Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Postmenopause”

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
PubMed1980

Testosterone and 17 beta-oestradiol secretion of the human ovary. II. normal postmenopausal women, postmenopausal women with endometrial hyperplasia and postmenopausal women with adenocarcinoma of the endometrium.

A study of the concentration of testosterone and of 17 beta-estradiol in blood drawn from the ovarian and cutal veins of normal oestrogen-deficient postmenopausal women and of postmenopausal women with signs of oestrogen activity, and the subsequent computation of the ovarian production rates of these two hormones, show that in the latter group of women there is a high ovarian secretion of testosterone. The theory is advanced that this ovarian-secreted testosterone is rapidly converted into 17 beta-oestradiol, and that, by thus increasing the levels of circulating oestrogens, ovarian-secreted testosterone contributes, albeit indirectly, to endometrial hyperplasia and possibly to endometrial carcinoma.

Adenocarcinoma↗
PubMedDate not supplied

Effect of long-term hormone replacement therapy on angiotensin-converting enzyme activity and bradykinin in postmenopausal women with essential hypertension and normotensive postmenopausal women.

OBJECTIVE: Hormone replacement therapy (HRT) reduces the incidence of cardiovascular disease in postmenopausal women. Three-month short-term HRT in postmenopausal women with essential hypertension increased the plasma concentrations ofbradykinin with decreased serum angiotensin-converting enzyme (ACE) activity, which may be partially responsible for the cardioprotective effects of HRT. The objective was to determine whether 12-month long-term HRT in postmenopausal women with essential hypertension would maintain the decreased ACE activity and increased bradykinin levels and whether long-term HRT would increase the plasma bradykinin concentrations of normotensive postmenopausal women who had shown no significant changes in the 3-month HRT study, despite their decreased serum ACE activity. DESIGN: Twenty hypertensive and 15 normotensive postmenopausal women were treated with conjugated estrogens (0.625 mg/day) and medroxyprogesterone (2.5 mg/day) for 12 months. Twenty hypertensive and 15 normotensive postmenopausal women were used as controls. The controls were not treated with HRT. Serum ACE activity and plasma bradykinin concentrations were measured at baseline and at 12 months. RESULTS: Long-term HRT in both hypertensive and normotensive postmenopausal women significantly decreased serum ACE activity from 15.5+/-0.7 IU/L and 16.0+/-0.9 IU/L, respectively, at baseline to 13.3+/-0.5 IU/L and 14.2+/-0.9 IU/L, respectively, 12 months after the start of HRT (p < 0.05 and p < 0.05, respectively). Long-term HRT in both hypertensive and normotensive postmenopausal women also significantly increased plasma bradykinin concentrations from 22.1+/-4.4 pg/mL and 19.2+/-3.0 pg/mL, respectively, at baseline to 86.7+/-21.2 pg/mL and 73.5+/-23.0 pg/mL, respectively, 12 months after the start of HRT (p < 0.01 and p < 0.05, respectively). No significant changes in serum ACE activity or plasma bradykinin concentrations were observed in the control groups. CONCLUSIONS: Long-term HRT in hypertensive and normotensive postmenopausal women decreases their serum ACE activity and increases their plasma bradykinin concentrations. Thus, maintenance of elevated bradykinin with decreased serum ACE activity by HRT may be useful in reducing the risk of cardiovascular disease in both hypertensive and normotensive postmenopausal women.

Administration, Oral↗
PubMed2006

CD38 is associated with premenopausal and postmenopausal bone mineral density and postmenopausal bone loss.

