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PubMed2003

Phytoestrogens: recent developments.

Phytoestrogens are polyphenolic non-steroidal plant compounds with estrogen-like biological activity. Based on their chemical structure, phytoestrogens can be classified into four main groups, i. e., isoflavonoids, flavonoids, stilbenes, and lignans. For each group, the chemistry, dietary sources and biotransformation of the most interesting compounds will be discussed. Since phytoestrogens are structurally very similar to the estrogen 17beta-estradiol, they may exhibit selective estrogen receptor modulating activities. Therefore, special attention will be given to the hormonal effects of various isoflavonoids, including genistein, daidzein, coumestrol and equol, several prenylated flavonoids, especially 8-prenylnaringenin, and the stilbene resveratrol. Furthermore, their non-hormonal effects will be discussed briefly. Finally, the latest developments on the potential protective properties of phytoestrogens and phytoestrogen-containing foods against hormone-dependent breast and prostate cancers and cardiovascular diseases, and as estrogen replacement therapy for postmenopausal women will be discussed.

Antineoplastic Agents, Phytogenic↗
PubMed1999

Clinical efficacy of raloxifene in postmenopausal women.

A new class of compounds known as selective estrogen receptor modulators (SERMs) may possess the optimal combination of characteristics desirable in a drug designed for use in postmenopausal women. Among this class of compounds, raloxifene is the most studied and is currently available for clinical use in some countries for the prevention of osteoporosis in post-menopausal women. Raloxifene is a non-steroidal benzotiophene derivative shown to prevent bone loss at axial and appendicular sites and reduce serum cholesterol, like estrogen, in oophorectomized rats and in postmenopausal women. In animal models, unlike estrogen, raloxifene does not stimulate breast or uterine tissues. These appealing attributes make raloxifene a potential treatment for osteoporosis and other menopause related risks in middle aged and elderly women. Multicenter studies have been performed in early postmenopausal women, randomly assigned to receive raloxifene 30, 60, or 150 mg/day or placebo. All subjects received a calcium supplement. Bone mineral density, which was measured twice a year over 24 months by dual X-ray absorptiometry, decreased significantly at all skeletal sites with placebo, and significantly increased with raloxifene at the spine, hip, and total body at the three doses. At 24 months, the mean increase with raloxifene 60 mg compared with placebo was 2.4% at the lumbar spine and at the total hip, and 2% at the total body. Markers of bone formation (serum osteocalcin and bone specific alkaline phosphatase) and of resorption (urinary CrossLaps) decreased significantly to the premenopausal range within 3-6 months of treatment with raloxifene. In addition, total serum and low-density lipoprotein cholesterol decreased significantly in all raloxifene therapy groups in a dose-related fashion. Serum HDL-cholesterol and triglycerides were not significantly changed by therapy. The most commonly observed side-effect was hot flushes, with patients taking raloxifene reporting a slightly higher rate of flushes (25%) than those on placebo (18%). This adverse event usually occurred within the first few months of therapy, was generally mild, and did not result in excess study dropout (raloxifene 1.5%, placebo 2.1%). Preliminary 2-year data indicated that raloxifene is not associated with an increased risk of breast cancer. In summary, the clinical efficacy and safety of raloxifene is very promising and this compound will offer a particularly attractive choice for postmenopausal women.

Cardiovascular Diseases↗
PubMed2002

Therapies to improve bone mineral density and reduce the risk of fracture: clinical trial results.

Osteoporosis is a skeletal disorder that is associated with lowered bone mineral density and increased risk of fracture. Numerous clinical trials have been conducted to study drugs and lifestyle changes that can either prevent bone loss in perimenopausal women or prevent fractures in women with established osteoporosis. The role of estrogen alone or in combination with androgen as hormone replacement therapy is discussed for its potential value in osteoporosis prevention and treatment. Additional therapies that are examined for prevention and treatment of osteoporosis include tibolone, bisphosphonates (alendronate and risedronate), selective estrogen-receptor modulators, calcitonin and parathyroid hormone. Experimental therapies that are in different phases of evaluation in osteoporosis management include statins as well as tumor necrosis factor-receptor antagonists. Other strategies include nonpharmacologic interventions, such as calcium supplements, vitamin D and exercise.

Aged↗
PubMed2003

Estrogen receptor-alpha and Sp1 interact in the induction of the low density lipoprotein-receptor.

