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PubMedDate not supplied

Vitamin D receptor alleles, bone mineral density and turnover in postmenopausal osteoporotic and healthy women.

OBJECTIVE: Vitamin D receptor (VDR) gene polymorphisms and bone metabolic markers were investigated as potential genetic markers for osteoporosis in postmenopausal Turkish women. The relationship between their VDR gene polymorphisms and bone states was determined. MATERIALS AND METHODS: Restriction fragment length polymorphisms at the VDR gene locus (i.e., for BsmI, ApaI, and TaqI) was investigated in 75 postmenopausal osteoporotic (53.16 +/- 1.31 years) and 66 healthy (52.62 +/- 1.69 years) Turkish women and the genotypes were related to bone mineral density (BMD) at femoral neck (FN), lumbar spine (L1-4), trochanter, Ward's triangle (Ward's) and metabolic parameters of bone turnover. RESULTS: In osteoporotic women, TaqI genotype-related differences of the VDR gene were found to be significant at all BMD sites; TT genotype had higher L1-4 BMD values than Tt and tt (p < 0.05); tt genotype had significantly lower BMD at FN (p < 0.05), trochanter (p < 0.01), and Ward's (p < 0.05) compared to TT genotype. The tt genotype was found to be associated with higher (p < 0.05) serum osteocalcin levels compared to Tt and TT genotypes in the osteoporotic women, whereas no such association was found for the healthy women. CONCLUSION: Our data showed an association between VDR TaqI genotype and BMD at the FN, L1-4, trochanter and Ward's triangle in nonobese postmenopausal osteoporotic women. Thus the VDR gene Taql polymorphism modulates differences in BMD in the postmenopausal osteoporotic women.

Body Mass Index↗

PubMed2004

Effects of combined estriol/pravastatin therapy on intima-media thickness of common carotid artery in hyperlipidemic postmenopausal women.

BACKGROUND: Several studies show that 17beta-estradiol (E2) has protective effects on atherosclerosis in the arterial wall in postmenopausal women. Little information is, however, available regarding the effect of estriol (E3) on atherosclerosis. This study was conducted to investigate the effects of E3 alone and combined E3/pravastatin therapy on intima-media thickness (IMT) of common carotid artery in postmenopausal women. METHODS: Thirty-three postmenopausal women were allocated to four groups: daily treatment with E3 (2 mg) alone (E3 group, n = 10), pravastatin (10 mg) alone (pravastatin group, n = 6), combined treatment with E3 (2 mg) and pravastatin (10 mg; E3/pravastatin group, n = 7) and untreated control group (n = 10). All women attended the Kobe University Hospital once a year for routine gynecological and ultrasonographic examinations for the evaluation of atherosclerosis. RESULTS: A significant decrease in IMT was noted in the E3/pravastatin group compared with that in the untreated control group (p < 0.05), whereas there was no significant difference in the reduction rate of IMT in the pravastatin group, E3 group and untreated control group. CONCLUSIONS: The combined E3/pravastatin therapy appeared to retard the progression of atherosclerosis in postmenopausal women.

Arteriosclerosis↗

PubMed2005

Transvaginal ultrasonography of the endometrium in postmenopausal Japanese women.

AIMS: To determine the cut-off level of endometrial thickness for detecting endometrial disease on a large scale of screening and to examine the usefulness of transvaginal ultrasonography (TVS) for endometrial disease screening in asymptomatic postmenopausal Japanese women. METHODS: The study involved 1,400 postmenopausal women in whom endometrial thickness was measured with TVS, and then compared with the histopathological diagnosis of endometrial specimens. RESULTS: The prevalence of endometrial disease in asymptomatic and symptomatic cases was 2.3 and 21%. In symptomatic cases, at a cut-off limit of 3 mm for endometrial thickness, the sensitivity for detecting endometrial disease was 94%, specificity 70% and positive predictive value 46%. With an endometrial thickness < or = 3 mm, the probability that endometrial disease would be overlooked was 0.025. In asymptomatic cases, the corresponding figures at a cut-off limit of 3 mm were 90, 84, 12% and 0.003. CONCLUSIONS: TVS does not appear to be an effective screening method in asymptomatic postmenopausal Japanese women because of the low prevalence of endometrial disease in this population. We recommend a normal cut-off level for endometrial thickness of 4 mm in symptomatic postmenopausal Japanese women.