One goal of osteoporosis research is to identify the genes and environmental factors that contribute to low bone mineral density (BMD) and fracture. Linkage analyses have identified quantitative trait loci (QTLs), however, the genes contributing to low BMD are largely unknown. We examined the potential association of an intronic polymorphism in CD38 with BMD and postmenopausal bone loss. CD38 resides in 4p15, where a QTL for BMD has been described. CD38-/- mice display an osteoporotic phenotype at 3 months, with normalization of BMD by 5 months. The CD38 polymorphism was identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis in 457 postmenopausal and 173 premenopausal Caucasian women whose spine and hip BMD was measured by dual energy X-ray absorptiometry (DXA). Influence of the CD38 polymorphism on bone loss was analyzed in 273 postmenopausal women over a follow-up of 2.94 +/- 1.50 years. The CD38-PvuII polymorphism was significantly associated with premenopausal and postmenopausal (P = 0.001) lumbar spine BMD. Women homozygous for the G allele had >14% lower spinal BMD than women with GC/CC genotypes. An allele dose effect was observed at the spine in premenopausal (P = 0.002) and postmenopausal (P < 0.001) cohorts. The CD38-PvuII polymorphism was significantly associated with femoral neck BMD in pre- and postmenopausal women (P = 0.002 and P = 0.011, respectively). However, significance was lost following adjustment of hip BMD for covariates in the postmenopausal cohort (P = 0.081). The CD38-PvuII polymorphism was weakly associated with bone loss at the spine (P = 0.024), in postmenopausal women not taking hormone replacement therapy. We suggest that the CD38-PvuII polymorphism may influence the attainment and maintenance of peak BMD and postmenopausal bone loss.

ADP-ribosyl Cyclase 1↗
PubMed1987

Obesity and postmenopausal bone loss: the influence of obesity on vertebral density and bone turnover in postmenopausal women.

This study was undertaken to evaluate the effect of obesity on the postmenopausal bone mass. Bone mineral density, measured by dual photon absorptiometry of the lumbar spine, serum osteocalcin (OC), fasting urinary calcium to creatinine (Ca:Cr), serum estradiol (E2) dehydroepiandrosterone (DHA) and testosterone (T) were measured in 176 women aged 45-71 years. Women were divided into four groups according to their menopausal status and their weight: 49 perimenopausal, 28 obese perimenopausal, 49 obese postmenopausal. Within each population (perimenopausal and postmenopausal), mean age was the same, only weight was significantly different (p less than 0.0001). For the two groups of postmenopausal women mean interval since menopause (YSM) was the same (5.8 +/- 3 and 5.4 +/- 5 yr). Comparison between groups revealed a significant effect of menopausal status and obesity on BMD and bone turnover. As compared to perimenopausal women, BMD was lower, OC and Ca: Cr higher only in nonobese-postmenopausal women. E2, T, DHA did not differ between the two groups of postmenopausal women. The results of this study suggest that even moderate obesity can play a protective role on postmenopausal bone loss.

Aged↗
PubMed1996

Fracture rate, pre- and postmenopausal bone mass and early and late postmenopausal bone loss are not associated with vitamin D receptor genotype in a high-endemic area of osteoporosis.

To investigate a possible association between vitamin D receptor genotype and development of postmenopausal osteoporosis, a longitudinal study from 1977 to 1995 was carried out on women living in Oslo, Norway. One hundred and eighteen premenopausal women born in 1930 were included in a study of pre- and postmenopausal bone loss in 1977. In 1995, blood samples for vitamin D receptor genotyping were available in 72, 42 and 49 of the women eligible for the determination of premenopausal bone mineral content, early postmenopausal appendicular bone loss and late postmenopausal bone mineral content, bone loss and fractures, respectively. Bone mineral density was measured in the distal and proximal right forearm annually from 1977 to 1987, and in the lumbar spine, proximal femur, right forearm and total body, including ultrasound measurements of the right calcaneus, in 1993 and 1995. Non-spinal fractures were also recorded. The results were compared to the individual vitamin D receptor genotype and it was found that vitamin D receptor genotype was neither associated with non-spinal fractures, pre- and post-menopausal bone mass nor with early and late postmenopausal bone loss within the age of 65 years. In conclusion, premenopausal bone mass, postmenopausal bone loss and the subsequent risk of osteoporosis and fractures were not predicted by vitamin D receptor genotype in a high-endemic area of osteoporosis.

