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PubMed2004

Quantitative ultrasound (QUS) of bone in the management of postmenopausal women.

OBJECTIVES: Postmenopausal osteoporosis is becoming a major problem for healthcare institutions as it has a growing social and economic impact. The incidence of osteoporotic fractures is constantly increasing due to the increase in life expectancy. The gynaecologist plays an important role in establishing a "biological zero" in each perimenopausal patient, and controlling the rate of bone loss during postmenopausal period. RESULTS: Dual energy X-ray absorptiometry (DXA) has been widely used for the diagnosis and management of osteoporosis and represents a strong risk factor for fractures, but it presents several limitations with regards to diagnosis, treatment follow-up and differential diagnosis of secondary osteoporosis. In these last years quantitative ultrasound (QUS) technique has been introduced for the evaluation of bone status in postmenopausal women and several in vitro and clinical studies have demonstrated the reliability of the examination in terms of: reproducibility, evaluation of fracture risk, treatment follow-up, differential diagnosis. QUS has proven to be equally capable in the prediction of future osteoporosis related fractures in comparison to DXA. Large-scale cross-sectional and longitudinal studies have demonstrated the applicability of QUS in screening the female population during the climacteric period. QUS technique seems to be very efficient in identifying "fast losers", identifying subjects at risk for osteoporosis requiring second-level investigation (DXA, X-ray), diagnosing secondary osteoporosis. CONCLUSION: If QUS is used in a systematic and rational manner in clinical practice, it is a valid technique for the prevention of osteoporosis in postmenopausal women.

Bone and Bones↗

PubMed1998

Metabolic effects of tibolone in postmenopausal women with non-insulin dependent diabetes mellitus.

OBJECTIVE: Postmenopausal women with non-insulin dependent diabetes (NIDDM) are frequently obese, hypertensive and hyperlipidaemic and hence at particular risk of coronary heart disease (CHD). They might therefore benefit from menopausal therapy. In view of the improvement in insulin sensitivity and the reduction in triglyceride levels induced by tibolone in healthy postmenopausal women we evaluated the effects of 12 months of tibolone on glycaemic control, serum insulin and lipid levels in postmenopausal women with NIDDM. DESIGN: A prospective 12 months before/after intervention study. PATIENTS: Fourteen postmenopausal women (mean age 58.14 +/- 1.25 years; mean duration of menopause 121.21 +/- 13.42 months; mean BMI: 26.55 +/- 0.97) with NIDDM (mean duration of diabetes 113.79 +/- 13.89 months). MEASUREMENTS: Fasting and postprandial blood glucose levels were assessed monthly, serum fructosamine, fasting and postprandial insulin every 3 months and serum lipids (total cholesterol, triglyceride, HDL-cholesterol and LDL-cholesterol) every 6 months. RESULTS: Changes in blood glucose, both fasting and postprandial, were not statistically significant during the treatment period. Serum fructosamine concentration increased significantly after 9 months. A significant decrease in fasting and postprandial insulin concentrations was observed after 9 months. A non-significant decrease was observed in total cholesterol, LDL cholesterol and triglyceride but no change in HDL cholesterol. Body weight did not change during the period of observation. CONCLUSION: A slight deterioration in glycaemic control, a fall in insulin concentration and no change in serum lipids were observed in women with NIDDM during 12 months treatment with tibolone.

Anabolic Agents↗

PubMed1998

Long-term effects of percutaneous estradiol on bone loss and bone metabolism in postmenopausal hysterectomized women.

