Deficiency In Postmenopausal Women Research Articles

Nitric oxide and bone

Age-associated decrease in nitric oxide (NO) production may be related to an increase in cardiovascular events, sexual dysfunction, and osteoporosis. Relative NO deficiency is a plausible biological basis for NO replacement therapy. Hormone replacement therapy (HRT) enhances local NO production and rectifies NO deficiency in postmenopausal women. However, excess local production of NO aggravates bone destruction in inflammatory arthropathies. In addition to its use in alleviating angina and erectile dysfunction, NO compounds could be a valuable supplemental therapy for chronic conditions including osteoporosis. Estrogen mediates its beneficial effects in bone, in part via the NO/cGMP pathway; hence NO donor therapy is an alternative to estrogen, estrogen agonists-antagonists, and androgen receptor modulator therapy in the prevention and treatment of osteoporosis. Large numbers of animal studies and human pilot studies support the concept of using NO donors for preventing bone loss. Administration of exogenous NO or prolonging endogenous NO activity are practical ways to supplement NO.

Estrogen receptor β protects against in vivo injury in RPE cells

Epidemiological data suggest that estrogen deficiency in postmenopausal women may contribute to the severity of AMD. We discovered that 17β-estradiol (E 2) was a crucial regulator of the severity of extracellular matrix turnover (ECM) dysregulation both in vivo and in vitro. We also found in vitro that the presence of estrogen receptor (ER)β regulates MMP-2 activity. Therefore in an attempt to delineate the role of the ER subtypes, female estrogen receptor knockout (ERKO) mice were fed a high-fat diet, and the eyes were exposed to seven 5-second doses of nonphototoxic levels of blue-green light over 2 weeks. Three months after cessation of blue light treatment, transmission electron microscopy was performed to assess severity of deposits, Bruchs membrane changes, and choriocapillaris endothelial morphology. We found that changes in the trimolecular complex of pro-MMP-2, MMP-14 and TIMP-2 correlated with increased Bruch's membrane thickening or sub-retinal deposit formation (basal laminar deposits) in ERKOβ mice. In addition RPE isolated from ERKOβ mice had an increase in expression of total collagen and a decrease in MMP-2 activity. Finally we found that ERK an intermediate signaling molecule in the MMP pathway was activated in RPE isolated from ERKOβ mice. These data suggest that mice which lack ERβ are more susceptible to in vivo injury associated with environmental light and high fat diet.

Vitamin D deficiency in postmenopausal women with osteoporosis in Venezuela

Vitamin D deficiency in postmenopausal women with osteoporosis in Venezuela

Nitric oxide: novel therapy for osteoporosis

Background: Relative nitric oxide (NO) deficiency is responsible for many pathophysiological processes, including in postmenopausal women providing a plausible biological basis for use of NO replacement therapy in humans. Excess or inappropriate local production of NO aggravates bone destruction in some diseases such as septic shock, rheumatoid and other inflammatory arthropathies. Results: A variety of in vitro and in vivo data have revealed the efficacy of nitroglycerin and nitrates on bone cells. Since some part of the beneficial effects of estrogen on bone is mediated via the NO–cGMP pathway, NO donor therapy is an attractive alternative to estrogen therapy to prevent and treat osteoporosis. When the body cannot generate adequate amounts of NO for biological homeostasis, administration of exogenous NO or prolongation of the actions of endogenous NO are practical ways to supplement NO, especially in postmenopausal women. Conclusion: Postmenopausal NO deficiency is rectified with hormone replacement therapy, which enhances local production of NO. Declining local NO production secondary to estrogen deficiency in postmenopausal women, and perhaps in older men, could be one of the key reasons for age-related increased incidences of cardiovascular events, sexual dysfunction as well as osteoporosis. Thus, in addition to supplementation of NO compounds in acute situations such as alleviating angina and erectile dysfunction, it could be a valuable addition to the armamentarium of therapies for chronic conditions such as osteoporosis.