Adult↗

PubMed2006

Postmenopausal bleeding: a diagnostic approach for both private and public sectors.

OBJECTIVE: To assess the optimal diagnostic approach to women with postmenopausal bleeding by comparing transvaginal ultrasound and endometrial sampling with office hysteroscopy. METHODS: A prospective collective study was performed on 102 consecutive patients with postmenopausal bleeding who were evaluated by ultrasound measurement of the endometrial thickness (EL), endometrial sampling by Accurette and outpatient hysteroscopy and directed biopsy. RESULTS: Accurette was inadequate for histological diagnosis in 65 of 136 samples and many repeat investigations were required. In all 16 cases of endometrial polyps, ultrasound measurement of the EL was > or =4 mm and hysteroscopy confirmed the findings. Accurette detected only 5 polyps. All 7 cases of endometrial hyperplasia were detected using an EL of > or =4 mm and hysteroscopy confirmed the findings. Accurette failed to detect 5 out of 7 cases of endometrial hyperplasia. Five cases of endometrial cancer were diagnosed: all had an EL > or =4 mm but were inadequately sampled for diagnostic purposes in 3 cases. A definitive diagnosis was made on hysteroscopy in 4 cases (1 patient did not have a hysteroscopy). CONCLUSION: Accurette is not a good sampling device for the diagnosis of postmenopausal bleeding. An ultrasound measurement of the EL > or =4 mm in patients with postmenopausal bleeding warrants further investigation. Outpatient office hysteroscopy is an accurate and sensitive modality to employ as a first line investigation for definitive diagnosis.

Adenocarcinoma↗

PubMed1997

High frequency of adenomyosis in postmenopausal breast cancer patients treated with tamoxifen.

Pathologic evaluation for adenomyosis in uterine specimens as well as demographic characteristics, health habits and risk factors for endometrial cancer were compared in 28 postmenopausal breast cancer patients with tamoxifen (TAM) treatment and in 11 similar patients without TAM treatment in order to determine the association between postmenopausal TAM exposure and the frequency of adenomyosis. The same comparison was also made between TAM-treated patients with adenomyosis and TAM-treated patients without adenomyosis. Adenomyosis was histologically diagnosed in 53.6% TAM-treated patients and in 18.2% non-TAM patients. Overall, there were no significant statistical differences in all parameters tested between the 2 groups, as well as between the TAM-treated patients with adenomyosis and the TAM-treated patients without adenomyosis. It can be concluded that adenomyosis was significantly more common among postmenopausal breast cancer patients who were treated with TAM as compared to similar patients without TAM treatment (p = 0.0186). This significant high rate of adenomyosis may be attributed to the continuous and unopposed exposure to TAM. It is, however, impossible to predict which postmenopausal breast cancer patient will develop adenomyosis after treatment with TAM.

Aged↗

PubMed1996

The importance of endometrial fluid collection in postmenopause.