OBJECTIVE: To determine whether percutaneous estradiol (pE2) (1.5 mg/day) is able to counteract the postmenopausal bone loss in postmenopausal hysterectomized women, in a double-blind study versus oral estriol (E3) (2 mg/day). METHODS: The bone mineral density of the lumbar spine (LS) and of the proximal femur (PF) was measured every 3 months by dual energy X-ray absorptiometry for 2 years in 43 hysterectomized postmenopausal women (21 in the E2 group and 22 in the E3 control group), and in a subset of patients for a 3rd year. The statistical analyses were performed on Macintosh using Stat View II. RESULTS: A significant bone loss of 1.2 (0.4%)% and of 1.3 (0.3)% per year was observed in the control group, respectively at LS and at PF, versus a significant gain of 1.2 (0.5)% per year in the treated group at the LS. No significant change at PF occurred in the treated group. In the 20 patients followed up for a 3rd year on pE2, an increase of 1.2 (0.9) and 2.5 (1.4)% at LS in the 12 former active group patients and the eight formerly control patients, respectively was seen. The same trend was observed at the proximal femur. CONCLUSION: pE2 (1.5 mg E2) is able to counteract the postmenopausal bone loss in hysterectomized women, whereas E3 (2 mg/day administered orally) is unable to maintain bone mass.

Administration, Cutaneous↗

PubMed1997

Endometrial sonographic and histologic findings in women with and without hormonal replacement therapy suffering from postmenopausal bleeding.

OBJECTIVES: To evaluate, in women with postmenopausal bleeding, the effect of hormonal replacement (HRT) therapy on the endometrial thickness as measured by transvaginal sonography in relation to endometrial histology. METHODS: 1110 women with sequential/progestin treatment (E + P) (n = 202), with Estriol treatment (n = 149) or without HRT (n = 759) and postmenopausal bleeding were examined by transvaginal sonography (TVS) prior to curettage, with special reference to the relation of endometrial thickness to its histopathology. RESULTS: The distribution of endometrial pathology was different in those women with E + P and Estriol compared with those without HRT. Endometrial pathology was found most frequently in women with an endometrium exceeding 8 mm in thickness. Furthermore, the incidence was found to increase with increasing endometrial thickness in all treatment groups. Atrophy was found significantly more often in women without HRT. Hormonal effects on the endometrium were found significantly more often in women with E + P and Estriol. Endometrial hyperplasia was found most commonly in women with Estriol in the thickness group 5 8 mm (P < 0.001) as compared to those with HRT and without HRT. Endometrial cancer occurs most in women without HRT, in those women with an endometrium exceeding 8 mm in thickness as compared both to the E + P (P < 0.001) group and to the Estriol (P < 0.001) group. Endometrial cancer did not occur in any woman (with E + P, Estriol or without HRT) with an endometrial thickness of < or = 4 mm. CONCLUSIONS: TVS is of value for excluding endometrial pathology in women with HRT and postmenopausal bleeding. The distribution of endometrial findings and histopathological diagnosis in women with abnormal postmenopausal bleeding was different in women with E + P than in women without HRT. Furthermore, the cut-off for excluding endometrial abnormalities is the same in both groups i.e. < or = 4 mm.

Endometrium↗

PubMed1998

Inhibin A and B in peri- and postmenopause.

OBJECTIVE: The aim of the study was to investigate the origin of inhibin A and B during the last years of the reproductive age and after menopause by measuring their levels in the ovarian and peripheral venous blood. METHODS: The study population consisted of 43 women, aged 42-69 years (mean 50), who underwent hysterectomy with ovarian removal for a benign disease. A total of 24 of them were in follicular phase, 11 in luteal phase, and eight were postmenopausal. Peripheral and ovarian venous blood was collected for measurement of inhibin A and B. In addition, sex steroid hormone and gonadotropin levels were measured. RESULTS: Ovarian venous inhibin B correlated significantly with ovarian estradiol secretion (r = 0.5, P = 0.001). The levels of inhibin B were significantly higher in the ovarian vein than in the peripheral vein (P = 0.006). The highest inhibin B concentrations were detected in the mid-proliferative (mid-follicular) phase (median 31.6 pg/ml range 25.9-47.9). In postmenopausal women, inhibin B was not detectable. No correlation between FSH and ovarian inhibin B was found. Inhibin A rose rapidly in late proliferative (late follicular) phase (median 28.5, range < 2-51.8) and dominated in the circulation throughout the luteal phase (median 20.9, range 8.8-60). For inhibin A, no concentration gradient existed between the ovarian and peripheral vein. Unlike inhibin B, inhibin A was detectable in ovarian and peripheral blood in postmenopausal women. A significant negative correlation between ovarian and peripheral inhibin A and FSH was found (r = -0.386, P = 0.015; r = -0.345, P = 0.034, respectively). CONCLUSION: Inhibin B correlates with ovarian estradiol secretion and seems to reflect follicular function. Inhibin A dominates in circulation during the luteal phase but is detectable at low concentrations both in follicular phase and even in postmenopause. Our findings suggest that inhibin A may play a role in FSH suppression in the female reproduction. In addition to the ovary, there may be extragondal source(s) of inhibin A.