Urban air pollution is a risk factor for vitamin D deficiency in postmenopausal women

Urban air pollution is a risk factor for vitamin D deficiency in postmenopausal women

Nitric oxide: new evidence for novel therapeutic indications

Background: Nitric oxide (NO) deficiency is implicated in many pathophysiological processes in mammals. NO is a ubiquitous molecule involved in multiple cellular functions. Uncontrolled or inappropriate production of NO may lead to several disease states including septic shock, rheumatoid and inflammatory arthropathies, and expansion of cerebral damage after stroke. However, to date, there are no therapeutic agents available that can overcome these conditions. Similarly, underproduction of NO by NO synthase or enhanced breakdown of NO also leads to diseases such as hypertension, ischemic conditions, pre-eclampsia, premature delivery, among others. NO donor therapies are indicated in these conditions. Results: Nitroglycerin and nitrates (NO donors) have been used as therapeutic agents for the past century, particularly to treat vascular disease, and the only significant adverse effects are headaches. NO donors are highly cost-effective and have beneficial effects in multiple body systems. When the body cannot generate NO via NO synthase or due to rapid turnover leading to inadequate amounts of NO available for biological homeostasis, administration of exogenous NO, or prolongation of the actions of endogenous NO, are practical ways to supplement NO. Conclusion: Recipients of such therapy include patients with angina pectoris, coronary artery disease, hypertension, osteoporosis, gastrointestinal motility disorders, pregnancy-related disorders including premature delivery, pre-eclampsia, vulvodynia, and erectile dysfunction in men. Postmenopausal NO deficiency is rectified with hormone replacement therapy, which enhances local production of NO. Declining local NO production secondary to estrogen deficiency in postmenopausal women and perhaps in older men could be one of the reasons for age-related increased incidences of cardiovascular events and sexual dysfunction. Thus, in addition to supplementation of NO compounds in acute situations like alleviating angina and erectile dysfunction, chronic NO therapy is cost-effective in decreasing cardiovascular events, and improving the urogenital system and skeletal health.

Centrally located body fat is related to inflammatory markers in healthy postmenopausal women

C-reactive protein and fibrinogen are established atherosclerotic cardiovascular disease risk factors. These acute-phase proteins and the proinflammatory cytokines tumor necrosis factor alpha, interleukin-6, and interleukin-1beta may be elevated in obesity and with menopause. The purpose of this multicenter study was to identify whether centrally located fat and/or overall adiposity were related to these inflammatory markers in healthy postmenopausal women. We used dual-energy x-ray absorptiometry to assess overall and regional body composition (fat mass in particular) in 242 postmenopausal women in relation to plasma fibrinogen, serum C-reactive protein, and these proinflammatory cytokines. Multiple regression analyses revealed that 36% of the variability in C-reactive protein (F = 32.4, P <or= 0.0001) was accounted for by androidal fat mass (16.1%, P <or= 0.0001), white blood cells (5.6%, P <or= 0.0001), and age (2.3%, P = 0.0045). Regression analyses revealed that 30% of the variability in fibrinogen (F = 24.5, P <or= 0.0001) was accounted for by white blood cells (3.1%, P = 0.0015), hip fat mass (2.2%, P = 0.0081), years since menopause (0.9%, P = 0.082), and geographic site (P <or= 0.0001). Our results indicated that androidal fat mass and hip fat mass contributed to C-reactive protein and fibrinogen, respectively, whereas we found no association between whole-body or regional fat measures and cytokines. Further study is warranted to determine the responsiveness of these acute-phase proteins and cytokines to loss of body fat through exercise and dietary intervention in postmenopausal women.

The effect of a combined oral calcium and vitamin D supplement for treating mild to moderate vitamin D deficiency in postmenopausal women

To evaluate the efficacy of a combined calcium and vitamin D (Ca-D3) supplement for vitamin D deficiency in a small group of postmenopausal women. A prospective open label 3 month-study. 23 postmenopausal women (mean age 61.2 yrs) with vitamin D deficiency were given a combined oral Ca-D3 supplement called "Osteoblast". The supplement comprises 500 mg elemental calcium and 500 IU ofcholecalciferol. The dosing regimen comprised a loading dose of 1000 IU of cholecalciferol per day for one month (two tablets) and thereafter a maintenance dose of 500 IU of cholecalciferol per day for 2 months (one tablet). Serum was collected for calcium, 25 hydroxyvitamin D3 (25OHD3), and PTH measurements, as well as early morning 2-hour urine calcium/creatinine excretion index (Uca/creat). Specimens were collected at baseline and after 3 months of therapy. Data are reported as mean +/- 1 standard error and 95% confidence intervals. Data was available for the 21 subjects who completed the study. Two subjects (9%) withdrew because of gastrointestinal intolerance. There were 3 subjects with moderate (12.5-24 nmol/L) and 18 with mild (25-49 nmol/L) vitamin D deficiency. Ten subjects (48%) had secondary hyperparathyroidism. Following the oral Ca-D3 combination, serum 25OHD3 levels normalised in all subjects with 18 (86%) subjects achieving values of greater than 70 nmol/L. Serum 25OHD3 levels increased from 36 (31-41) to 91 (79-102) nmol/L (p = 0.0001), increasing by an average of 152% over the 3-month period. There was a corresponding 38% decrease in serum PTH concentrations at 3 months (5.1 + 0.6 pmol/L), compared with baseline (8.0 + 1 pmol/L) (p = 0.001). No subject developed hypercalcemia, but an elevated Uca/creat excretion index occurred in one subjects. A combined oral Ca-D3 product (Osteoblast) is effective for treating vitamin D deficiency and is adequately tolerated.

