrent endometrial cancer: Hormonal therapy, chemotherapy and molecularly targeted therapies.

Hormonal therapy and chemotherapy play a major role in the management of advanced or recurrent endometrial cancer. Progesterone therapy obtains overall response rates ranging from 11% to 25% in patients with endometrioid-type tumours, and oral medroxyprogesterone acetate 200mg daily appears to be a reasonable therapeutic option for those lesions that are well differentiated and/or have a high progesterone receptor (PgR) content. However, the activity of progestins is often compromised by the down-regulation of PgR within the target tissues, and therefore therapeutic strategies designed to enhance PgR expression are warranted. Little data are currently available about the new aromatase inhibitors and selective estrogen receptor modulators. As for chemotherapy, the combination of doxorubicin [DOX]+cisplatin [CDDP] achieves overall response rates ranging from 34% to 60%, and the addition of paclitaxel (TAX) seems to improve response rates, progression-free survival and overall survival, but to worsen toxicity profile. A phase III study is currently comparing TAX+DOX+CDDP versus the less toxic combination of TAX+carboplatin. Chemotherapy is active against both endometrioid-type carcinoma and uterine serous papillary carcinoma. However, this latter endometrial malignancy is less chemosensitive than the histologically similar high-grade serous ovarian carcinoma. Interesting fields of research are represented by investigational agents directed against specific intracellular signal transduction pathways involved in the proliferation, invasiveness and metastatic spread of endometrial cancer. Mammalian target of the rapamycin (mTOR) inhibitors, epidermal growth factor receptor inhibitors (gefitinib, erlotinib, lapatinib, the monoclonal antibody cetuximab), imatinib, the monoclonal antibody trastuzumab, and the Clostridium perfrigens enterotoxin are currently under evaluation as molecularly targeted therapies for endometrial cancer. Further investigations addressed to better understand the signal transduction pathways that are disregulated in endometrial carcinogenesis could identify novel biological targets suitable for tailored therapies.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2004

Effects of zearalenone on mRNA expression and activity of cytochrome P450 1A1 and 1B1 in MCF-7 cells.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a ubiquitous pollutant and promoter of carcinogenesis with both estrogenic and antiestrogenic effects in mammal epithelium. Zearalenone (ZEA) is a naturally occurring estrogenic contaminant of moldy feeds and is present in high concentrations in dairy products and cereals. Numerous studies describe a possible correlation between xenoestrogens and breast cancer risk. A potential mechanism for the etiology of breast cancer involves altered cytochrome P450 (CYP) enzymes. Since cocontamination of multiple compounds in our environmental and occupational circumstances likely happens and since few studies have addressed the molecular consequences of combinations of contaminants, we decided to investigate the effects of ZEA on basal and TCDD-induced mRNA expression and enzymic activity of CYP1A1 and CYP1B1 in human breast cancer MCF-7 cells. CYP1A1 enzyme activity was measured by the CYP1A1-referential activity assay, ethoxyresorufin O-deethylase (EROD), in MCF-7 cells. To investigate CYP1B1 activity, we employed the microsomal EROD assay prepared from baculovirus-infected insect cells expressing human cDNA CYP1B1. Reverse transcription-polymerase chain reaction was used to detect mRNA expression of CYP1A1 and CYP1B1 in MCF-7 cells. The results demonstrated that 10nM TCDD could readily induce a significant increase in the enzyme activity and mRNA expression of CYP1A1 in MCF-7 cells and 5 nM estradiol (E2) significantly reduced both basal and TCDD-induced activity and mRNA expression in MCF-7 cells. The same pattern was observed with 50nM ZEA. The estrogen receptor antagonist 4-hydroxytamoxifen could attenuate these inhibitive effects of both E2 and ZEA. Interestingly, Both E2 and ZEA could promote basal and TCDD-induced CYP1B1 activity but with no effect on CYP1B1 mRNA expression. These results suggest that the effect of ZEA on the TCDD-induced CYP1A1 activity and gene expression involved the estrogen receptor pathway and that the increase in the CYP1B1/CYP1A1 ratio underlying the basal or TCDD-treated condition might constitute one of the mechanisms underlying the synergic carcinogenic action of these compounds.

Aryl Hydrocarbon Hydroxylases↗
PubMed2005

Effect of tamoxifen, raloxifen and tibolon on bile components in ovariectomized rats.