Adult↗

PubMed1999

A longitudinal study of the effect of vitamin K2 on bone mineral density in postmenopausal women a comparative study with vitamin D3 and estrogen-progestin therapy.

OBJECTIVES: To investigate the effect of vitamin K2 treatment for a year on spinal bone mineral density (BMD) in postmenopausal women, comparing with vitamin D3 hormone replacement therapy and to determine the factors which affect the efficacy of vitamin K2 therapy. SUBJECTS AND METHODS: Seventy-two postmenopausal women were randomized into four groups and treated with respective agents. Before the therapy, 6 and 12 months after the treatment, their lumbar spine BMD were measured by dual energy X-ray absorptiometry. The rates of change in BMD (delta BMD) were calculated. Correlations of BMD with age, year since menopause and the initial BMD were determined. RESULTS: Vitamin K2 suppressed the decrease in spinal BMD as compared with no treatment group. BMD in women treated with vitamin K2 was inversely correlated with their age (r = -0.54; P < 0.05). CONCLUSIONS: Vitamin K2 therapy may be a useful method for preventing postmenopausal spinal bone mineral loss. In addition, the therapy should be started early in postmenopausal period.

Bone Density↗

PubMed1999

Depressive vulnerability is not an independent risk factor for osteoporosis in postmenopausal women.

Major depression has been repeatedly but not consistently reported to be associated with low bone mineral density (BMD) and to an increased risk for fracture in women. We have investigated, in healthy postmenopausal women, whether depressive symptomatology, assessed by the General Health Questionnaire (GHQ), was associated to a significant decrease in BMD, hence supporting the hypothesis of an independent pathogenetic link between the two disorders. We investigated 121 postmenopausal women, aged 48-77 years, spontaneously attending a screening visit for osteoporosis in an outpatient facility. BMD of the spine and the non-dominant hip (total and neck areas) were measured by Dual Energy X-Ray absorptiometry. All subjects completed to the 'General Health Questionnaire' translated and validated in French. No significant correlations were observed between the GHQ score and BMD of the spine (P = 0.54), the total hip area (P = 0.65), or the femoral neck area (P = 0.65). No differences in terms of spinal or femoral BMD were observed between women with GHQ score < 5 or > or = 5. When comparing values of BMD between women within the upper and the lower quartiles for GHQ score, no difference was observed for spine (P = 0.69), total hip (P = 0.80), or femoral neck (P = 0.93). Similarly, GHQ scores were not significantly different when comparing women in the upper and lower quartiles of BMD distribution at the spine or the hip. In conclusion, notwithstanding the clinical pattern of postmenopausal osteoporosis can lead to depression and, on the other hand, hormonal and behavioral disturbances reported in depression might be enhancing factors for accelerated bone loss, our present results do not support the hypothesis that otherwise healthy postmenopausal women with increased depressive complaints are also more prone to exhibit osteoporotic fractures.

Aged↗

PubMed2001

Attenuation of endothelin-1 induced vasoconstriction by 17beta estradiol is not sustained during long-term therapy in postmenopausal women with coronary heart disease.