Both estrogen and selective estrogen receptor modulators (SERMs) such as tamoxifen and raloxifene have been demonstrated to lower plasma low density lipoprotein (LDL)-cholesterol concentrations by stimulation of LDL receptor gene expression. To determine the molecular mechanisms of estradiol- and tamoxifen-induced LDL receptor expression, we performed transient transfection experiments with luciferase reporter gene-constructs under transcriptional control of the human LDL receptor promoter. We demonstrate, that estradiol and tamoxifen stimulate LDL receptor gene expression in human HepG2 hepatoma cells only when estrogen receptor (ER)-alpha but not when ER-beta is cotransfected. Deletion mutants and point mutations of the LDL receptor promoter reveal that estradiol- and tamoxifen-stimulated expression of this gene depends on an intact repeat 3 in the LDL receptor promoter, a cis-element previously shown to interact with Sp1. Gel mobility analyses demonstrated estradiol- and tamoxifen-stimulated binding of nuclear proteins to repeat 3 (bp -56 to bp -36) of the LDL receptor promoter. These data provide an alternative mechanism of LDL receptor gene expression by non-classical estradiol- and tamoxifen-stimulated induction through an ER-alpha/Sp1 complex.

Cell Line, Tumor↗
PubMed1999

Thrombophilic state in breast cancer.

Tumor cell metastasis and thrombosis are the major causes of death in cancer patients. Thrombosis in cancer patients may occur when physiologic antithrombotic systems are defective or when prothrombotic activities defeat normal physiologic antithrombotic mechanisms. Malignancies by themselves may already predispose to a hypercoagulable state in cancer patients. Tumor cells can either directly activate the blood clotting system or indirectly stimulate mononuclear cells to synthesize and express various procoagulants, subsequently leading to prothrombin activation, fibrin formation, and generation of a thrombus. In addition, other comorbid predisposing factors effecting thrombosis in cancer patients have to be considered, including surgery, bed rest, infection, long-term indwelling central venous catheters, anticoagulation, and chemotoxic or steroidal anticancer drugs used in adjuvant or palliative cancer treatment. Reliable information on the incidence of thromboembolism in cancer patients is available for breast cancer; less data have been reported for other malignancies. Chemo- and/or hormone therapy in patients with primary or metastatic breast cancer is associated with an increased thromboembolic risk, although the benefits of treatment far outweigh the risks. The current literature discussing the effect of chemo/hormone therapy on blood clotting factors and the associated risk of thrombosis is reviewed, with emphasis on new developments in the area of tissue-specific SERMs (selective estrogen receptor modulators). SERMs are employed as adjuvant therapy in primary breast cancer and in the palliation of advanced breast cancer and may be clinically useful as potential substitutes for long-term hormone replacement therapy, in the treatment of osteoporosis, and for cancer prevention therapy.

Antineoplastic Agents↗
PubMed2000

Osteoporosis prevention, detection, and treatment. A mandate for primary care physicians.

Prevention of bone loss through healthy lifestyle choices offers the greatest promise of minimizing fracture incidence. Safe, effective therapeutic options are available when drug therapy is prudent. Newer bisphosphonates, selective estrogen receptor modulators, and HRT delivery systems will soon be available to offer an even larger menu of choices for osteoporosis prevention and treatment. By implementing appropriate treatment, we can prevent bone loss, reduce fracture incidence, and improve function and quality of life, even in patients who have previously experienced fractures.

Alendronate↗
PubMed2004

Effects of conjugated equine estrogen vs. raloxifene on serum insulin-like growth factor-i and insulin-like growth factor binding protein-3: a 2-year, double-blind, placebo-controlled study.