The aim of the study was to investigate the effect of ovariectomy on the bile composition in order to estimate the ability of selective estrogen receptor modulators (SERMS) (tibolon, tamoxifen, raloxifen) to modify the ovariectomy-induced disorders. The study was carried out on the ovariectomized female Wistar rats. Tibolon (1 mg kg(-1) 24 h(-1)), tamoxifen (5 mg kg(-1) 24 h(-1)) and raloxifen (10 mg kg(-1) 24 h(-1)) were administered for 42 days. Under anesthesia bile was collected during 6h period. The ovariectomy increased significantly the excretion of biliary acids and calcium in bile and decreased the excretion of cholesterol and chloride. In rats treated with tamoxifen and raloxifen the excretion and concentration of cholesterol in bile were significantly reduced in comparison with ovariectomized rats. In rats treated with tibolon these values were increased. Moreover in rats treated with tamoxifen and raloxifen the concentrations of calcium in bile were significantly reduced. Tibolon had no significant effect on bile calcium concentrations. The therapy with tamoxifen, raloxifen and tibolon decreased the serum cholesterol concentrations, whereas the bile acid concentrations were increased in comparison with ovariectomized control. The drugs studied had no significant effect on calcium and chloride serum concentrations. Our results suggest that the therapy with tamoxifen and raloxifen may have the positive effect on bile composition in ovariectomized rats and probably may prevent the gallstone formation.

Animals↗
PubMed2004

Treatment with tamoxifen reduces hypoxic-ischemic brain injury in neonatal rats.

Tamoxifen, an estrogen receptor modulator, is neuroprotective in adult rats. Does tamoxifen reduce brain injury in the rat pup? Seven-day-old rat pups had the right carotid artery permanently ligated followed by 2.5 h of hypoxia (8% oxygen). Tamoxifen (10 mg/kg) or vehicle was given i.p. 5 min prior to hypoxia, or 5 min after reoxygenation, with a second dose given 6 h after the first. Brain damage was evaluated by weight deficit of the right hemisphere 22 days following hypoxia and gross and microscopic morphology. Tamoxifen pre-treatment reduced brain weight loss from 21.5+/-4.0% in vehicle pups (n=27) to 2.6+/-2.5% in the treated pups (n=22, P<0.05). Treatment 5 min after reoxygenation reduced brain weight loss from 27.5+/-4.0% in vehicle pups (n=42) to 12.0+/-3.9% in the treated pups (n=30, P<0.05). Tamoxifen reduces brain injury in the neonatal rat.

Animals↗
PubMed2006

Long-term fracture risk among women with proven endometriosis.

OBJECTIVE: To determine whether women with pelvic endometriosis are at increased fracture risk. DESIGN: Historical cohort study. SETTING: Population-based investigation using the data resources of the Rochester Epidemiology Project. PATIENT(S): From Olmsted County, Minnesota, 987 women with endometriosis that was first surgically visualized or histologically proven in 1970-1989. INTERVENTION(S): None, observational study. MAIN OUTCOME MEASURE(S): Follow-up for fractures through complete inpatient and outpatient community medical records. RESULT(S): In 17,408 person-years of follow-up, 256 women experienced 449 different fractures. The cumulative incidence after 20 years (30.8%) was not elevated relative to that expected (30.6%). The independent predictors of any fracture included age (hazard ratio [HR] per 10 years: 1.61; 95% confidence interval [CI] 1.42-1.84]), corticosteroid use (HR: 2.78; 95% CI 1.48-5.24), prior hip, spine, or forearm fracture (HR: 1.82; 95% CI 1.10-3.02), and use of the selective estrogen receptor modulators, tamoxifen or raloxifene (HR: 4.34; 95% CI 2.14-8.81); physical activity was protective (HR: 0.40; 95% CI 0.18-0.88). There was no significant influence on fracture risk of surgery or other medical treatments for endometriosis. CONCLUSION(S): Despite reported adverse effects of treatment on bone density, there was no overall increase in long-term fracture risk in this unselected cohort of women with proven endometriosis.

Adolescent↗
PubMed2006

[Is the clinical profile of women treated with tibolone similar to that of women receiving a classical estrogen-progestogen therapy? Data from a nationwide survey in France].