OBJECTIVES: The goal of this study was to determine the long-term effects of estrogen replacement therapy on the response to endothelin-1 (ET-1) in postmenopausal women with coronary heart disease. BACKGROUND: It is thought that the vasoconstrictor ET-1 is involved in the development and progression of atherosclerosis. Estrogen replacement may slow the development of atherosclerosis in postmenopausal women. METHODS: Nineteen of 20 postmenopausal women randomized to either three months of 2 mg oral estradiol or placebo completed the double-blind placebo-controlled protocol. Change in forearm blood flow (FBF) in response to a 60 min brachial arterial infusion of ET-1 (5 pmol/min) was measured before randomization, after one month of randomized therapy and after three months of therapy using venous occlusion plethysmography. RESULTS: Estrogen treatment had no effect on baseline FBF. Systolic and diastolic blood pressure and heart rate did not change in response to estrogen therapy or ET-1. Before randomization, in response to ET-1, FBF was reduced by -21.9% (mean response over 60 min) in the placebo group and -19.0% in the estradiol group (p = 0.67). After one month of therapy, the response was attenuated in the estrogen group, -10.0%, compared with the placebo group, -23.6 (difference in means 13.6%, 95% confidence interval [0.7%, 26.6%], p = 0.041). After three months of therapy, there was no difference in response between the placebo group, -27.0%, and estrogen group, -30.2% (p = 0.65). CONCLUSIONS: In postmenopausal women with coronary heart disease, estrogen therapy inhibits the vasoconstrictor response to ET-1 after one month of therapy. This effect is lost after three months of therapy, suggesting that tachyphylaxis to one potentially beneficial action of estradiol develops during chronic treatment.

Aged↗

PubMed2001

Relationship between the angiotensin-converting enzyme genotype and the forearm vasodilator response to estrogen replacement therapy in postmenopausal women.

OBJECTIVES: We sought to evaluate the relationship between the angiotensin-converting enzyme (ACE) genotype and the change in forearm vasoreactivity in response to a three-month course of oral estrogen in postmenopausal women. BACKGROUND: The ACE genotype is a known predictor of the response to an ACE inhibitor drug; however, it is not clear whether it can modify the effect of estrogen replacement therapy (ERT) on endothelial function in postmenopausal women. METHODS: Fifty-five postmenopausal women received 0.625 mg of conjugated equine estrogen daily for three months. Forearm blood flow (FBF) was measured by strain-gauge plethysmography. RESULTS: Twenty-one, 25 and 9 patients had the insertion/deletion (ID), II and DD genotypes, respectively. Plasma ACE activity was significantly higher at baseline in patients with either the DD or ID genotype than in those with the II genotype (p < 0.05). A significant decrease in plasma ACE activity with ERT was seen in the ID and II genotypes (p < 0.05), but not in the DD genotype. There were no significant differences in the FBF responses to reactive hyperemia at baseline between the three groups. Estrogen replacement therapy did not alter the FBF response to reactive hyperemia in the DD genotype (4.0 +/- 1.3%), although ERT significantly increased the FBF response in the ID and II genotypes (32.6 +/- 7.5% and 30.6 +/- 6.5%, respectively; p < 0.05). Forearm blood flow after administration of sublingual nitroglycerin did not change over three months in any of the three groups. CONCLUSIONS: These findings suggest that the effect of ERT in postmenopausal women on forearm endothelial function may be determined in part by the genotype of the ACE gene.

Administration, Oral↗

PubMed2002

Oral conjugated equine estrogen increases plasma von Willebrand factor in postmenopausal women.

OBJECTIVES: We sought to test whether one month of daily oral conjugated equine estrogen (CEE) or transdermal estradiol alters hemostatic factors in postmenopausal subjects. BACKGROUND: Estrogen replacement therapy and hormonal replacement therapy (HRT) effect an early increase in cardiovascular events in postmenopausal women. Circulating plasma von Willebrand factor (vWF) antigen is a marker of generalized endothelial dysfunction and atherothrombosis. METHODS: Thirty-eight healthy postmenopausal women (average 59 +/- 7 years) were randomized to receive daily oral CEE, 0.625 mg (n = 21); transdermal estradiol, 0.1 mg/day (n = 7); or oral placebo (n = 10) for one month. Blood samples were collected at baseline and after two weeks and four weeks of therapy for measurement of circulating plasma hormones, lipid concentrations, and hemostatic factors. RESULTS: Oral CEE decreased total cholesterol (p < 0.01) and low-density lipoprotein cholesterol (p < 0.01), although it increased both triglycerides (p < 0.05) and high-density lipoprotein cholesterol (p < 0.01). Transdermal estradiol had no significant effect on lipids. Plasminogen activator inhibitor-1 antigen declined in both oral CEE and transdermal estradiol users, but did not achieve statistical significance. Fibrin D-dimer antigen did not vary significantly in any group. However, oral CEE users had a significant increase in vWF from baseline to four weeks (p < 0.03) and a decrease in tissue-type plasminogen activator antigen from baseline to four weeks (p < 0.004), which was significantly different from the change observed in the transdermal estradiol group (p < 0.05). CONCLUSIONS: These data suggest that the oral CEE-mediated increase in plasma vWF may have clinical relevance given the early atherothrombotic effects of HRT in postmenopausal women.