OBJECTIVE: To assess and compare the effect of conjugated estrogen and of the selective estrogen receptor modulator raloxifene on serum levels of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) and on the IGF-I/IGFBP-3 ratio. DESIGN: A 2-year randomized, double-blind, placebo-controlled study. SETTING: Endocrinology outpatient department. PATIENT(S): Fifty-six postmenopausal, hysterectomized women. INTERVENTION(S): Women received raloxifene hydrochloride in doses of 60 mg/day (n = 15) or 150 mg/day (n = 13), conjugated equine estrogen (CEE) in doses of 0.625 mg/day (n = 15), or a placebo (n = 13) over the course of 2 years. MAIN OUTCOME MEASURE(S): At baseline and after 6, 12, and 24 months of treatment, serum levels of IGF-I, IGFBP-3, and insulin were measured, and an IGF-I/IFGBP-3 ratio was calculated. RESULT(S): Both raloxifene and CEE decreased serum IGF-I concentration. In contrast to CEE, which had no effect, both raloxifene doses of 60 and 150 mg/day significantly increased serum IGFBP-3 during the 2 years. Compared with placebo, the decrease in IGF-I/IGFBP-3 ratio was -32.5% (95% CI: -20.1; -44.8%) for CEE; -16.4% (95% CI: -3.6; -29.2%) for raloxifene at 150 mg/day; and -15.4% (95% CI: -1.0; -29.8%) for raloxifene at 60 mg/day. No effect of CEE or raloxifene was found on insulin concentration at any time point. CONCLUSION(S): Long-term use of both CEE and raloxifene decreases serum IGF-I and the IGF-I/IGFBP-3 ratio, but, unlike CEE, raloxifene produced a significant yet small increase in IGFBP-3.

Double-Blind Method↗
PubMed2005

Effects of dehydroepiandrosterone, Premarin and Acolbifene on histomorphology and sex steroid receptors in the rat vagina.

To assess the specific estrogenic and/or androgenic effects of a potential novel hormone replacement therapy, we have examined the morphology of the rat vagina 9 months after ovariectomy (OVX) and treatment of OVX animals with dehydroepiandrosterone (DHEA), conjugated estrogens Premarin and the selective estrogen receptor modulator Acolbifene. OVX led to atrophy and inflammatory changes while Acolbifene reduced the inflammation incidence and induced mucification of the vaginal epithelium. Premarin induced a typical keratinized stratified squamous epithelium while DHEA induced stimulation of the vaginal epithelium, with mucous cells typical of an androgenic effect, combined with increased collagen fiber compactness of the lamina propria. On the other hand, after OVX, the vaginal muscle layer decreased by 46%, an effect which was 41 and 100% reversed by DHEA and Premarin, respectively. The present data show particularly interesting effects of DHEA on the three layers of the vaginal wall, namely a highly mucified epithelium, an increased muscularis thickness and increased collagen fiber compactness in the lamina propria. DHEA exerts both androgenic and estrogenic effects on the vaginal mucosa, thus providing a more physiological replacement therapy.

Animals↗
PubMed2006

Comparative gene expression profiling reveals partially overlapping but distinct genomic actions of different antiestrogens in human breast cancer cells.

Antiestrogens used for breast cancer (BC) treatment differ among each other for the ability to affect estrogen receptor (ER) activity and thereby inhibit hormone-responsive cell functions and viability. We used high-density cDNA microarrays for a comprehensive definition of the gene pathways affected by 17beta-estradiol (E2), ICI 182,780 (ICI), 4OH-tamoxifen (Tamoxifen), and raloxifene (RAL) in ER-positive ZR-75.1 cells, a suitable model to investigate estrogen and antiestrogen actions in hormone-responsive BC. The expression of 601 genes was significantly affected by E2 in these cells; in silico analysis reveals that 86 among them include one or more potential ER binding site within or near the promoter and that the binding site signatures for E2F-1, NF-Y, and NRF-1 transcription factors are significantly enriched in the promoters of genes induced by estrogen treatment, while those for CAC-binding protein and LF-A1 in those repressed by the hormone, pointing to novel transcriptional effectors of secondary responses to estrogen in BC cells. Interestingly, expression of 176 E2-regulated mRNAs was unaffected by any of the antiestrogens tested, despite the fact that under the same conditions the transcriptional and cell cycle stimulatory activities of ER were inhibited. On the other hand, of 373 antiestrogen-responsive genes identified here, 52 were unresponsive to estrogen and 25% responded specifically to only one of the compounds tested, revealing non-overlapping and clearly distinguishable effects of the different antiestrogens in BC cells. As some of these differences reflect specificities of the mechanism of action of the antiestrogens tested, we propose to exploit this gene set for characterization of novel hormonal antagonists and selective estrogen receptor modulators (SERMs) and as a tool for testing new associations of antiestrogens, more effective against BC.

Breast Neoplasms↗
PubMed2004

Effect of raloxifene on activated protein C (APC) resistance in postmenopausal women and on APC resistance and homocysteine levels in elderly men: two randomized placebo-controlled studies.