Aged↗
PubMed1995

Alcohol effects on hormone levels in normal postmenopausal women and in postmenopausal women with alcohol-induced cirrhosis.

The effects of alcoholic beverage consumption on the hormonal status of postmenopausal women will be reviewed. Focused attention on the effect of social drinking 244 normal postmenopausal women has revealed that moderate alcohol intake exerts a major influence not only on estradiol, testosterone, and the estimate of aromatization of testosterone to estradiol but also on the estrogen-responsive pituitary hormones in normal postmenopausal women. The hormonal status of 66 postmenopausal women with alcohol-induced cirrhosis is compared with normal alcohol-abstaining control women. As expected, there are significant differences in levels of all hormones; furthermore, hormonal interrelationships are also disrupted. Of major interest are findings that hormone levels in alcoholic cirrhotic postmenopausal women are related to the severity of liver disease. This observation supports a role for cirrhosis per se in the hormonal disruptions noted. Of further interest are findings that hormone levels may have prognostic value in postmenopausal women with alcohol-induced liver disease.

Alcohol Drinking↗
PubMed1997

Can we measure prior postmenopausal estrogen/progestin use? The Postmenopausal Estrogen/Progestin Interventions Trial. The PEPI Investigators.

The objective of this study was to assess: 1) the accuracy of a single self-report question about postmenopausal estrogen use; and 2) the performance and repeated measures agreement of a standardized hormone use interview. Women (n = 863) in the Postmenopausal Estrogen/Progestin Interventions Trial (PEPI) completed a self-report baseline questionnaire (BQ) at enrollment and a History of Hormone Use interview (HHU) at the 3-month follow-up visit (HHU3mos). A subsample of 101 women completed a second HHU interview 3 years later (HHU3yrs). As determined by the HHU3mos, 479 (56%) of women had ever used postmenopausal estrogen and 261 (30%) had ever used postmenopausal progestin. The mean number of years since last estrogen or progestin use was 2.2 and 1.3 years, respectively. Overall, there was 95% agreement between self-reported estrogen use on the BQ and the HHU3mos (kappa = 0.91). Using the HHU3mos as the criterion standard, the BQ misclassified 2.3% of women as false positives and 6.3% as false negatives. The average duration of estrogen use in the false-negative classifications was 1.9 years (range: 1-9 years). On the HHU3mos, 39.7% of participants could not recall at least one of the specific details of estrogen use (preparation, dose, route, or starting or stopping year); similar patterns of recall were found for progestin use. Factors associated with discordant reporting of ever-use of ERT (BQ vs. HHU3mos) or incomplete reporting of estrogen/progestin use on the HHU3mos were: route of administration, recency of hormone use, duration of hormone use, and race. Age, years since menopause, education, income, and hysterectomy status were not related to discordant and/or incomplete reporting. Agreement between the HHU3mos and HHU3yrs for ever-use of estrogen was 85.2% (kappa = 0.71). In sum, a single self-report question was adequate to ascertain ever-use of postmenopausal estrogen. When a structured interview form was used, details of postmenopausal estrogen and progestin use were not well remembered. Some features of hormone use and participant characteristics were associated with completeness of recalled hormone use, which suggests the potential for differential misclassification.

Age Factors↗
PubMed1986

Bone mineral content in early-postmenopausal and postmenopausal osteoporotic women: comparison of measurement methods.