OBJECTIVES: To compare the pre-existing risk profiles for breast or endometrial cancer of menopaused women receiving tibolone or another hormone replacement therapy in France, with a view to examining the possibility of biases of selection of patients and of detection of these cancers in the Million Women Study. PATIENTS AND METHODS: Nationwide survey conducted in France among a representative sample of 153 gynaecologists. The particulars of the last two consulting menopaused women treated with tibolone (N = 306) and of the last two treated with a classical estrogen-progestogen therapy (N = 306) were collated then analysed. RESULTS: Compared to those treated with a classical estrogen-progestogen therapy, more women receiving tibolone were aged 60 years or over (40 vs 31%; P < 0.01). More of them had risk factors for breast cancer (history of mastodynia or mastopathy, elevated mammographic breast density) (6 vs 50%; P < 0.01). More of them had a history of uterine investigation or exploration or of irregular bleeding (61 vs 53% of women with a history of irregular bleeding; P < 0.05). Overall, 84% of women treated with tibolone had at least one risk factor for breast or endometrial cancer vs 75% of those receiving a classical estrogen-progestogen therapy (P < 0.01). DISCUSSION AND CONCLUSION: Owing to its specific properties, tibolone is generally prescribed to women with a higher risk profile for breast or endometrial cancer than those receiving a classical estrogen-progestogen therapy, which may entail patient selection and cancer detection biases in non-randomised, open-label, observational studies.

Age Factors↗
PubMed2005

Resveratrol as an anticancer nutrient: molecular basis, open questions and promises.

The polyphenol resveratrol is an anticancer nutrient that was shown to inhibit cancer initiation and promotion [Jang M, Cai L, Udeani GO, Slowing KV, Thomas CF, Beecher CW, et al. Cancer chemopreventive activity of resveratrol, a natural product derived from grapes. Science 1997;275:218-20]. The absorption, transport and metabolism of resveratrol will be reviewed as well as its actions in multiple pathways involved in the regulation of the cell cycle and the induction of apoptosis. Resveratrol acts as a selective estrogen receptor modulator (SERM) and regulates proteins involved in DNA synthesis and cell cycle, such as p(53) and Rb/E2F, cyclins, cyclin-dependent kinases (CDKs) and their inhibitors. Resveratrol affects the activity of transcriptional factors involved in proliferation and stress responses, such as NF-kB, AP1 and Egr1. Part of these events is mediated by mitogen-activated protein kinases (MAPKs) and tyrosine kinases (e.g., Src) and leads to the modulation of survival and apoptotic factors [e.g., Bcl2 family members, inhibitors of apoptosis (IAPs), ceramide] as well as enzymes involved in carcinogenesis [cyclooxygenases (COXs), nitric oxide synthase (NOS), phase I and II enzymes]. Moreover, resveratrol affects the expression and the activity of cotranscriptional factors such as p(300) and sirtuin 1. Thus, resveratrol potential as an anticancer chemopreventive and chemotherapeutic agent and its implication in the prosurvival versus prodeath pathway induction will be discussed.

Animals↗
PubMed2004

Effect of hormone replacement therapy and tibolone on serum leptin levels in postmenopausal women.

OBJECTIVE: To evaluate the effect of estrogen replacement therapy (ERT), continuous combined hormone replacement therapy (HRT) and tibolone on serum leptin levels in healthy postmenopausal women. METHODS: Eighty-four healthy postmenopausal women aged 43-63 years were studied prospectively. Hysterectomized women (n = 16) received conjugated equine estrogens (CEE) 0.625 mg. Women with an intact uterus were randomly allocated either to CEE+medroxyprogesterone acetate (CEE/MPA) 5 mg or tibolone 2.5 mg. Serum leptin levels were assessed at baseline and after 6 months of treatment. RESULTS: The three groups did not differ with respect to age, body mass index (BMI) or baseline serum leptin levels. Overweight women (BMI > 25 kg/m2) had higher baseline leptin levels (27.0 +/- 11.4 ng/ml) compared to their lean counterparts (BMI < or = 25 kg/m2; leptin: 16.5 +/- 8.1 ng/ml, P = 0.0001). Neither CEE nor CEE/MPA had any effect on serum leptin levels at the end of 6 months either in overweight or in lean women (overweight: CEE baseline 34.4 +/- 13.3 ng/ml, 6 months 36.9 +/- 15.8, P = 0.89, CEE/MPA baseline 22.4 +/- 9.8 ng/ml, 6 months 26.8 +/- 8.7 ng/ml, P = 0.1; lean: CEE baseline 12.6 +/- 4.4 ng/ml, 6 months 13.2 +/- 5.8 ng/ml, P = 0.36, CEE/MPA baseline 17.2 +/- 10.6 ng/ml, 6 months 18.8 +/- 8.8 ng/ml, P = 0.31). Similarly serum leptin remained unchanged at the end of the study in both lean and overweight women on tibolone (overweight: baseline 22.9 +/- 8.1 ng/ml, 6 months 18.5 +/- 12 ng/ml, P = 0.37; lean: baseline 13.2 +/- 5.6 ng/ml, 6 months 17.3 +/- 8.4 ng/ml). CONCLUSION: BMI is a strong determinant of serum leptin levels in healthy postmenopausal women. Neither ERT/HRT nor tibolone exert any effect on serum leptin after 6 months in lean or overweight postmenopausal women. Further studies are required to verify the exact role of estrogen and tibolone on leptin production and function in postmenopausal women.