Raloxifene, a selective estrogen receptor modulator, like hormonal replacement therapy increases the risk of venous thromboembolism in postmenopausal women. A possible explanation for the increased thrombotic risk could be an increase in acquired resistance to activated protein C (APC). In two randomized, placebo-controlled, double-blind studies we determined the effect of raloxifene on the normalized APC sensitivity ratios (nAPCsr). The nAPCsr were determined with the thrombin generation-based APC resistance test. In the first study 83 postmenopausal women (age, 51.1 +/- 2.7 years) randomly received daily 0.625 mg conjugated equine estrogen and 2.5 mg medroxyprogesterone acetate (n=17), 60 mg raloxifene (n=23), 150 mg raloxifene (n=20) or placebo (n=23) for 24 months. At baseline and after 6, 12 and 24 months the nAPCsr were measured. In the second study 30 elderly men (age, 64.4 +/- 2.4 years) randomly received 120 mg raloxifene (n=15) or placebo (n=15) for 3 months. At baseline and after 3 months the nAPCsr and fasting homocysteine levels were measured. In postmenopausal women conjugated equine estrogen/medroxyprogesterone acetate significantly increased the nAPCsr from 1.26 +/- 0.82 to 2.87 +/- 0.86 at 24 months (P <0.0005 compared with placebo). Raloxifene had no significant effect on nAPCsr compared with placebo in both women and men. The results did not change after excluding carriers of factor V Leiden. Also fasting homocysteine levels were not affected by raloxifene in the aging men. It is concluded that raloxifene, in contrast to combined hormonal replacement therapy, does not increase APC resistance.

Activated Protein C Resistance↗
PubMed1997

Raloxifene inhibits aortic accumulation of cholesterol in ovariectomized, cholesterol-fed rabbits.

BACKGROUND: The beneficial effect of long-term hormone replacement therapy in terms of a decreased risk of cardiovascular disease is now generally accepted. Raloxifene, a selective estrogen receptor modulator, has demonstrated hypolipidemic properties while leaving the endometrium unstimulated. METHODS AND RESULTS: For our study of the effects of raloxifene on atherosclerosis, 75 rabbits were ovariectomized and treated with either raloxifene, 17beta-estradiol, or placebo; 25 rabbits were sham operated and treated with placebo. After 45 weeks, the raloxifene group had two thirds of the aortic atherosclerosis, as evaluated by the cholesterol content of the proximal inner part of the aorta, found in the placebo group (placebo, 577+/-55.1 nmol/mg protein; raloxifene, 397+/-53.6 nmol/mg protein; P<.05); the estrogen group had one third of the aortic atherosclerosis in the placebo group (estrogen, 177+/-32.1 nmol/mg protein; P<.001). The sham-operated group (473+/-59.6 nmol/mg protein) was not significantly different from placebo. These effects were only partly explained by the changes in serum lipids and lipoproteins, and treatment with both estrogen and raloxifene independently predicted the response in aorta cholesterol. Because plasma levels of total raloxifene were low relative to clinical values in postmenopausal women, dose-response data for raloxifene are required. CONCLUSIONS: Our findings indicate that raloxifene hydrochloride has a potentially important antiatherogenic effect, analogous to that observed with estrogen in this model.

Animals↗
PubMed2005

An estrogen receptor chimera senses ligands by nuclear translocation.

We have developed a new mammalian cell-based assay to screen for ligands of the estrogen receptor. A fluorescently tagged chimera between the glucocorticoid and the estrogen receptors, unlike the constitutively nuclear estrogen receptor, is cytoplasmic in the absence of hormone and translocates to the nucleus in response to estradiol. The chimera maintains specificity for estrogen receptor alpha ligands and does not show cross-reactivity with other steroids, providing a clean system for drug discovery. Natural and synthetic estrogen receptor alpha agonists as well as phytoestrogens effectively translocate the receptor to the nucleus in a dose-dependent manner. Antagonists of the estrogen receptor can also transmit the structural signals that result in receptor nuclear translocation. The potency and efficacy of high-affinity ligands can be evaluated in our system by measuring the nuclear translocation of the fluorescently labeled receptor in response to increasing ligand concentrations. The chimera is transcriptionally competent on transient and replicating templates, and is inhibited by estrogen receptor antagonists. Interestingly, the nucleoplasmic mobility of the chimera, determined by FRAP analysis, is faster than that of the wild type estrogen receptor, and the chimera is resistant to ICI immobilization. The translocation properties of this chimera can be utilized in high content screens for novel estrogen receptor modulators.