Administration, Cutaneous↗

PubMed2003

Effects of raloxifene on endothelium-dependent dilation, lipoproteins, and markers of vascular function in postmenopausal women with coronary artery disease.

OBJECTIVES: We sought to assess the effects of raloxifene, a selective estrogen receptor modulator, on arterial physiology and biology in postmenopausal women with coronary artery disease (CAD). BACKGROUND: Raloxifene improves endothelial function and markers of vascular health in vitro in experimental animals and in healthy postmenopausal women. In women whose arteries are affected by advanced atherosclerosis, however, the vascular effects of estrogen receptor modulation are unknown. METHODS: We conducted a prospective, randomized, double-blinded, placebo-controlled, crossover trial of raloxifene, 60 mg/day for 8 weeks, in 33 consecutively eligible and consenting postmenopausal women age 50 to 75 years with known CAD. Parameters measured at the beginning and end of each treatment period included brachial artery flow-mediated dilation (FMD), the primary end point, as well as nitroglycerin-induced dilation, peripheral artery tonometry, serum lipoprotein levels, and markers of vascular function, including urinary prostaglandin, serum endothelin-1, and fibrinogen levels. RESULTS: Baseline FMD was impaired in these women, as expected (2.84 +/- 0.60%), but there was no significant difference between the effect of raloxifene (0.26 +/- 0.66% increase) and placebo (0.01 +/- 0.63% decrease) on this marker of endothelial function (p = 0.82). No significant raloxifene-related effects were observed on derived aortic pressure, pulse pressure, augmentation index, total cholesterol or low- and high-density lipoprotein subfractions, markers of thrombosis, or vasoconstrictor or vasodilator substances. CONCLUSIONS: In postmenopausal women with treated CAD, selective estrogen receptor modulation with raloxifene does not improve a comprehensive set of parameters examining vascular function and serum lipoprotein levels.

Aged↗

PubMed1998

The effect of hormone replacement therapy alone and in combination with simvastatin on plasma lipids of hypercholesterolemic postmenopausal women with coronary artery disease.

OBJECTIVES: This study sought to compare hormone replacement therapy (HRT), simvastatin and their combination in the management of hypercholesterolemia in postmenopausal women with coronary artery disease (CAD). BACKGROUND: Lipid-lowering therapy reduces mortality in hypercholesterolemic women with CAD. In postmenopausal women HRT seems to increase survival, particularly those with ischemic heart disease, and this is partly due to changes in lipid levels. METHODS: We studied 16 postmenopausal women with CAD and fasting total cholesterol <200 mg/dl and low-density lipoprotein (LDL) cholesterol <130 mg/dl. We compared HRT (0.625 mg of conjugated estrogen and 2.5 mg of medroxyprogesterone acetate daily) with simvastatin (20 mg daily) and their combination in a randomized, crossover, placebo-controlled study. Each treatment period was 8 weeks long with a 4-week washout interval between treatments. RESULTS: Simvastatin, HRT and their combination significantly reduced total and LDL cholesterol by 35%, 13%, and 33% and 45%, 20%, and 46%, respectively, compared to placebo (p < 0.001). However, simvastatin and the combination was superior to HRT (p < 0.001), and none of our patients had total cholesterol <180 mg/dl and LDL cholesterol <100 mg/dl on HRT alone. High-density lipoprotein cholesterol was not significantly affected by any of the active treatments, and triglycerides were lower during simvastatin therapy compared to placebo (p < 0.01). Apolipoprotein B was significantly reduced by simvastatin, alone and combined with HRT, by 39% and 35%, respectively, compared to placebo (p < 0.001). Alone and in combination with simvastatin, HRT significantly increased apolipoprotein A-I by 11% and 12%, respectively, compared to placebo (p < 0.05) and decreased lipoprotein (a) by 23% and 33%, respectively, compared to placebo (p < 0.05), whereas simvastatin had no significant effect on either of these parameters. CONCLUSIONS: In hypercholesterolemic postmenopausal women with CAD, HRT exerts beneficial effects on plasma lipids but the levels currently recommended for secondary prevention are not achieved. Hormone replacement therapy combined with simvastatin is well tolerated and extremely effective, as the two therapies seem to be additive.