The Effects of Trabecular-Bone Loading Variables on the Surface Signaling Potential for Bone Remodeling and Adaptation

It is widely believed that mechanical forces affect trabecular bone structure and orientation. The cellular mechanisms involved in this relationship, however, are poorly understood. In earlier work we developed a theoretical, computational framework, coupling bone-cell metabolic expressions to the local mechanical effects of external bone loading. This theory is based on the assumption that osteocytes within the bone tissue control the recruitment of bone-resorbing osteoclasts and bone-forming osteoblasts, by sending strain-energy-density (SED) related signals to trabecular surfaces through the osteocytic, canalicular network. The theory explains the known morphological effects of external bone-loading variations in magnitude and frequency. It also explains the development of osteoporosis, as an effect of increased osteoclast resorption due to estrogen deficiency in postmenopausal women, and to reduced physical activity levels in general. However, the theory uses lumped variables to represent the mechanisms of osteocyte mechano-sensing and signaling. The question is whether these mechanisms could not be specified in a more realistic way. On the one hand, anabolic osteocyte signals might be triggered by the local mechanical loading variables they experience directly, as we assumed in our original theory. On the other hand, osteocyte signals might be triggered by fluid flow in the osteocytic network at large, as was suggested by others. For that purpose we compared the effects of SED, maximal principal strain and volumetric strain as representing local loading variables, to their spatial gradients on the morphological predictions of our computational model. We found that, in concept, they all produced reasonable trabecular structures. However, the predicted trabecular morphologies based on SED as the triggering variable were more realistic in dimensions and relevant metabolic parameters.

Immune effects of surgical menopause and estrogen replacement therapy in peri-menopausal women

The complex relationship between sex hormones and immune function suggests that sex hormone deficiency and estrogen replacement therapy (ERT) in post-menopausal women may have pleiotropic effects on immune function. For this reason, we aimed to investigate short-term effects of surgical menopause and ERT on immunity profile in peri-menopausal women. Seventeen healthy peri-menopausal women who were to undergo total abdominal hysterectomy and bilateral salpingo-oopherectomy (TAH + BSO) for uterine myoma were enrolled into this study. Three blood samples were collected from each patient: 1-day prior to surgery, 30 days after the operation (before ERT) and 30 days after transdermal ERT. The percentages of peripheral blood lymphocyte subpopulations, serum interleukin-4 (IL-4) and interferon-gamma (IFN-γ) concentrations were determined by flow-cytometry and ELISA, respectively. Following TAH + BSO, the percentage of CD8 + cells was increased ( P<0.001) while the percentage of CD19 + cells, serum IL-4, and IFN-γ concentration and the ratio of CD4 + to CD8 + cells were decreased ( P<0.001, P<0.001, P<0.002, and P<0.05, respectively ). After ERT, this trend reversed and a decrease in the CD8 + cells ( P<0.001), increase in the CD19 + cells percentages ( P<0.02) and increase in serum IFN-γ concentration ( P<0.002) were observed. Although an increasing trend in the CD4 + to CD8 + ratio occurred by ERT, this was not significant. However, the decrease in the serum IL-4 concentration after TAH + BSO was not reversed by ERT. Hormone deficiency in post-menopausal women may cause an impaired immune response, and ERT can restore this phenomenon. Estrogen seems to have an important role in the regulation of immune function.