OBJECTIVE: We sought to determine the importance of postmenopausal endometrial fluid collection, which has almost invariably been accepted as a finding of a malignant process. METHODS: Out of 1,500 postmenopausal patients admitted to our center mainly for their postmenopausal symptoms, endometrial fluid collection was detected in 15 cases during transvaginal pelvic ultrasonographic evaluations. These patients were evaluated with cervical smears as well as endocervical and endometrial curretages. The fluid collections were aspirated and measured. RESULTS: The mean age and mean menopausal age were 51.7 +/- 1.3 and 5.7 +/- 9.8 years, respectively. Six of the patients were already on hormone replacement therapy. Nine were asymptomatic and the others had vaginal discharge and pelvic pain. Ten patients had normal findings on pelvic examination, and in the others benign cervical polyps, previous cervical amputation, cervical erosion, and nabothian cysts were detected. The volume of the directly measured fluid was 7.9 +/- 4.0 cm3. The cervical smears, the cytological examinations of the fluids, the colposcopic examinations and the endocervical curretages were negative, and the histopathological evaluation of the endometrial curretage specimens revealed no premalignant or malignant disease, but blood and fibrin in 1 patient, inactive endometria in 9 patients, proliferative endometria in 4 patients and senile cystic atrophy in 1 patient. CONCLUSION: Although there was no malignancy in our series, the conflicting results of the limited number of studies made us cautious and we still consider that postmenopausal patients with endometrial fluid collection may be at risk for gynecologic cancers and that every effort should be made in order to rule out such a condition.

Cervix Uteri↗

PubMed2003

Effect of lower dosage of oral conjugated equine estrogen on inflammatory markers and endothelial function in healthy postmenopausal women.

OBJECTIVE: Although oral estrogen replacement therapy (ERT) in postmenopausal women improves endothelial function, it also increases plasma C-reactive protein (CRP) and interleukin-6 (IL-6) concentration. The proinflammatory effect of oral ERT may explain the increased risk of coronary heart disease (CHD) associated with this treatment. Recent observational studies have demonstrated that a lower dose of oral estrogen reduces the risk for CHD. The purpose of the present study was to investigate the effects of low-dose oral estrogen on vascular inflammatory markers and endothelium-dependent vasodilation in postmenopausal women. METHODS AND RESULTS: Postmenopausal women were randomized into 3 groups to receive no treatment (n=14) or oral conjugated equine estrogen (CEE) at a dosage of 0.625 mg (n=15) or 0.3125 mg (n=15) daily for 3 months. CEE at a dosage of 0.625 mg resulted in significant increases in plasma concentrations of CRP from 690.9+/-749.5 to 1541.9+/-1608.0 ng/mL, serum amyloid A from 6.12+/-4.15 to 8.25+/-4.40 microg/mL, and IL-6 from 1.45+/-0.73 to 2.35+/-1.16 pg/mL. In contrast, CEE at a dosage of 0.3125 mg had no effect on these inflammatory markers. Both dosages of estrogen significantly decreased E-selectin concentration, whereas the concentrations of intercellular and vascular cell adhesion molecules remained unchanged. In both CEE groups, flow-mediated vasodilation in the brachial artery was increased significantly, whereas nitroglycerine-induced vasodilation was unaltered. CONCLUSIONS: Oral CEE at a low dose of 0.3125 mg in postmenopausal women eliminated the adverse effects of high-dosage oral CEE on vascular inflammatory markers in addition to preserving the favorable effects of estrogen on cell adhesion molecules and endothelial function.

Administration, Oral↗

PubMed1994

Effects of hormone replacement therapy on lipoprotein(a) and lipids in postmenopausal women.

High concentrations of lipoprotein(a) [Lp(a)], an independent risk factor for atherosclerosis, cannot be managed by the usual lipid-lowering agents. It has been suggested that Lp(a) levels are related to female sex hormones. Estrogen replacement therapy makes the lipid profiles favorable for delaying atherosclerosis in postmenopausal women. The effects of the combination therapy of estrogen and progesterone on lipids are controversial. This study was designed to evaluate the effect of female sex hormones on the concentration of Lp(a) and to clarify the influence of progesterone on the effect of estrogen in postmenopausal women. Postmenopausal women (n = 184) were divided into four groups: control; 0.625 mg conjugated equine estrogen (CEE) plus 10 mg medroxyprogesterone acetate (MPA); 0.625 mg CEE plus 5 mg MPA; and 0.625 mg CEE only. Medication for 2 months lowered the concentrations of Lp(a) by 20% in all treated groups. The decrease was more pronounced in subjects with a relatively higher basal Lp(a) concentration. Estrogen replacement therapy raised the concentration of high-density lipoprotein cholesterol and decreased low-density lipoprotein cholesterol without changing total cholesterol. The combination therapy of estrogen and progesterone abolished the effect of estrogen on high-density lipoprotein cholesterol. Hormone replacement therapy lowered Lp(a) levels in postmenopausal women. The effect was prominent in subjects with high basal Lp(a) levels. This decrease may be one of the mechanisms of the cardioprotective effects of estrogen. The cardioprotective effect of estrogen cannot be applied to the combination therapy due to the adverse effect of progesterone on high-density lipoprotein cholesterol.