Active Transport, Cell Nucleus↗
PubMed2001

Monitoring treatment for osteoporosis by using bone densitometry.

In recent years, the range of treatments available for patients with osteoporosis has greatly increased. A decade ago, the only proven therapy was estrogen, but today the choices include bisphosphonates, selective estrogen-receptor modulators, calcitonin, and parathyroid hormone. Clinical trials involving bone mineral density (BMD) scans of the spine and femur have had an important role in the evaluation of these new therapies. In particular, the efficacy of treatments has now been verified in large studies powered to show reductions in fracture risk. In contrast with the use of BMD scans in research studies, their value for monitoring response to treatment in individual patients is less certain. In many cases, the increases in BMD are too small to reliably distinguish between true changes and measurement error. However, experience with estrogen and bisphosphonates suggests that these treatments have a beneficial effect on bone in most patients. Follow-up scans for patients taking these agents are therefore of limited value, apart from offering reassurance to the patient and the doctor. However, when new therapies are first introduced, follow-up scans have a useful role in building up the physician's experience and confidence.

Absorptiometry, Photon↗
PubMed1998

Post-menopausal women and osteoporosis: available choices for maintenance of skeletal health.

OBJECTIVE: To briefly summarize the therapeutic choices for osteoporosis prevention which are currently available to post-menopausal women. METHODS: Results of randomized clinical trials and epidemiological studies in postmenopausal women, and pre-clinical studies in ovariectomized rats were summarized. RESULTS: Estrogen combined with progestogen in hormone replacement therapy (HRT) is effective in relieving perimenopausal symptoms and maintaining bone mineral density. However, the increased breast cancer risk associated with long-term HRT use makes it a less desirable option for many women. Selective estrogen receptor modulators (SERMs), such as raloxifene, are also effective in maintaining bone density, without stimulating the breast or uterus. However, SERMs do not relieve perimenopausal hot flashes. CONCLUSION: HRT is effective for acute relief of perimenopausal symptoms, but for women who are unwilling or unable to take HRT long-term, SERMs such as raloxifene are a useful therapy for the prevention of osteoporosis.

Animals↗
PubMed1998

Management of postmenopausal osteoporosis for primary care.

OBJECTIVE: The shift in health care delivery from a subspecialty to primary care system has transferred the responsibility of preventing osteoporotic fractures from specialists in metabolic bone disease to the web of physicians--family practitioners, general internists, pediatricians, and gynecologists--who provide the bulk of primary care. The challenge for this group of physicians is to decrease the rising prevalence of osteoporotic hip and vertebral fractures while operating within the cost parameters. It is the goal of this brief summary to provide primary practitioners with focused guidelines for the management of postmenopausal osteoporosis based on new and exciting developments. Prevention and treatment will change rapidly over the next decade and these advances will require changes in these recommendations. DESIGN: We identified patients at risk for osteoporosis and provided indications for bone mass measurement, criteria for diagnosis of osteoporosis, therapeutic interventions, and biochemical markers of the disease. RESULTS: Prevention and treatment are discussed, including hormone replacement therapy and use of calcitonin, sodium fluoride, bisphosphonates, and serum estrogen receptor modulators. CONCLUSIONS: Postmenopausal osteoporosis should no longer be an accepted process of aging. It is both preventable and treatable. Primary care physicians must proactively prevent and treat osteoporosis in their daily practice, and combination therapies are suggested.

Absorptiometry, Photon↗
PubMed2003

Chronic effects of toremifene on the vasculature of menopause-induced rats.

