Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Osteoporosis, Postmenopausal”

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 19 recordsLinked to original sources
PubMed1989

A rational approach to the prevention and treatment of postmenopausal osteoporosis.

Postmenopausal osteoporosis is a common disorder. Its importance is measured by the mortality and morbidity associated with increasing numbers of fractures and the enormous social and economic cost to the community. Although the precise aetiology of postmenopausal osteoporosis remains unclear, prevention is now possible and treatment may be effective if commenced early enough in the course of the disease. Combination therapy with oestrogens and progestogens is currently the treatment of choice for prevention, in conjunction with calcium supplementation and changes in lifestyle. Prophylaxis should be offered to women at 'high risk', although the identification of this group is difficult at present. Treatment of existing disease is less effective, although oestrogens should be tried first, with calcitonin as a second choice. There is no place at present for vitamin D, anabolic steroids or parathyroid hormone. The use of fluoride or diphosphonates cannot be recommended outside research centres until further long term studies are completed, which will enable a comparison of the relative risks and benefits. Postmenopausal osteoporosis is now a preventable disease; however, further knowledge of risk factors and the identification of those at risk is essential. Treatment can then be directed at women who need it and healthy women can be spared a lifetime of unnecessary medication.

Estrogens↗
PubMed1994

[Therapeutic concepts in the treatment of postmenopausal osteoporosis].

Postmenopausal osteoporosis is not a well-defined disease, but summarizes women with different severity of changes in bone metabolism and different clinical complaints. The only common feature in women with 'postmenopausal osteoporosis' is the deficiency of estrogen. Postmenopausal women can be subdivided into four groups, according to their risk for fractures: 1. women without evident increase of fracture risk (bone mineral content between 0 and 2 SD of age-related normal range, no known risk factors from history); 2. women with possible increase of fracture risk (bone mineral content between 0 and -2 SD of age-related normal range, with or without known risk factors from history); 3. women with clear increase of fracture risk (bone mineral content below age-related normal range, with or without known risk factors from history); 4. women with already occurred fracture (manifest osteoporosis). Therapeutic intervention in postmenopausal women should be adapted to the risk for fracture. In all four groups a secondary prevention or basic therapy should be performed, focusing on calcium intake, vitamin D supply and sufficient physical activity. Calcium intake should be 1500 mg/day in women without estrogen substitution and 1000 mg in women with estrogen substitution. In patients living mainly inside or with malnutrition, a daily substitution of 500 E. Vitamin D3 is recommended. In group 2, regular control of bone mass is recommended to start additional estrogen replacement therapy, if accelerated loss of bone mass occurs. In group 3, estrogen replacement therapy is recommended urgently and is the therapy of first choice to prevent development of fractures. In group 4 (manifest osteoporosis), therapy should aim on improvement of the patient's symptoms and on increase of bone stability to avoid further fractures. The symptomatic therapy includes pain medications and an intensive physical therapy adapted to the patient's needs. Physical therapy should be performed for long time to reduce complaints and to improve musculoskeletal function in order to prevent falls. Different agents influencing bone metabolism by inhibition of bone resorption (estrogens, calcitonin, bisphosphonates) or stimulation of bone formation (fluoride) are used in manifest osteoporosis to increase bone stability. But the present efficacy to avoid further fractures has not been shown sufficiently for all available agents, so that a final evaluation and recommendation can't be done. Therapy decisions in manifest osteoporosis are often influenced by the possible side effects of the drugs (bleeding, gastrointestinal problems, joint pain), other, not bone-related effects of the drugs (improvement of climacteric complaints, pain relief) and other concomitant diseases and medications.

Aged↗
PubMed2003

Management of postmenopausal osteoporosis.