Adult↗

PubMed2001

Postmenopausal hormone therapy and risk of stroke: The Heart and Estrogen-progestin Replacement Study (HERS).

BACKGROUND: Observational studies have shown that postmenopausal hormone therapy may increase, decrease, or have no effect on the risk of stroke. To date, no clinical trial has examined this question. To investigate the relation between estrogen plus progestin therapy and risk of stroke among postmenopausal women, we analyzed data collected from the Heart & Estrogen-progestin Replacement Study (HERS), a secondary coronary heart disease prevention trial. METHODS AND RESULTS: Postmenopausal women (n=2763) were randomly assigned to take conjugated estrogen plus progestin or placebo. Primary outcomes for these analyses were stroke incidence and stroke death during a mean follow-up of 4.1 years. The number of women with strokes was compared with the number of women without strokes. A total of 149 women (5%) had 1 or more strokes, 85% of which were ischemic, resulting in 26 deaths. Hormone therapy was not significantly associated with risk of nonfatal stroke (relative hazard [RH] 1.18; 95% CI 0.83 to 1.66), fatal stroke (RH 1.61; 95% CI 0.73 to 3.55), or transient ischemic attack (RH 0.90; 95% CI 0.57 to 1.42). Independent predictors of stroke events included increasing age, hypertension, diabetes, current cigarette smoking, and atrial fibrillation. Black women were at increased risk compared with white women, and unexpectedly, body mass index was inversely associated with stroke risk. CONCLUSIONS: Hormone therapy with conjugated equine estrogen and progestin had no significant effect on the risk for stroke among postmenopausal women with coronary disease.

Aged↗

PubMed2002

Characterization of an animal model of postmenopausal hypertension in spontaneously hypertensive rats.

Blood pressure (BP) increases in postmenopausal women. The mechanisms responsible are unknown. The present study was performed to characterize a model of postmenopausal hypertension in the rat and to determine the role that oxidative stress may play in mediating the postmenopausal hypertension. Spontaneously hypertensive rats were ovariectomized (ovx) or left intact (PMR) at 8 months and were aged to 18 months. These animals were compared with young females (YF; 4 or 8 months of age) and old males (18 months) for some measurements. Estradiol levels were decreased in PMR rats to levels not different from YF rats in proestrous or from old males. BP increased progressively with age in PMR rats but not in ovx or male rats, such that the gender difference in hypertension disappeared by 18 months. Glomerular filtration rate was lower in ovx and PMR rats than in YF rats. Renal plasma flow and renal vascular resistance were similar between YF and ovx rats, but lower and higher, respectively, in PMR rats. Serum testosterone increased by 60% in ovx rats and 400% in PMR rats compared with YF rats. Plasma renin activity also increased in PMR rats but not in ovx rats. Chronic treatment (for 8 months beginning at 8 months of age) of PMR rats with vitamins E and C, but not tempol, resulted in a significant reduction in BP and excretion of F2-isoprostanes. In contrast, tempol, but not vitamins E and C, reduced BP in old males. These data suggest that the PMR rats, but not ovx rats, may be a suitable model for the study of postmenopausal hypertension, and that oxidative stress plays a role in the increased BP.

Age Factors↗

PubMed2004

Pulse pressure and coronary atherosclerosis progression in postmenopausal women.