Immune effects of surgical menopause and estrogen replacement therapy in peri-menopausal women

The complex relationship between sex hormones and immune function suggests that sex hormone deficiency and estrogen replacement therapy (ERT) in post-menopausal women may have pleiotropic effects on immune function. For this reason, we aimed to investigate short-term effects of surgical menopause and ERT on immunity profile in peri-menopausal women. Seventeen healthy peri-menopausal women who were to undergo total abdominal hysterectomy and bilateral salpingo-oopherectomy (TAH + BSO) for uterine myoma were enrolled into this study. Three blood samples were collected from each patient: 1-day prior to surgery, 30 days after the operation (before ERT) and 30 days after transdermal ERT. The percentages of peripheral blood lymphocyte subpopulations, serum interleukin-4 (IL-4) and interferon-gamma (IFN-γ) concentrations were determined by flow-cytometry and ELISA, respectively. Following TAH + BSO, the percentage of CD8 + cells was increased ( P <0.001) while the percentage of CD19 + cells, serum IL-4, and IFN-γ concentration and the ratio of CD4 + to CD8 + cells were decreased ( P <0.001, P <0.001, P <0.002, and P <0.05, respectively ) . After ERT, this trend reversed and a decrease in the CD8 + cells ( P <0.001), increase in the CD19 + cells percentages ( P <0.02) and increase in serum IFN-γ concentration ( P <0.002) were observed. Although an increasing trend in the CD4 + to CD8 + ratio occurred by ERT, this was not significant. However, the decrease in the serum IL-4 concentration after TAH + BSO was not reversed by ERT. Hormone deficiency in post-menopausal women may cause an impaired immune response, and ERT can restore this phenomenon. Estrogen seems to have an important role in the regulation of immune function.

A prospective, randomized, placebo-controlled study of the dose effect of oral estradiol on bone mineral density in postmenopausal Chinese women

Objectives: One of the long-term consequences of estrogen deficiency in postmenopausal women is an increased risk of osteoporosis. Fractures of the hip and lumbar spine are associated with considerable morbidity and mortality. Estrogen replacement therapy reduces the risk of osteoporosis, but there is no clear agreement on the most appropriate doses to be used. The aim of this study was to compare changes in bone mineral density (BMD) measurements using conventional and lower dose estradiol. Methods: A prospective, randomized, placebo-controlled 12-month study of the effect of 1 and 2 mg estradiol on BMD in 152 hysterectomized postmenopausal Chinese women with no contraindication to the use of estrogen replacement therapy. Results: Over 12 months, spinal BMD in placebo treated patients decreased by a mean of 2% from baseline (−0.02±0.03 g/cm 2) while it increased by 2% in the 1 mg (0.02±0.03 g/cm 2) and 3% in the 2 mg group (0.03±0.03 g/cm 2). Mean changes in BMD over 12 months in the hip were −0.02±0.02 g/cm 2 (−2%), 0.01±0.02 g/cm 2 (+1%) and 0.01±0.03 g/cm 2 (+1%) in the placebo, 1 and 2 mg estradiol groups, respectively ( P<0.05). Relative to placebo, increases in BMD in both 1 and 2 mg groups were statistically significant for both spine and hip ( P<0.05). However, there was no significant difference in the increase in BMD between the 1 and 2 mg doses for either lumbar spine or hip ( P=0.82, 0.53, respectively). Conclusion: The results of our study show that a 1 mg dose of oral estradiol is effective in preventing bone loss in postmenopausal Chinese women.

Association of tumor necrosis factor receptor 1 gene polymorphism with bone mineral density

Background: Estrogen deficiency in postmenopausal women causes an increased production of proinflammatory cytokines such as interleukin (IL)‐1, IL‐6, and tumor necrosis factor (TNF)‐α. These cytokines are associated with an increase of bone turnover and an acceleration of bone loss. Tumor necrosis factor‐α is known to promote osteoclastogenesis via TNFR1, one of the tumor necrosis factor receptors (TNFR). Therefore, the purpose of the present report was to investigate the association of TNFR1 gene polymorphism with bone mineral density (BMD) in postmenopausal Japanese women.Methods: The question of whether a polymorphism of the TNFR1 gene would correlate with osteoporosis in 320 unrelated healthy postmenopausal women in Japan, was investigated. A single nucleotide polymorphism (SNP) located at Pro12 (CCA to CCG) in exon 1 of TNFR1 was utilized.Results: The subjects were categorized into three genotypes: AA, AG, and GG. The frequency of each genotype was 72.2%, 23.8%, and 4.0%, respectively. The association of this polymorphism with BMD of the lumbar spine and total body, and several bone metabolic markers was then examined. Concerning the TNFR1 gene, the AA group had significantly low total body BMD, compared with the AG + GG group (Z score; 0.285 vs 0.568; P = 0.03), although BMD of the lumbar spine was not statistically different.Conclusion: These results suggest an association between this SNP of the TNFR1 gene and BMD, and an involvement of TNFR1 in postmenopausal osteoporosis among Japanese.