Postmenopausal osteoporosis is associated with significant morbidity, mortality, reduction in quality of life, and increasing health care costs. It is estimated that 1.5 million women in the United States have one or more osteoporosis-related fractures annually. Fractures may occur at any site, but vertebral fractures are the most common. Longitudinal studies have demonstrated a decreased life expectancy associated with both vertebral and nonvertebral fractures. Once an initial fracture occurs, there is a fivefold increased risk of a second fracture within 1 year. The management of osteoporosis today incorporates multiple modalities of therapy. In addition to early detection, patient education, exercise, and nutritional supplementation, multiple therapeutic agents should be implemented early in an attempt to prevent initial and subsequent fractures. This article reviews currently approved modalities of therapy for the prevention and treatment of postmenopausal osteoporosis.

Aged↗
PubMed2003

[How to chose HRT or bisphosphonate for postmenopausal osteoporosis?].

Postmenopausal osteoporosis is caused by an increased bone loss after menopause. Both estrogen and bisphosphonate have a potent anti-resorptive effect on bone and are proved to be useful for treatment of osteoporosis. Treatment regimen for osteoporosis should be determined after considering presence of estrogen-deficiency related symptoms such as climacteric symptoms, hyperlipidemia and so on. From the view point of gynecologist, HRT should be chosen first for prevention and treatment of postmenopausal osteoporosis.

English Abstract↗
PubMed2005

Clinical effects of strontium ranelate in women with postmenopausal osteoporosis.

Postmenopausal osteoporosis has long-term physical, psychological, and social consequences with a major impact on patients' daily life. Treatment for such a chronic disease needs to be clinically effective and well tolerated, and should ultimately result in a beneficial effect on quality of life. The antifracture efficacy of strontium ranelate, 2 g/day orally, an agent that appears to have dissociation effects on resorption and formation, has been assessed in two large, randomized, double-blind, placebo-controlled clinical studies: the Spinal Osteoporosis Therapeutic Intervention (SOTI) trial and the TReatment Of Peripheral Osteoporosis Study (TROPOS), including more than 6,700 postmenopausal women. Pending the results of TROPOS, a 3-year analysis of SOTI results shows that strontium ranelate significantly reduces new vertebral and clinical vertebral fracture incidence in postmenopausal osteoporotic women. This significant reduction in the risk of clinical and new vertebral fractures has been demonstrated as early as after 1 year of treatment (RR = 0.48, p = 0.003; and RR = 0.51, p < 0.001, respectively) and is maintained over 3 years (RR = 0.62, p < 0.001; and RR = 0.59, p < 0.001, respectively). This is accompanied by decreased back pain and body height loss in the strontium ranelate group compared with the placebo group. As strontium ranelate appears to improve clinical signs and is, furthermore, well tolerated especially in the upper gastrointestinal region, this treatment is expected to result in an improved health-related quality of life (HRQoL). Strontium ranelate thus offers significant clinical benefits in terms of efficacy, tolerability, and ease of administration in the treatment of postmenopausal women with vertebral osteoporotic fractures.

Aged↗
PubMed1993

Postmenopausal osteoporosis.

Postmenopausal osteoporosis is a major health problem. This presentation discusses how an 'unusual' stress fracture site in a postmenopausal woman was diagnosed. The significance of CT scanning in reaching the diagnosis and that of bone densitometry in confirming the presence of osteoporosis are highlighted.

Alkaline Phosphatase↗
PubMed1997

Increase in cytokine production (IL-1 beta, IL-6, TNF-alpha but not IFN-gamma, GM-CSF or LIF) by stimulated whole blood cells in postmenopausal osteoporosis.