During menopause, women have a higher propensity for developing cardiovascular diseases. Recent studies have shown that treatment with selective estrogen receptor modulators (SERMs) improves cardiovascular status in menopausal women. The mechanisms involved, however, have not been elucidated. The present study evaluates the effect of toremifene (10 mg/kg/day), a new member of SERM family, on the vasculature of ovariectomized (Ovx) Sprague-Dawley rats that have been treated with the drug for a 4-week period. Age-matched sham, Ovx-untreated, and Ovx 17beta-estradiol-treated rats were used as controls. Aortic rings from treated and untreated animals were used to determine vascular responses to norepinephrine, acetylcholine, and sodium nitroprusside. Systolic blood pressure (SBP), plasmatic nitric oxide (NO) concentration, estrogen levels, aortic wall thickness, and cholesterol profiles were also determined. Toremifene displaces the concentration-response curve (CRC) for the acetylcholine-induced relaxation to the left and increases the Emax by 34% (from 59.2 +/- 4.2% in Ovx-untreated to 90.2 +/- 3.1% in Ovx-treated rats, n = 9, P < .05). Toremifene increases the Emax (by 22%) without modifying the EC5o for the NE-induced contraction. In addition, toremifene amplifies the relaxing responses to sodium nitroprusside compared to Ovx-untreated group (P < .05). SBP was significantly reduced in the Ovx toremifene-treated group when compared to the Ovx-untreated group (124 +/- 3.5 mm Hg for Ovx toremifene-treated vs. 161 +/- 4.3 mm Hg for Ovx-untreated, n = 10, P < .05). Rats treated chronically with toremifene also exhibited a significantly higher plasmatic NO levels, and a decrease in basal resting tension and aortic wall thickness. The drug, however, did not affect the plasmatic high-density lipoprotein (HDL)/total cholesterol ratio. These results suggest that chronic administration of toremifene improves cardiovascular performance in menopause-induced rats by reversing endothelial dysfunction and decreasing vascular resting tone. Thus, use of toremifene may help to diminish total peripheral resistance and improve cardiovascular status in Ovx rats.

Animals↗
PubMed2004

Targeting steroid hormone receptor pathways in the treatment of hormone dependent cancers.

Sex steroid hormones play a central role in the development and progression of prostate and breast cancers. The biological functions of these and other steroid hormones are mediated by a family of closely related steroid hormone receptors (SHRs), with the androgen receptor (AR) mediating the effects of testosterone and related androgens, and the classical estrogen receptor (ERalpha) mediating the effects of estradiol. Recent studies have begun to elucidate the complex pathways through which SHRs regulate gene expression, and their interaction with other cellular pathways. These studies have also begun to reveal molecular mechanisms underlying the diverse spectrum of effects mediated by steroid hormone analogues in different tissues. A major advance has been the finding that certain drugs induce unique conformational changes in SHRs that alter their interactions with transcriptional coactivator and corepressor proteins, resulting in cell type specific responses. These unique conformational changes appear responsible for the tissue specific effects of the selective estrogen receptor modulators (SERMs) in breast cancer. SHRs are clearly well established therapeutic targets in cancer, and drug development has continued to focus on agents that either block steroid hormone production or bind to and modulate their receptors. The identification of multiple proteins and pathways that mediate the downstream functions of SHRs may eventually provide additional therapeutic targets. This review outlines the basic biology of SHR structure and function, with a focus on AR and ERalpha. Hormonal therapies in prostate and breast cancer that directly target AR and ERalpha, respectively, are then presented and possible novel drug targets in the SHR pathway are discussed.

Animals↗
PubMed1999

Postmenopausal osteoporosis.

UNLABELLED: Osteoporosis affects approximately 28 million Americans and costs about $14 billion a year. Low bone density is the most important risk factor for osteoporosis. The National Osteoporosis Foundation recommends bone density testing for all women over 65 and earlier (around the time of menopause) for women who have risk factors or who are considering therapy. Biochemical markers of bone remodeling, such as urine collagen cross links, may be useful to decide if treatment is needed and to determine the effectiveness of treatment. Once the diagnosis of osteoporosis is made, it is time to consider management options. A healthy life style is important for everyone: an adequate intake of calcium and vitamin D and regular weight-bearing exercise. Pharmacologic agents are indicated for all patients with fragility fractures and for many patients with low bone density. Estrogen is the agent of choice for both prevention and treatment of postmenopausal osteoporosis; however, once estrogen is stopped, bone mass levels drop fairly quickly. Long-term adherence to hormone replacement therapy is not good. Effective alternatives for prevention of bone loss in recently menopausal women include alendronate (a bisphosphonate) and raloxifene (a selective estrogen-receptor modulator). Effective alternatives for treatment of established osteoporosis include alendronate and nasal calcitonin. TARGET AUDIENCE: Obstetricians & Gynecologists, Family Physicians LEARNING OBJECTIVES: After completion of this article, the reader will be able to understand the clinical impact and sequlae of osteoporosis in women, how to identify the high risk patient and those patient that should be screened, the various tests that are available for screening and monitoring, and the various pharmacologic therapies for osteoporosis.

Biomarkers↗