Pulse pressure, an index of large artery stiffness, has been associated with coronary events. However, mechanisms for this association remain unclear. In this study, we examined the relationship between pulse pressure and the progression of coronary atherosclerosis and the effects of hormone replacement therapy (HRT) on pulse pressure in postmenopausal women with angiographically confirmed coronary disease followed for 3.2 years in the Estrogen Replacement in Atherosclerosis (ERA) trial. In the ERA trial, 309 postmenopausal women (mean age 66+/-7 years) with coronary disease were randomized to estrogen, estrogen plus progestin, or placebo, and followed for 3.2 years. Ten standardized epicardial segments were measured for minimal diameter values at baseline and follow-up using quantitative coronary angiography. For this study, mixed-model analysis of covariance was used to: (1) test the association between pulse pressure and change in mean minimum diameter (MMD) adjusted for baseline MMD and (2) the effect of HRT on follow-up pulse pressure. After adjustment for potential confounders, there was a significant graded increase in progression of coronary stenosis with increasing quartiles of baseline pulse pressure (P test for trend=0.0001). The progression rate in women with the highest quartile of baseline pulse pressure was 5-fold higher than in women in the lowest quartile (P<0.01). In postmenopausal women with coronary disease, increased levels of baseline pulse pressure are associated with subsequent progression of coronary atherosclerosis in postmenopausal women. HRT had no detectable effect on pulse pressure.

Aged↗

PubMed2005

Antihypertensive effects of drospirenone with 17beta-estradiol, a novel hormone treatment in postmenopausal women with stage 1 hypertension.

BACKGROUND: Drospirenone (DRSP) is a novel progestin with antimineralocorticoid activity that has been developed for hormone therapy in combination with 17beta-estradiol (E2) in postmenopausal women. In prior studies with DRSP in postmenopausal women that were focused on relief of menopausal symptoms, DRSP/E2 yielded significant reductions in blood pressure (BP). METHODS AND RESULTS: The effects of 3 mg DRSP/1 mg E2 on clinic and 24-hour ambulatory BP as well as potassium homeostasis were evaluated in postmenopausal women with stage 1 hypertension (systolic, 140 to 159 and/or diastolic, 90 to 99 mm Hg) in a 12-week, multicenter, double-blind, randomized, placebo-controlled study. Clinic BPs were measured at baseline and at 2, 4, 6, 8, and 12 weeks of therapy, whereas potassium was measured at 2, 6, and 12 weeks of therapy. Ambulatory BP was performed in a substudy at baseline and at the end of the trial. In the intention-to-treat population of 213 women, the clinic BP was reduced significantly on DRSP/E2 (clinic BP, -14.1/-7.9 for DRSP/E2 versus -7.1/-4.3 mm Hg for placebo, P<0.0001). In the subgroup of 43 women with ambulatory BP monitoring, the 24-hour BP fell by -8.5/-4.2 mm Hg versus -1.8/-1.6 mm Hg on placebo (P=0.002/0.07). There were no significant changes from baseline in potassium levels or in the incidence of hyperkalemia (> or =5.5 meq/L) on DRSP/E2 compared with placebo. CONCLUSIONS: Combination therapy with DRSP/E2 significantly lowered both clinic and 24-hour systolic BP in postmenopausal women with stage 1 systolic hypertension. This characteristic may lead to benefit for cardiovascular risk reduction in this population.

Aged↗

PubMed2002

Comparative effects of estrogen and angiotensin-converting enzyme inhibition on plasminogen activator inhibitor-1 in healthy postmenopausal women.