Postmenopausal osteoporosis is a progressive disorder characterized by a decreased bone mass and increased susceptibility to fractures. Several investigations have suggested that one of the mechanisms through which estrogen prevents bone loss was a modulation on secretion or release of various cytokines that are known to influence bone remodeling, even if some recent data have challenged this hypothesis. However, in established osteoporosis, the possibility that enhanced cytokines activity may account for the progression of this disease remains unclear and controversial. We sought here to determine whether production of IL-1 beta, IL-6, TNF-alpha, IFN-gamma, GM-CSF and LIF, after direct stimulation in whole blood, was different in healthy (n = 30) or osteoporotic postmenopausal women (n = 24) and whether lumbar bone density (1-BMD) correlated with the values of cytokine production observed in these conditions. A significant difference was observed between the osteoporotic and control subjects for IL-1 beta (p < 0.0001), IL-6 (p < 0.001) and TNF-alpha (p = 0.027) productions, the values being higher in the osteoporotic women. No significant differences between the groups were observed for IFN-gamma (p = 0.51), GM-CSF (p = 0.70) or LIF (p = 0.97). In the whole population, statistically significant negative correlations were observed between lumbar BMD and IL-1 beta (r = -0.46) (p < 0.0005), IL-6 (r = -0.50) (p < 0.0001) and TNF-alpha (r = -0.39) (p < 0.005) production while no such correlations were observed for IFN-gamma, GM-CSF or LIF. In conclusion, the study of cytokine production by immune cells cultured in autologous whole blood suggests that in women more than 10 years past the menopause and presenting a decrease in lumbar bone density corresponding to the new WHO definition of "osteoporosis', production of IL-1 beta, IL-6 and TNF-alpha is still increased compared to controls matched for age and ovarian function, while no differences are reported for IFN-gamma, GM-CSF or LIF production.

Bone Density↗
PubMed1987

Screening for postmenopausal osteoporosis.

Postmenopausal osteoporosis is an area of increasing concern to the gynecologist. Fractures will develop in approximately 15% to 25% of women in their later years and preventive therapy is best aimed specifically at this group. Predicting who will be the ones to sustain fracture is a difficult and imprecise clinical task. The clinical, laboratory, and radiologic methods available for this purpose are reviewed. A rational approach to this problem in today's setting is outlined.

Absorptiometry, Photon↗
PubMed1987

Postmenopausal osteoporosis.

Postmenopausal osteoporosis is a common disabling condition, which is almost completely preventable with oestrogen therapy. Unfortunately unjustified anxiety about the safety of oestrogens still limits the acceptability of this therapy. The role of calcium and the calcium-regulating hormones in the aetiology, prevention and treatment remains unproven.

Aged↗
PubMed1997

Elimination and biochemical responses to intravenous alendronate in postmenopausal osteoporosis.

Postmenopausal women with established vertebral osteoporosis were studied for 2 years to determine the terminal elimination half-life and the duration of response to treatment with intravenous alendronate (30 mg) given over 4 days. The urinary excretion of alendronate followed a multiexponential decline. Approximately 50% of the total dose was excreted over the first 5 days, and a further 17% was excreted in the succeeding 6 months. Thereafter, there was a much slower elimination phase with an estimated mean terminal half-life of greater than 10 years (n = 11). Urinary excretion of hydroxyproline and calcium decreased significantly from pretreatment values by day 3, reaching a nadir by 1 week (40% and 67% decrease, respectively). Thereafter, hydroxyproline remained suppressed for the following 2 years. In contrast, urinary calcium excretion returned gradually toward pretreatment values over the first year and during the second year was comparable to pretreatment values. Serum activity of alkaline phosphatase activity decreased over 3 months (23% reduction), increased gradually thereafter, and returned to pretreatment values at month 24. Bone mineral density measured at the spine increased by approximately 5% during the first year and remained significantly higher than pretreatment values at 2 years. We conclude that a short course of high doses of intravenous alendronate is associated with a prolonged skeletal retention of the agent. This open study also suggests that this regimen has a sustained effect on bone turnover persisting for at least 1 year.

Aged↗
PubMed2002

Meta-analyses of therapies for postmenopausal osteoporosis. VIII: Meta-analysis of the efficacy of vitamin D treatment in preventing osteoporosis in postmenopausal women.