Adult↗
PubMed2005

Nitric oxide in postmenopausal women taking three different HRT regimens.

OBJECTIVE: To search and compare the effects of three different HRT regimens on nitric oxide levels of postmenopausal women. METHODS: Four groups of postmenopausal women were included in this prospective, randomised, placebo controlled study. 34 women used 0.625 mg conjugated estrogen continuously combined with 5 mg medroxyprogesterone acetate, 32 women used 2.5 mg tibolone, 26 women used 50 mcg transdermal estrogen alone continuously and 32 women used placebo for 12 months. Before the treatment and after 1 year, serum NO (nitrate/nitrite) and some other biochemical parameters were evaluated. RESULTS: All HRT using groups had increased serum nitric oxide levels significantly compared to placebo group and also there was not any difference among three HRT using groups concerning to increases in nitric oxide levels. CONCLUSION: Both conjugated estrogen combined with continuous progestin and transdermal estrogen alone and also tibolone increases serum nitric oxide levels of postmenopausal women equally for 12-months of treatment.

Administration, Cutaneous↗
PubMed2005

Vascular reactivity and atheromatous plaques in post-menopausal women on tibolone treatment. Open prospective study with Doppler ultrasonography in internal carotid artery.

BACKGROUND: Arteriosclerosis is the main cause of ischaemic ictus. The middle cerebral and anterior cerebral arteries, which irrigate over 70% of the entire cerebral tissue, spring from the internal carotid. Additionally, it is in the extracraneal vessels that embolism, thrombosis and stenosis originate more frequently. AIM: To evaluate the variations in blood flow (pulsatility index: PI) and to assess the evolution of atherogenic lesions (thickening of the vascular intima and the presence of atheromatous plaques) in the internal carotid artery after tibolone therapy. SUBJECTS AND METHODS: A total of 116 healthy menopausal women were included in this open, prospective and comparative study. Of them, 101 subjects completed the 48 weeks follow-up. Subjects were allocated in two groups: group T (n = 55) received 2.5mg/day of tibolone daily and group C (n = 61) was a free-treatment control group. To evaluate both resistance to blood flow and the existence and evolution of atheromatous plaques in the internal carotid, an ultrasonograph with a pulsed Doppler was used. The PI was used as the parameter of vascular tone. To study atherosclerotic lesions in the internal carotid artery, we used morphological criteria. Measurements were done before entering in the study, and at 12, 24, 36 and 48 weeks of treatment. RESULTS: After tibolone treatment the PI in the internal carotid artery was observed markedly diminished. Moreover, tibolone reduces both the thickness and length of atheromatous plaque and the degree of vascular stenosis. CONCLUSION: tibolone administration reduced the carotid atheromatous plaque in thickness and length and improved cerebral perfusion.

Arteriosclerosis↗
PubMed2005

The role of hormone replacement therapy in endometrial polyp formation.

OBJECTIVE: To evaluate the iatrogenic effect of different protocols of hormone replacement therapy (HRT) on endometrial polyp formation adjusting for the confounding effects of other factors such as age, parity, weight and menopausal status at menopause. METHODS: Out of 2685 menopause patients 375 (13.9%) eligible patients were enrolled. Patients were randomized to three HRT types and three equal groups were formed. The first group received Premelle 2.5 mg (Group-I) (0.625 mg conjugated estrogen + 2.5 mg medroxyprogestorone), the second received Kliogest (Group-II) (2 mg estradiol + 1 mg norethisterone) and the last received Livial (Group-III) (2.5 mg tibolone) at least for 36 months without giving a break. After the first 18 months patients had their first office hysteroscopy and it was repeated in every 6 months until the end of third year to find out new and recurrent endometrial polyps. RESULTS: Multiple regression analysis revealed that the type of HRT, late menopause and obesity increased the occurrence of endometrial polyps. In Group-I five polyps, in Group-II ten polyps and in Group-III two polyps were detected. There were significant differences between G-II and G-I and G-II and G-III (P < 0.05), but there was no significant difference between G-I and G-III (P > 0.05). 82.3% of the polyps were detected in the third and fourth hysteroscopic examinations. Endometrial polyp recurrence was encountered in 4 (23.5%) patients, 1 in G-I and 3 in G-II without a significant difference (P > 0.05). No malignancy was detected in any of the specimen. CONCLUSION: We observed that endometrial polyp formation may be dependent on the type and dosage of the estrogen and progestogen. Especially a progestogen with high antiestrogenic activity may play an important preventive role in the development of endometrial polyps.