To investigate associations among methods for noninvasive measurement of skeletal bone mass, we studied 40 healthy early postmenopausal women and 68 older postmenopausal women with osteoporosis. Methods included single- and dual-energy quantitative computed tomography (QCT) and dual-photon absorptiometry (DPA) of the lumbar spine, single-photon absorptiometry (SPA) of the distal third of the radius, and combined cortical thickness (CCT) of the second metacarpal shaft. Lateral thoracolumbar radiography was performed, and a spinal fracture index was calculated. There was good correlation between QCT and DPA methods in early postmenopausal women and modest correlation in postmenopausal osteoporotic women. Correlations between spinal measurements (QCT or DPA) and appendicular cortical measurements (SPA or CCT) were modest in healthy women and poor in osteoporotic women. Measurements resulting from one method are not predictive of those by another method for the individual patient. The strongest correlation with severity of vertebral fracture is provided by QCT; the weakest, by SPA. There was a high correlation between single- and dual-energy QCT results, indicating that errors due to vertebral fat are not substantial in these postmenopausal women. Single-energy QCT may be adequate and perhaps preferable for assessing postmenopausal women. The measurement of spinal trabecular bone density by QCT discriminates between osteoporotic women and younger healthy women with more sensitivity than measurements of spinal integral bone by DPA or of appendicular cortical bone by SPA or CCT.

Adult↗
PubMed1996

Changes in vitamin-D metabolites and parathyroid hormone in plasma following cholecalciferol administration to pre- and postmenopausal women in the Netherlands in early spring and to postmenopausal women in Curaçao.

To study the effect on plasma 25-hydroxycholecalciferol (25(OH)D), 1,25-dihydroxycholecalciferol (1,25(OH)2D) and parathyroid hormone (PTH) we supplemented premenopausal (aged 30 (SD 7) years) and postmenopausal (aged 61 (SD 2) years) white women living in The Netherlands in late winter/early spring, and elderly black and white women (aged 75 (SD 6) years) living in Curaçao (Dutch Antilles) with either 10 or 20 micrograms cholecalciferol/d for 4, 5 and 9 weeks respectively. Baseline plasma 25(OH)D concentration of Dutch women was lower than that of Curaçao women. Postmenopausal Dutch women had a higher PTH concentration in plasma than premenopausal Dutch and postmenopausal Curaçao women. There were no differences in plasma 1,25(OH)2D. Cholecalciferol administration increased 25(OH)D in all groups, 1,25(OH)2D in postmenopausal Curaçao women and PTH in postmenopausal Curaçao women and premenopausal Dutch women. Serum and urinary Ca and phosphate concentrations did not change. There were no response differences between 10 and 20 microgram doses. Oral cholecalciferol administration (either 10 or 20 micrograms/d) to women living at northern latitudes in late winter/early spring increased 25(OH)D levels to the baseline levels of elderly people living in the tropics.

Administration, Oral↗
PubMed2003

Predictors of postmenopausal body mass index and waist hip ratio in the oklahoma postmenopausal health disparities study.

OBJECTIVE: The goal of the current study has been to examine systematically the respective roles of nutrition, exercise, menopausal weight gain, moderate drinking and smoking as determinants of body mass index (BMI) and waist hip ratio (WHR) in a setting in which the role of race or ethnic group could be simultaneously or individually evaluated as predictors of BMI and WHR. Because the use of estrogen replacement has been reported to affect estimates of body fat mass in postmenopausal women, endocrine factors have also been evaluated. METHODS: The design is cross-sectional with historical prospective elements. The study has a biomedical focus and is not an epidemiologic study. Data are from 649 women recruited into The Postmenopausal Health Disparities Study in Oklahoma. The study population was composed of 649 postmenopausal women: American Indian: 226 (34.9%), Asian: 21 (3.2%), Black: 78 (12.0%), Hispanics: 54 (8.3%) and Whites: 270 (41.6%). Recruitment occurred between 1994 and late 1999 in Oklahoma. RESULTS: In this multi-racial, multi-ethnic study population, there was statistical heterogeneity in all nutrition/dietary and exercise variables as well as in other potential determinants of BMI and WHR. In contrast to the literature available for postmenopausal women in which postmenopausal status, estrogen replacement and race have rarely been taken into account, the results of multi-linear regression revealed the following: Significant predictors for BMI, with or without WHR specified, included the neuroendocrine factors, menopausal weight gain, smoking, mean fitness (i.e., difficulty performing physical activities), fat as percent of total calories, moderate drinking and being Asian or Black. When WHR was not included, total calories and socioeconomic status also entered the model. The statistical predictors of WHR in the total study population with BMI in the equation included BMI and the neuroendocrine variables of FSH, E2, but not ERT, as well as the interaction of higher intensity exercise fitness with frequency, socioeconomic status and being American Indian or Asian. When BMI was not included in the model, in addition to the neuroendocrine factors, the interaction of lower intensity exercise fitness with frequency, fat as percent of total calories, age living alone and being American Indian or and Black were significant predictors of WHR. The predictors of both BMI and WHR were found to differ among individual racial and ethnic groups. CONCLUSIONS: Given the role of increased body fat and obesity in disease risk and the substantial differences in life expectancy among the racial and ethnic groups, the findings of this study, particularly in contrast to literature reports, strongly suggest that a whole variety of factors including hormonal status and race need to be considered when examining the role of dietary factors and physical activity in relation to estimates of body fat mass and disease risk.