OBJECTIVE: To review the effect of vitamin D on bone density and fractures in postmenopausal women. DATA SOURCE: We searched MEDLINE and EMBASE from 1966 to 1999 and examined citations of relevant articles and proceedings of international meetings. We contacted osteoporosis investigators and primary authors to identify additional studies and to obtain unpublished data. STUDY SELECTION: We included 25 trials that randomized women to standard or hydroxylated vitamin D with or without calcium supplementation or a control and measured bone density or fracture incidence for at least 1 yr. DATA EXTRACTION: For each trial, three independent reviewers assessed the methodological quality and abstracted data. DATA SYNTHESIS: Vitamin D reduced the incidence of vertebral fractures [relative risk (RR) 0.63, 95% confidence interval (CI) 0.45-0.88, P < 0.01) and showed a trend toward reduced incidence of nonvertebral fractures (RR 0.77, 95% CI 0.57-1.04, P = 0.09). Most patients in the trials that evaluated vertebral fractures received hydroxylated vitamin D, and most patients in the trials that evaluated nonvertebral fractures received standard vitamin D. Hydroxylated vitamin D had a consistently larger impact on bone density than did standard vitamin D. For instance, total body differences in percentage change between hydroxylated vitamin D and control were 2.06 (0.72, 3.40) and 0.40 (-0.25, 1.06) for standard vitamin D. At the lumbar spine and forearm sites, hydroxylated vitamin D doses above 50 microg yield larger effects than lower doses. Vitamin D resulted in an increased risk of discontinuing medication in comparison to control as a result of either symptomatic adverse effects or abnormal laboratory results (RR 1.37, 95% CI 1.01-1.88), an effect that was similar in trials of standard and hydroxylated vitamin D. CONCLUSIONS: Vitamin D decreases vertebral fractures and may decrease nonvertebral fractures. The available data are uninformative regarding the relative effects of standard and hydroxylated vitamin D.

Female↗
PubMed2002

Meta-analyses of therapies for postmenopausal osteoporosis. V. Meta-analysis of the efficacy of hormone replacement therapy in treating and preventing osteoporosis in postmenopausal women.

OBJECTIVE: To review the effect of hormone replacement therapy (HRT) on bone density and fractures in postmenopausal women. DATA SOURCE: We searched MEDLINE and EMBASE from 1966 to 1999, the Cochrane Controlled Register, citations of relevant articles, and proceedings of international meetings for eligible randomized controlled trials. We contacted osteoporosis investigators to identify additional studies, and primary authors for unpublished data. STUDY SELECTION: We included 57 studies that randomized postmenopausal women to HRT or a control (placebo or calcium/vitamin D) and were of at least 1 yr in duration. Seven of these studies reported fractures. DATA ABSTRACTION: For each study, three independent reviewers assessed the methodological quality and abstracted the data. DATA SYNTHESIS: HRT showed a trend toward reduced incidence of vertebral fractures [relative risk (RR) 0.66, 95% confidence interval (CI) 0.41-1.07; 5 trials] and nonvertebral fractures (RR 0.87, 95% CI 0.71-1.08; 6 trials). HRT had a consistent effect on bone mineral density (BMD) at all sites. The difference between HRT and control in the percent change in bone density at 2 yr was 6.76 (5.83, 7.89; 21 trials) at the lumbar spine and 4.53 (3.68, 5.36; 14 trials) and 4.12 (3.45, 4.80; 9 trials) at the forearm and femoral neck, respectively. CONCLUSIONS: HRT has a consistent, favorable and large effect on bone density at all sites. The data show a nonsignificant trend toward a reduced incidence in vertebral and nonvertebral fractures.

Estrogen Replacement Therapy↗
PubMed2006

Update of current therapeutic options for the treatment of postmenopausal osteoporosis.