Adult↗
PubMed2005

Assessment of DNA damage in postmenopausal women under hormone replacement therapy.

OBJECTIVE: To evaluate the possible DNA damage in peripheral blood leukocytes of postmenopausal women under different hormone replacement therapies (HRT), comet assay, a standard method for assessing genotoxicity has been used. METHOD: 46 women were categorized in three groups-Group A: 15 surgical menopausal women who underwent surgery for benign conditions, receiving conjugated equine estrogen, 0.625 mg/day (CEE) for 2.3 +/- 1.5 years, Group B: 16 spontaneous menopausal women receiving conjugated equine estrogen, 0.625 mg/day plus medroxyprogesteron acetate, 5mg/day (CEE + MPA) for 2.4 +/- 1.0 years and Group C: 15 spontaneous menopausal women receiving tibolone, 2.5mg/day for 2.4 +/- 1.3 years. Control group consisted of 15 spontaneous menopausal women who never had HRT. RESULTS: Significant differences in terms of DNA damage were observed between Group A and B with controls as mean total comet scores 23.93 +/- 5.84, 19.44 +/- 6.19 and 10.07 +/- 2.40, but no significance (P > 0.05) were detected between Group C and controls as mean total comet scores 12.07 +/- 3.65 and 10.07 +/- 2.40, respectively. CONCLUSION: Reduced DNA damage were observed with tibolone compared to CEE or CEE + MPA therapy. Studies of this approach are needed.

Case-Control Studies↗
PubMed2005

Postmenopausal hormone therapy and mammographic breast density.

OBJECTIVE: The aim of this study was to evaluate the effects of different types of hormone replacement therapy (HRT) on mammographic density. MATERIALS AND METHODS: In a prospective 1-year study, 103 postmenopausal women were randomized to receive tibolone 2.5 mg/die, continuous conjugated equine estrogens 0.625 mg/die plus medroxyprogesterone acetate (MPA) 5mg/die or placebo. Mammograms were performed at baseline and after 12 months of treatment. Mammographic density was quantified according to the Wolfe classification. RESULTS: After 12 months of HRT 16 of the 35 patients (45.1%) receiving continuous combined hormonal therapy showed an increase of breast density change in the Wolfe classification. After treatment with tibolone, an up grading in breast density, according to Wolfe's classification, was found in 2 of the 43 patients (2.3%). No changes were recorded in the 25 patients of the control group. The difference between the group treated with continuous combined hormonal therapy and the control group was highly significant (p<0.001). The difference in breast density between patients in treatment with tibolone and the control group was not statistically significant (p=0.34). DISCUSSION: Continuous combination HRT may be more commonly associated with an increase of mammography density than tibolone treatment.

Breast↗
PubMed2005

Tibolone: clinical recommendations and practical guidelines. A report of the International Tibolone Consensus Group.

An international multidisciplinary panel of experts in the management of the menopause met at the 4th Amsterdam Menopause Symposium in October 2004 to determine the specific place of tibolone, a synthetic steroid with a unique clinical profile, within the wide range of currently available postmenopausal therapy options. The consensus was that tibolone is a valuable treatment option for women with climacteric complaints. As well as relieving vasomotor symptoms, tibolone has positive effects on sexual well-being and mood, and improves vaginal atrophy and urogenital symptoms. Prevention of bone loss with tibolone is comparable to that seen with estrogen therapy (ET) and estrogen/progestogen therapy (EPT). As tibolone rarely causes endometrial proliferation, no additional progestogen is required. It also has good tolerability, being associated with a low incidence of vaginal bleeding and of breast pain. Tibolone does not increase mammographic density. Absolute numbers of women at increased risk for breast cancer are estimated to be low or absent with both tibolone and ET, and the risk with tibolone should be significantly lower than that with EPT. Tibolone might therefore be preferable to EPT in certain women who have not been hysterectomised. Based on the evidence available, the panel proposed a number of subgroups of postmenopausal women with vasomotor symptoms in whom tibolone might have added value; these included women with sexual dysfunction, mood disorders, fibroids and urogenital complaints, as well as those with breast tenderness or high mammographic breast density with EPT use.

Estrogen Receptor Modulators↗