BACKGROUND: This study compares the effect of estrogens and ACE inhibition on plasminogen activator inhibitor-1 (PAI-1) concentrations in healthy postmenopausal women, genotyped for a 4G/5G polymorphism in the PAI-1 promoter, a polymorphism shown to influence PAI-1 concentrations. Methods and Results- Morning estradiol, PAI-1, tissue plasminogen activator, plasma renin activity, angiotensin II, and aldosterone were measured in 19 postmenopausal women (5G/5G:4G/5G:4G4G=5:10:4, respectively) at baseline and during randomized, single-blind, crossover treatment with conjugated equine estrogens 0.625 mg per os per day, ramipril 10 mg per os per day, and combination estrogens and ramipril. Estradiol (P<0.005) and angiotensin II (P<0.01) were significantly higher during estrogens. Plasma renin activity was significantly increased during ACE inhibition (P<0.05). Both conjugated estrogens [PAI-1 antigen from 12.5 (7.6, 17.4) [mean (95% CI)] baseline to 6.6 (2.6, 10.7) ng/mL, P<0.01] and ACE inhibition [8.3 (4.9, 11.7) ng/mL, P<0.005] decreased PAI-1 without decreasing tissue plasminogen activator. The effect of combined therapy on PAI-1 [5.6 (2.3, 8.8) ng/mL] was significantly greater than that of ramipril alone (P<0.05). There was a significant effect of PAI-1 4G/5G genotype on baseline PAI-1 concentrations (P=0.001) and a significant interactive effect of 4G/5G genotype and treatment, such that genotype influenced the change in PAI-1 during ramipril (P=0.011) or combined therapy (P=0.006) but not during estrogens (P=0.715). CONCLUSIONS: ACE inhibition with ramipril and conjugated estrogens similarly decrease PAI-1 antigen concentrations in postmenopausal women. Larger studies that use clinical outcomes are needed to determine whether PAI-1 4G/5G genotype should influence the choice of conjugated estrogens or ACE inhibition for the treatment of healthy postmenopausal women.

Aldosterone↗

PubMed2002

Weight loss reduces C-reactive protein levels in obese postmenopausal women.

BACKGROUND: C-reactive protein (CRP) has been proposed as an independent risk factor for cardiovascular disease and has been positively associated with body weight and body fatness. We examined the hypothesis that weight loss would reduce plasma CRP levels in obese postmenopausal women. METHODS AND RESULTS: In a sample of 61 obese (body mass index, 35.6 +/- 5.0 kg/m(2)), postmenopausal women (age, 56.4 +/- 5.2 years), we found that plasma CRP levels were positively associated with dual x-ray absorptiometry-measured total body fatness (r=0.36, P<0.005) and CT-measured intra-abdominal body fat area (r=0.30, P<0.02). Significant correlations were also found between plasma CRP and triglyceride levels (r=0.33, P<0.009) and glucose disposal measured by the hyperinsulinemic-euglycemic clamp technique (r=-0.29, P<0.03). Twenty-five of the 61 women tested at baseline completed a weight loss protocol. The average weight loss was 14.5 +/- 6.2 kg (-15.6%, P<0.0001), with losses of 10.4 +/- 5.4 kg fat mass (-25.0%, P<0.0001) and 2.8 +/- 1.4 kg fat-free mass (-6.0%, P<0.0001). Visceral and subcutaneous fat areas were reduced by -36.4% and -23.7%, respectively (P<0.0001). Plasma CRP levels were significantly reduced by weight loss: average -32.3%, from 3.06 (+0.69, -1.29) to 1.63 (+0.70, -0.75) microgram/mL (P<0.0001, medians and interquartile differences). Changes in body weight and in total body fat mass were both positively associated with plasma CRP level reductions. CONCLUSIONS: Adiposity was a significant predictor of plasma CRP in postmenopausal women on a cross-sectional basis. Moreover, caloric restriction-induced weight loss decreased plasma CRP levels. Weight loss may represent an important intervention to reduce CRP levels, which may mediate part of its cardioprotective effects in obese postmenopausal women.

Absorptiometry, Photon↗

PubMed2002

Effect of medroxyprogesterone acetate on vascular inflammatory markers in postmenopausal women receiving estrogen.