Osteoporosis in men treated with androgen suppression therapy for prostate cancer.

Men with advanced or metastatic prostate cancer commonly receive long-term treatment with luteinizing hormone-releasing hormone (LHRH) agonist therapy. This prolonged treatment causes a hypogonadal state of chronic testosterone deficiency. Similar to estrogen deficiency in postmenopausal women, testosterone deficiency among these men negatively affects bone metabolism through a complex self-regulating, negative feedback system and subsequent reduction in bone formation. If left undetected or untreated, the risk for osteoporosis rises. Osteoporosis increases the likelihood of fracture, especially of the hips. Researchers are studying the effects of LHRH agonist therapy on osteoporosis and other related conditions to determine whether interventions, such as pharmacologic agents (e.g., bisphosphonates), dietary supplements (e.g., calcium, vitamin D), and exercise, can slow or prevent the process and assist healthcare providers in knowing how to counsel patients. Current recommendations are found in the literature on glucocorticoid-induced and menopausal osteoporosis. Nurses need to stay abreast of current knowledge in this area, as it is expanding rapidly.

Review of risk factors for osteoporosis with particular reference to a possible aetiological role of dietary salt

Laboratory animal, clinical and epidemiological studies in the published literature have been reviewed in order to establish whether excessive salt intake is an important risk factor for the development of osteoporosis and whether an intervention strategy based on salt restriction would be beneficial in the prevention of osteoporosis. Genetic factors appear to be far more important than the combination of nutritional, hormonal, environmental and lifestyle factors in the pathogenesis of osteoporosis. The most important single non-genetic factor is oestrogen deficiency in postmenopausal women. Preventive measures should be aimed at maximizing peak bone mass at skeletal maturity and retarding bone loss thereafter. Apart from postmenopausal oestrogen deficiency, various factors have been incriminated as risk factors for osteoporosis, and these include age at menarche, age at and years since menopause, insufficient physical exercise, alcohol, smoking, low calcium intake, low or high protein intake and high intake of phosphorus, sodium or caffeine. Many of the risk factors are considered to be weak, although when combined they could impact significantly on bone health. Increased intakes of various nutritional factors (potassium, magnesium, zinc, vitamin C), fibre and alkaline-producing fruit and vegetables favour adult bone health. Calcium homeostasis is normally well regulated such that increased calcium loss via the urine leads to increased calcium absorption from the gut. However, the duration of this adaptive process may be greater than that of many of the studies demonstrating that increased salt intake leads to both increased sodium and calcium in the urine. In any case, higher urinary calcium output appears to be seen only in a minority of humans in response to increased salt intake. As numerous factors—genetic, nutritional, hormonal and lifestyle—are involved in the maintenance of calcium homeostasis, it is difficult to devise human studies which adequately take into account all the important factors. Another difficulty is that many past studies have relied on imprecise methods for the measurement of bone resorption. Nor have studies based on the use of the laboratory rat produced clear answers to the problem because the rat, as a species, is uniquely deficient in its ability to handle the relevant minerals. Limited studies to date indicate that increased sodium intake neither exerts a consistent effect on various biomarkers of bone health nor leads to irreversible changes in the bone modelling process in men or in pre- or postmenopausal women. We conclude from the available evidence that increased sodium (or salt) intake is not an important risk factor for osteoporosis and that a reduction of salt intake from 9 to 6 g/day in the diet would not be beneficial as an intervention measure in the prevention of osteoporosis. More research is needed to (i) assess the effects (especially long-term) of various nutrients including sodium on bone health, (ii) assess the long-term value of any intervention strategy involving reduced intake of a particular nutrient such as sodium; and (iii) determine whether subpopulations exist particularly in the elderly (e.g. sodium-responsive subjects) in which adaptation to sodium-induced hypercalciuria may be compromised. General prudence dictates that excessively high levels of dietary salt should be eschewed by those persons with raised blood pressure or a limited range of genetic disorders. However, for the generally healthy person there is no sound evidence that the consumption of salt at the present average level of 9 g/day constitutes a risk factor for osteoporosis.

Pathogenesis and management of recurrent urinary tract infection in women.