Alcohol Drinking↗
PubMed1981

Effects in postmenopausal women of natural and synthetic estrogens on calcitonin and calcium-regulating hormone secretion. Relevance to postmenopausal osteoporosis.

The major function of calcitonin in man appears to be the prevention of excessive or unwanted bone resorption. There is a marked sex difference in circulating levels, with a relative deficiency in women. As calcitonin secretion in young women is known to be increased by estrogens, long periods of estrogen lack - such as the postmenopause - are possibly associated with a more pronounced calcitonin deficiency. This exaggerated deficiency could be an important factor in the pathogenesis of postmenopausal bone loss, especially as the latter is believed to be due to excessive bone resorption. We have studied the effects of three exogenous estrogens on the circulating levels in postmenopausal women of calcitonin, parathyroid hormone, the vitamin D metabolites 1,25 dihydroxyvitamin D and 25 hydroxyvitamin D, and calcium and phosphate. The most striking finding was a sharp rise in the plasma levels of calcitonin. Estrogens are known to prevent postmenopausal bone loss but the mechanism of action remains obscure. We suggest that the beneficial effects of estrogens could be mediated, at least in part, through control of calcitonin secretion. Thus calcitonin may prove effective in the prevention of postmenopausal bone loss and its role in the treatment of established osteoporosis warrants further evaluation.

Adult↗
PubMed2000

Effects of hormone replacement therapy on bone mineral density in postmenopausal women with primary hyperparathyroidism: four-year follow-up and comparison with healthy postmenopausal women.

BACKGROUND: Long-term treatment of patients with asymptomatic primary hyperparathyroidism remains controversial, but the presence of osteoporosis is regarded as an indication for parathyroidectomy. Hormone replacement therapy (HRT) is a possible alternative therapy in osteopenic postmenopausal women with the disorder, and results of short-term studies suggest a beneficial effect on bone mass comparable to that achieved by parathyroidectomy. Longer-term data are required to further assess the efficacy of this treatment in chronic stable primary hyperparathyroidism. METHODS: We report the results of the extension from 2 to 4 years of a randomized, placebo-controlled trial of HRT in postmenopausal women with primary hyperparathyroidism. Of 23 postmenopausal women with primary hyperparathyroidism, 11 received active HRT with conjugated equine estrogen, 0.625 mg/d, and medroxyprogesterone acetate, 5 mg/d, and 12 received placebo. Bone mineral density was measured throughout the skeleton at 6-month intervals using dual-energy x-ray absorptiometry in these women and in 50 normocalcemic age-matched control subjects. None of the 23 patients withdrew during the extension period. RESULTS: Changes in bone mineral density were more positive in those taking HRT than placebo, with the between-group differences at 4 years being 4.6% in the total body, 7.5% in the lumbar spine, 7.4% in the femoral neck, 8.2% in the femoral trochanter, 6.8% in the legs, and 7.0% in the forearm (P<.01). At skeletal sites composed predominantly of cortical bone, there was a progressive divergence of the 2 groups. Biochemical markers of bone turnover remained lower throughout the study in women taking HRT. When rates of bone loss were compared between the placebo group and healthy women of comparable age, bone loss tended to be more marked throughout the skeleton in women with hyperparathyroidism, but only in the total body and its legs subregion was this difference significant. CONCLUSIONS: Hormone replacement therapy is efficacious in the long-term management of osteopenia in postmenopausal women with primary hyperparathyroidism and thus represents an important new therapeutic option for asymptomatic patients who do not have other indications for surgery. Bone loss seems to be accelerated in untreated primary hyperparathyroidism.