BACKGROUND: Estrogen increases C-reactive protein (CRP) in postmenopausal women. Estrogen also decreases cell adhesion molecules, whereas elevated CRP stimulates the expression of cell adhesion molecules. Because androgens have antiinflammatory effects, androgenic progestins such as medroxyprogesterone acetate (MPA) may inhibit proinflammatory effects of estrogen. We investigated the effects of MPA on estrogen-induced changes in acute inflammatory proteins and cell adhesion molecules in postmenopausal women. METHODS AND RESULTS: Postmenopausal women were treated daily with conjugated equine estrogen (CEE, 0.625 mg), CEE plus MPA 2.5 mg, or CEE plus MPA 5.0 mg for 3 months. CEE significantly increased CRP concentrations by 320.1+/-210.2% (P<0.05). The addition of MPA to CEE, however, inhibited the increase in CRP in a concentration-dependent manner (MPA 2.5 mg, 169.8+/-66.9%, P<0.05; MPA 5 mg, 55.0+/-30.4%, not significant). Similarly, CEE increased amyloid A protein concentrations, whereas MPA reversed this effect. Interleukin-6 concentration did not change significantly in any treatment group. CEE alone significantly decreased the concentration of E-selectin, but the concentrations of intercellular adhesion molecule and vascular cellular adhesion molecule did not change significantly. The addition of MPA tended to decrease the levels of cell adhesion molecules, and use of 5.0 mg MPA showed significant decreases in all cell-adhesion molecule concentrations. CONCLUSIONS: Concurrent MPA administration may attenuate estrogen's proinflammatory effect. Because MPA in combination with CEE decreased cell adhesion molecule concentrations, the anti-inflammatory effect of MPA may actually be responsible for the favorable effect of estrogen-progestogen combinations on cell adhesion molecules in postmenopausal women.

Adult↗

PubMed2001

Effect of medroxyprogesterone acetate on endothelium-dependent vasodilation in postmenopausal women receiving estrogen.

BACKGROUND: Estrogen increases endothelium-dependent vasodilation in postmenopausal women. However, use of progestins in combination with estrogen may counter beneficial effects of estrogen on endothelium. We investigated the effect of medroxyprogesterone acetate (MPA) on estrogen-induced increase in endothelium-dependent vasodilation in postmenopausal women. METHODS AND RESULTS: Postmenopausal women were treated daily with conjugated equine estrogen (CEE) 0.625 mg (n=14), CEE 0.625 mg and MPA 2.5 mg (n=15) or CEE 0.625 mg and MPA 5.0 mg (n=16) for 3 months. Plasma lipids and hormones were measured before and after treatment. Vasodilatory responses of the brachial artery were evaluated by measuring flow-mediated vasodilation (FMD) and nitroglycerin-induced vasodilation by use of high-resolution ultrasonography. Susceptibility of LDL to oxidation was analyzed by incubation with CuSO(4) while kinetics of conjugated diene formation was monitored. Plasma total and LDL cholesterol concentrations were decreased significantly in all groups. CEE increased FMD significantly, from 4.5+/-1.7% to 8.5+/-2.8% (P<0.001). Addition of MPA reversed this effect in a concentration-dependent manner (for MPA 2.5 mg, from 5.0+/-3.2% to 6.2+/-3.1%; for MPA 5.0 mg, from 4.9+/-3.4% to 3.6+/-3.7%; P=NS for each). No treatment significantly altered nitroglycerin-induced dilation. Lag time for conjugated diene formation was prolonged significantly in all groups, and the oxidation rate was significantly reduced. CONCLUSIONS: Concurrent MPA administration may offset favorable effects of estrogen on endothelial function in postmenopausal women. Because MPA did not diminish LDL-lowering and antioxidant effects of estrogen, MPA-induced inhibition of endothelium-dependent vasodilation may be independent of changes in oxidative susceptibility and plasma concentration of LDL.

Blood Flow Velocity↗

PubMed2001

Randomized, double-blind, placebo-controlled study on effects of raloxifene and hormone replacement therapy on plasma no concentrations, endothelin-1 levels, and endothelium-dependent vasodilation in postmenopausal women.