BACKGROUND: Osteoporosis is a common chronic condition in elderly women and is associated with decreased bone strength and an increased risk for fractures. As the incidence of osteoporotic fractures continues to rise, it is important to identify the most effective therapies for reducing patients' risk of fracture. OBJECTIVE: This article reviews the medication classes commonly used for treating osteoporosis and the efficacy, tolerability, and drug-interaction potential of specific medications. The evidence for the use of combination therapies is summarized, as are the agents under investigation. METHODS: Relevant articles were identified through a search of MEDLINE (August 1985-August 2005) using the terms osteoporosis, postmenopausal, fracture, and efficacy combined with drug therapy, calcium, vitamin D, estrogen, progesterone, selective estrogen modulators, calcitonin, strontium ranelate, bisphosphonates, alendronate, risedronate, ibandronate, pamidronate, parathyroid hormone, combination therapy, and zoledronic acid. The identified articles were reviewed for suitability, with priority given to meta-analyses. RESULTS: Among the therapeutic options for the treatment of osteoporosis, the bisphosphonates appear to provide the greatest antiresorptive efficacy, with some bisphosphonates providing 7% to 8% increases in bone mineral density and 60% to 70% decreases in markers of bone resorption. Bisphosphonates also may reduce the incidence of new vertebral fractures by 50% to 52%. CONCLUSIONS: Bisphosphonates are currently the first choice for the treatment of osteoporosis. Use of intermittent regimens of the newer bisphosphonates appears to be a promising alternative to administration of daily or weekly treatment.

Anabolic Agents↗
PubMed2002

Different effects of antiresorptive therapies on vertebral and nonvertebral fractures in postmenopausal osteoporosis.

In postmenopausal osteoporosis, controlled clinical trials with antiresorptive therapies have shown consistent effects on vertebral fracture incidence while their effects on nonvertebral fractures, especially at the hip, have been reported with some agents, but not others. These discrepancies stress the differences in the pathogenesis of vertebral and nonvertebral fractures as discussed below, and the need to further investigate the mechanisms of action of various antiresorptive agents.

Bone Density↗
PubMed2003

Risedronate for the prevention and treatment of postmenopausal osteoporosis.

BACKGROUND: Postmenopausal osteoporosis results in an increased susceptibility to low-trauma fractures due to reduced bone volume and microarchitectural deterioration. Risedronate, a third generation bisphosphonate, has been shown in multiple clinical trials to reduce fracture risk and improve bone mineral density in postmenopausal women with osteoporosis. First and second generation bisphosphonates are known to have gastrointestinal side-effects and risedronate may be better tolerated. OBJECTIVES: To systematically review the efficacy of risedronate on bone density, and fracture reduction in postmenopausal women. SEARCH STRATEGY: The Cochrane Controlled Trials Registry Medline, and Current Contents were searched from 1990 - 2001. The electronic search was supplemented by handsearching four osteoporosis journals and their conference proceedings, as well as contacting content experts and industry sources for unpublished data. SELECTION CRITERIA: We included eight trials that randomised women to risedronate or an alternative (placebo or calcium and /or vitamin D) and measured bone mineral density for at least one year. DATA COLLECTION AND ANALYSIS: For each trial three independent reviewers assessed the methodological quality and abstracted data. Data was extracted for outcomes of fracture, bone mineral density and adverse events. The more conservative random effects model was used to pool data. The quality of trials was assessed according to the Jadad five-point scale. MAIN RESULTS: Both vertebral and non-vertebral fractures were statistically and clinically reduced with risedronate. Eleven out of one hundred women who received risedronate had a vertebral fracture compared to 17 out of one hundred of those who received an alternative treatment (pooled relative risk for vertebral fractures of 0.64 (95% CI 0.52 - 0.77). Three percent of participants who received risedronate had a non-vertebral fracture compared to 4.6% of those who received an alternative treatment (pooled relative risk for nonvertebral fractures of 0.73 (95% CI 0.61 - 0.87). The weighted mean difference for the percent change from baseline for bone mineral density with 5 mg daily for lumbar spine, femoral neck and trochanter was 4.54% (95%CI 4.12 - 4.97), p<0.01; 2.75% (95% CI 2.32 - 3.17), p<0.01; and 4.38% (95% CI 3.51 - 5.25), p<0.01 respectively. REVIEWER'S CONCLUSIONS: There is good evidence for the efficacy of risedronate in the reduction of both vertebral and non-vertebral fractures. In addition, there is evidence from randomized trials that risedronate is able to achieve this without increasing risk for overall withdrawals due to adverse effects.

Bone Density↗