Absorptiometry, Photon↗
PubMed1997

The effect of postmenopause and postmenopausal HRT on measured voice values and vocal symptoms.

OBJECTIVES: To study the effect of postmenopause and postmenopausal hormone replacement therapy (HRT) on the measured fundamental frequency (F0) and sound pressure level (SPL) of sustained phonation and speaking voice samples and on subjective vocal/laryngeal symptoms. METHODS: Forty-three postmenopausal women (mean age 51.6) were divided into three groups: a group with no HRT, an estrogen group (daily oral dose of 2 mg of estradiol valerate), and an estrogen-progestin group (daily oral dose of 2 mg of 17-B-estradiol and 1 mg of northisterone acetate). Voice measurements were made before and after 1 year of treatment. Subjective symptoms were registered using a questionnaire. RESULTS: The mean F0 and SPL decreased significantly in the group with no HRT in spontaneous speech and reading samples as did SPL in the normal phonation sample. In both groups with HRT, the mean F0 decreased significantly only in the spontaneous speech sample and the decrease was smaller than in the group with no HRT. The mean SPL decrease in the estrogen group was significant in the normal phonation sample while in the estrogen-progestin group it was significant in both the normal phonation and the reading sample. The number of subjective symptoms was smallest in the estrogen group. CONCLUSIONS: The changes in the measured voice values and the subjective symptoms experienced suggest that at least the early postmenopausal years are associated with vocal changes and that HRT counteracts this phenomenon. This seems to be more pronounced with estrogen than with a combination of estrogen and progestin.

Cohort Studies↗
PubMed2004

The effect of exemestane on serum lipid profile in postmenopausal women with metastatic breast cancer: a companion study to EORTC Trial 10951, 'Randomized phase II study in first line hormonal treatment for metastatic breast cancer with exemestane or tamoxifen in postmenopausal patients'.

BACKGROUND: The impact of aromatase inhibitors (AIs) on non-cancer-related outcomes, which are known to be affected by oestrogens, has become increasingly important in postmenopausal women with hormone-dependent breast cancer. So far, data related to the effect of AIs on lipid profile in postmenopausal women is scarce. This study, as a companion substudy of an EORTC phase II trial (10951), evaluated the impact of exemestane, a steroidal aromatase inactivator, on the lipid profile of postmenopausal metastatic breast cancer (MBC) patients. PATIENTS AND METHODS: The EORTC trial 10951 randomised 122 postmenopausal breast cancer patients to exemestane (E) 25 mg (n = 62) or tamoxifen (T) 20 mg (n = 60) once daily as a first-line treatment in the metastatic setting. Exemestane showed promising results in all the primary efficacy end points of the trial (response rate, clinical benefit rate and response duration), and it was well tolerated with low incidence of serious toxicity. As a secondary end point of this phase II trial, serum triglycerides (TRG), high-density lipoprotein cholesterol (HDL), total cholesterol (TC), lipoprotein a (Lip a), and apolipoproteins (Apo) B and A1 were measured at baseline and while on therapy (at 8, 24 and 48 weeks) to assess the impact of exemestane and tamoxifen on serum lipid profiles. Of the 122 randomised patients, those who had baseline and at least one other lipid assessment are included in the present analysis. The patients who received concomitant drugs that could affect lipid profile are included only if these drugs were administered throughout the study treatment. Increase or decrease in lipid parameters within 20% of baseline were considered as non-significant and thus unchanged. RESULTS: Seventy-two patients (36 in both arms) were included in the statistical analysis. The majority of patients had abnormal TC and normal TRG, HDL, Apo A1, Apo B and Lip a levels at baseline. Neither exemestane nor tamoxifen had adverse effects on TC, HDL, Apo A1, Apo B or Lip a levels at 8, 24 and 48 weeks of treatment. Exemestane and tamoxifen had opposite effects on TRG levels: exemestane lowered while tamoxifen increased TRG levels over time. There were too few patients with normal baseline TC and abnormal TRG, HDL, Apo A1, Apo B and Lip a levels to allow for assessment of E's impact on these subsets. The atherogenic risk determined by Apo A1:Apo B and TC:HDL ratios remained unchanged throughout the treatment period in both the E and T arms. CONCLUSIONS: Overall, exemestane has no detrimental effect on cholesterol levels and the atherogenic indices, which are well-known risk factors for coronary artery disease. In addition, it has a beneficial effect on TRG levels. These data, coupled with E's excellent efficacy and tolerability, support further exploration of its potential in the metastatic, adjuvant and chemopreventive setting.