The endothelium is thought to play an important role in the genesis of atherosclerosis, and several lines of evidence suggest that the effect of an intervention on endothelial function might predict its involvement in coronary disease progression and in the rate of cardiovascular events. Estrogen has direct effects on the blood vessel wall, indicating that vascular endothelium may play a key role in the cardiovascular protective effects of hormone replacement therapy (HRT). Raloxifene relaxes coronary arteries in vitro by an estrogen receptor-dependent and NO-dependent mechanism, thus suggesting that this selective estrogen receptor modulator could also have beneficial effects on endothelial function. This study compared the effects of HRT and raloxifene on NO products, endothelin-1 plasma levels, and endothelium-dependent vasodilatation in postmenopausal women. Healthy postmenopausal women (n=90) were enrolled in a double-blind, randomized, placebo-controlled, 6-month trial. Women were randomly assigned to receive continuous HRT (1 mg 17beta-estradiol combined with 0.5 mg norethisterone acetate), raloxifene (60 mg/d), or placebo for 6 months. Flow-mediated endothelium-dependent vasodilation of the brachial artery, plasma NO concentrations, and endothelin levels were measured at baseline and after 6 months of therapy. The mean baseline level of NO breakdown products was 26.5+/-10.7 micromol/L and increased to 36.3+/-11.4 micromol/L after 6 months of treatment with raloxifene. The mean baseline plasma endothelin level was 17.3+/-8.9 pg/mL and decreased to 11.5+/-2.1 pg/mL after 6 months of treatment with the selective estrogen receptor modulator. The mean baseline ratio of NO (breakdown products) to endothelin was also significantly increased at the end of treatment with raloxifene. Postmenopausal women treated with HRT had similar changes in plasma nitrites/nitrates and endothelin levels as well as in the ratio of NO to endothelin. In contrast, these markers of endothelial function did not change in the placebo-treated women. Flow-mediated endothelium-dependent vasodilation of the brachial artery was 8.3+/-2.1% at baseline and increased to 12.3+/-2.1% after 6 months of treatment with raloxifene. HRT also caused a significant and similar increase in flow-mediated endothelium-dependent vasodilation. No change in flow-mediated vasodilation was observed in the participants treated with placebo. We conclude that raloxifene therapy and HRT influence endothelial function and improve flow-mediated endothelium-dependent vasodilation to a comparable extent in healthy postmenopausal women at least after a 6-month treatment period. However, further investigation is warranted to enhance our understanding of the mechanisms of the effect of raloxifene on vascular function and to determine whether its effect on endothelial function may contribute to the reduction in cardiovascular-related morbidity and mortality.

Aged↗

PubMed2003

Short-term use of estradiol for depression in perimenopausal and postmenopausal women: a preliminary report.

OBJECTIVE: The authors examined the effect of a 4-week course of estrogen therapy on depression in perimenopausal and postmenopausal women. METHOD: Twenty-two depressed women who were either perimenopausal (N=10) or postmenopausal (N=12) received open-label treatment with transdermal 17beta-estradiol (100 micro g/day) for 4 weeks. The Montgomery-Asberg Depression Rating Scale and the Beck Depression Inventory were used to assess depressive symptoms, the Greene Climacteric Scale was used to assess menopause-related symptoms, and the Clinical Global Impression (CGI) was used to assess global clinical improvement in these women at baseline and after treatment. Remission of depression was defined as a score <10 on the Montgomery-Asberg Depression Rating Scale and a score </=2 on the CGI at week 4. RESULTS: Remission of depression was noted in eight of the 20 women who completed the study; two of these women were postmenopausal, and six were perimenopausal. Antidepressant response was not associated with severity or subtypes of depression at study entry or with concomitant improvement in menopause-related symptoms. CONCLUSIONS: Some perimenopausal women with depression may benefit from short-term use of estrogen therapy, and its role for postmenopausal depressed women warrants further investigation. Antidepressant benefit associated with estrogen therapy may be independent of improvement in physical symptoms.

Administration, Cutaneous↗