A number of pathogenic factors for the development of recurrent urinary tract infection, such as prolonged vaginal colonization with uropathogenic Escherichia coli, nonsecretion of ABH blood-group antigens, impaired local immune response, oestrogen deficiency in postmenopausal women and altered vaginal milieu caused by the use of contraceptives, are involved. Long-term use of antimicrobial agents is the cornerstone of prevention of recurrent urinary tract infection. Other approaches currently used involve self-start (on demand) therapy, oestrogen replacement in postmenopausal women, behavioural changes and alternative therapies, such as acupuncture.

Individualizing therapy to prevent long-term consequences of estrogen deficiency in postmenopausal women.

Alendronate sodium and raloxifene hydrochloride were recently approved for the prevention of postmenopausal osteoporosis, but data on their clinical efficacy are limited. We compared these drugs with hormone replacement therapy (HRT) to help women and physicians guide postmenopausal treatment decisions. To help physicians understand how they can best help women choose the most beneficial therapy after menopause based on their individual risk profile. We developed a decision analytic Markov model to compare the effects of alendronate therapy, raloxifene therapy, and HRT on risks of hip fracture, coronary heart disease (CHD), breast cancer, and life expectancy. Regression models linked individual risk factors to future disease risks and were modified by drug effects on bone density, lipid levels, and associated breast cancer effects. Hormone replacement therapy, alendronate therapy, and raloxifene therapy have similar predicted efficacies in preventing hip fractures (estimated relative risk, 0.57, 0.54, and 0.58, respectively). Hormone replacement therapy should be more than 10 times more effective than raloxifene therapy in preventing CHD, but raloxifene therapy may not induce breast cancer. Women at low risk for hip fracture, CHD, and breast cancer do not benefit significantly from any treatment. Among women at average risk, HRT was preferred unless raloxifene therapy could reduce the risk of breast cancer by at least 66%, compared with a 47% increase for HRT. Women at high risk for CHD benefit most from HRT; women at high risk for breast cancer but low risk for CHD benefit most from raloxifene therapy, but only if it lowers the risk of breast cancer. Because of significant differences in the impact of these drugs, treatment choice depends on an individual woman's risk for hip fracture, CHD, and breast cancer.

Alzheimer’s disease in postmenopausal women: screening for cognitive decline in the OB/GYN office

Alzheimer’s disease is the most common cause of dementia diagnosed today, affecting nearly 10% of Americans over the age of 65. The prevalence of this neurodegenerative disease has been escalating and will continue to rise as the population ages. Recent studies suggest that estrogen deficiency in postmenopausal women increases the risk for Alzheimer’s disease and that hormone replacement therapy may prevent or delay disease progression. Therefore, OB/GYN physicians are becoming more interested in the potential prevention, detection and treatment of Alzheimer’s disease in menopausal patients. In response, we recommend that OB/GYNs incorporate a cognitive self-assessment tool, such as the self-administered questionnaire we have developed, in an attempt to recognize and follow the course of cognitive function in their ambulatory patients. Recognition of early cognitive decline will be increasingly important as novel treatments to delay disease progression emerge. This paper reviews the current etiology of Alzheimer’s disease, the effects of estrogen on brain function, and presents a prototype of a Cognitive Self-Assessment tool OB/GYNs can use in their office setting for following cognitive function in patients.

Beneficial Effects of Estrogen in Syndrome X of Postmenopausal Women

Background:There are many reports about the correlation between cardiovascular disorders and estrogen deficiency in postmenopausal women. The purpose of current study is to know that postmenopausal estrogen therapy may affect the lipid metabolism and endogenous fibrinolytic system and exercise tolerance. Method: We investigated the relation of estrogen treatment (srogen 0.625 mg/day to serum lipid levels, angiotensin converting enzyme activity, plasminogen activator inhibitor-1 and parameters of treadmill test in 22 post- menopausal women of normal coronary artery with abnormal exercise test complained with chest pain accompanied by postmenopausal symptoms. Results:Estrogen treatment significantly elevated the serum HDL- cholesterol level (42.8 to 50.1 mg/dl, p<0.05 and reduced the PAI-1 level (16.2 to 10.4 ng/dl, p<0.01 without considerable side effects. During the exercise test, the positivity appearance time and total exercise duration is significantly increased after estrogen treatment. Conclusion:The postmenopausal use of estrogen favorably changed the lipid level, fibrinolytic system and might improve the microcirculation which may protect against the ischemic heart disease risk without significant side effects. (Korean Circulation J 1999;29(3 :298-305

Vitamine D deficiency in postmenopausal women in region of paris

Vitamine D deficiency in postmenopausal women in region of paris