Adult↗
PubMed1998

Effect of postmenopausal hormone therapy on lipoprotein(a) concentration. PEPI Investigators. Postmenopausal Estrogen/Progestin Interventions.

BACKGROUND: Postmenopausal hormone therapy has been reported to decrease levels of lipoprotein (Lp)(a) in cross-sectional studies and small or short-term longitudinal studies. We report findings from a large, prospective, placebo-controlled clinical trial that allows a broad characterization of these effects for four regimens of hormone therapy. METHODS AND RESULT: The Postmenopausal Estrogen/Progestin Interventions study was a 3-year, placebo-controlled, randomized clinical trial to assess the effect of hormone regimens on cardiovascular disease risk factors in postmenopausal women 45 to 65 years of age. The active regimens were conjugated equine estrogens therapy at 0.625 mg daily, alone or in combination with each of three regimens of progestational agents: medroxyprogesterone acetate (MPA) at 2.5 mg daily (ie, continuous MPA), MPA at 10 mg days 1 to 12 (ie, cyclical MPA), and micronized progesterone at 200 mg days 1 to 12. Plasma levels of Lp(a) were measured at baseline (n = 366), 12 months (n = 354), and 36 months (n = 342). Assignment to hormone therapy resulted in a 17% to 23% average drop in Lp(a) concentrations relative to placebo (P<.0001), which was maintained across 3 years of follow-up. No significant differences were observed among the four active arms. Changes in Lp(a) associated with hormone therapy were positively correlated with changes in LDL cholesterol, total cholesterol, apolipoprotein B, and fibrinogen levels and were similar across subgroups defined by age, weight, ethnicity, and prior hormone use. CONCLUSIONS: Postmenopausal estrogen therapy, with or without concomitant progestin regimens, produces consistent and sustained reductions in plasma Lp(a) concentrations.

Aged↗
PubMed1993

Vertebral postmenopausal bone loss is reduced in overweight women: a longitudinal study in 155 early postmenopausal women.

To study the influence of excess body weight on vertebral postmenopausal bone loss, 155 healthy early postmenopausal women were divided into 2 groups according to their body mass index (BMI = weight/height2) and prospectively followed over a mean 31-month period. Spinal (L2-L4) bone mineral density was measured by dual photon absorptiometry. The annual rate of vertebral bone loss (percentage) was significantly reduced (-0.54 +/- 1.1% vs. -1.46 +/- 1.6%; P < 0.05) in the overweight group (BMI, > or = 25; n = 40) compared to that in the normal weight group (BMI, < 25; n = 115). At baseline, a significant decrease in the urinary calcium/creatinine ratio was observed in the overweight group, which suggested a decrease in bone turnover. A significant correlation was found between the annual rate of bone loss and the BMI (r = 0.21; P < 0.05), but not the body weight. The positive correlation between vertebral postmenopausal rate of bone loss and BMI was confirmed after adjustment for age and time since menopause. Moreover, plasma dehydroepiandrosterone sulfate levels were higher in the high BMI group than in the normal BMI group (P < 0.05). We conclude that within the first years after menopause, moderate excess body weight significantly reduces vertebral postmenopausal bone loss. This effect is probably related to excess adipose tissue through increased conversion of estrogen from adrenal precursors and/or increased production of adrenal androgens.

Body Mass Index↗
PubMed1997

Effect of postmenopausal hormone therapy on body weight and waist and hip girths. Postmenopausal Estrogen-Progestin Interventions Study Investigators.

Reports from cross-sectional comparisons, nonrandomized prospective studies, and relatively small clinical trials indicate that postmenopausal hormone therapy may slightly decrease the amount of weight typically gained by women during the decade following menopause. Despite this, widespread belief remains that hormone therapy may cause weight gain. We use data from the Postmenopausal Estrogen/Progestin Interventions trial to characterize the impact of postmenopausal hormone therapy on weight and fat distribution and to examine the consistency of this impact among subgroups of women defined by lifestyle, clinical, and demographic factors. The Postmenopausal Estrogen/Progestin Interventions trial was a 3-yr, placebo-controlled, randomized clinical trial of 875 women assessing the effects on cardiovascular risk factors of four hormone regimens: oral conjugated equine estrogen (CEE) therapy (0.625 mg daily alone), CEE in combination with medroxyprogesterone acetate (2.5 mg daily), CEE in combination with medroxyprogesterone acetate (10 mg daily on days 1-12), and CEE in combination with micronized progesterone (200 mg daily on days 1-12). Women randomly assigned to CEE with or without a progestational agent averaged 1.0 kg less weight gain at the end of 3 yr (P = 0.006) than those assigned to placebo. Assignment to CEE was also associated with averages of 1.2 cm less increase in waist girth (P = 0.01) and 0.3 cm less increase in hip (P = 0.07) girth. In regression models that included weight change as a covariate, none of these differences reached statistical significance. There were no significant differences in weight or girth changes among any of the four active hormone regimens. After accounting for the effects of assignment to active hormone therapy and baseline weight, older age (P 0.008) and higher physical activity level at baseline (P = 0.002) were also independently predictive of less weight gain. The impact of hormone therapy on weight gain was similar among subgroups, except for those defined by baseline smoking status (P = 0.04) and physical activity level at home (P = 0.02). Factors that were independently associated with smaller increases in girths were: for waist, greater overall activity (P = 0.005) and Hispanic ethnicity (P = 0.02); and for hip, work activity (P = 0.003) and greater alcohol consumption (P = 0.03). None of these factors significantly affected the observed overall relationships between estrogen and changes in girth.

Animals↗
PubMed2004

Prevention of postmenopausal bone loss: six-year results from the Early Postmenopausal Intervention Cohort Study.

We report the effect of continuous treatment with alendronate for 6 yr vs. placebo in the Early Postmenopausal Intervention Cohort study. A total of 1609 healthy, early postmenopausal women were recruited; we describe results for the 585 women who received continuous placebo or alendronate (2.5 or 5 mg) daily for 6 yr. Bone mineral density (BMD) was evaluated at the lumbar spine, hip, forearm, and total body at baseline and annually thereafter. Bone turnover markers were measured every 6 months from baseline to yr 2 and annually thereafter. Adverse experiences, including upper gastrointestinal events and fractures, were recorded throughout the study. Women receiving placebo experienced progressive decreases in BMD at all skeletal sites. Patients receiving alendronate experienced significant gains in spine and hip BMD that were maintained through yr 6. Significantly greater, dose-related decreases in bone turnover markers in the alendronate groups vs. placebo occurred within the first year and were sustained through yr 6. Women receiving alendronate had adverse experience incidences similar to those receiving placebo. Fractures occurred in 11.5, 10.3, and 8.9% of women taking placebo, 2.5 mg alendronate, or 5 mg alendronate daily, respectively. Therapy with alendronate is an effective and promising strategy for the prevention of postmenopausal osteoporosis.

Alendronate↗