Aged↗

PubMed1999

Individual and combined effects of estrogen/progestin therapy and lovastatin on lipids and flow-mediated vasodilation in postmenopausal women with coronary artery disease.

OBJECTIVES: We sought to examine the individual and combined effects of estrogen/progestin therapy versus lovastatin on lipids and flow-mediated vasodilation in postmenopausal women with heart disease. BACKGROUND: Little information is available regarding the relative benefits of estrogen replacement therapy versus reductase inhibitors and the potential utility of their combination as lipid-lowering therapy for postmenopausal women. METHODS: We conducted a randomized, double-blind, crossover trial in 24 postmenopausal women, each of whom received the following drug regimens during three consecutive six-week treatment periods: 1) hormone replacement (oral dose of 0.625 mg/day conjugated equine estrogens and 2.5 mg/day medroxyprogesterone acetate); 2) 20 mg lovastatin/day and 3) hormone replacement plus lovastatin. RESULTS: Total and low density lipoprotein (LDL) cholesterol were significantly lowered and high density lipoprotein (HDL) cholesterol was significantly increased by all three regimens compared with baseline (p < 0.05). Lovastatin was more effective than estrogen/progestin in reducing LDL (p < 0.001), but estrogen/progestin was slightly more effective in increasing HDL. The hormone replacement and lovastatin regimen blocked the estrogen-associated increase in triglycerides. Hormone replacement (alone and with lovastatin) resulted in increases in brachial artery flow-mediated vasodilator capacity (p = 0.01 for both regimens) and the area under the curve (p = 0.016 and p = 0.005, respectively) compared with baseline. Percent dilation was greatest after the hormone replacement regimen, whereas the area under the curve was greatest after hormone replacement plus lovastatin (69% improvement vs. baseline). CONCLUSIONS: In postmenopausal women with coronary disease and hyperlipidemia, conjugated equine estrogen produced significant improvements in lipids and vasodilator responses despite the concurrent administration of low dose medroxyprogesterone acetate. Low dose lovastatin produced greater reductions in LDL, but less dramatic improvements in vasodilator responses. Estrogen/progestin plus lovastatin may provide additional benefits via a greater reduction in the LDL/HDL ratio and attenuation of estrogen-associated hypertriglyceridemia. More information is needed about the safety and efficacy of such combinations of hormone replacement and reductase inhibitor therapy.

Aged↗

PubMedDate not supplied

Fatty acid compositions of serum phospholipids of postmenopausal women: a comparison between Greenland Inuit and Canadians before and after supplementation with fish oil.

OBJECTIVES: We compared serum phospholipid fatty acid compositions, in particular the status of omega-3 polyunsaturated fatty acid (PUFA), of postmenopausal Greenland Inuit women and postmenopausal Canadian women at baseline and after supplementing the Canadian women with a fish-oil product. METHODS: Fasting serum samples were collected from 15 Inuit subjects from Greenland and 16 non-Inuit subjects from Canada. In addition, eight Canadian subjects provided fasting serum samples after completing a long-chain omega-3 PUFA intervention (2.4 g of eicosapentaenoic acid [EPA] plus 1.6 g of docosahexaenoic acid [DHA] per day) for 28 d. Fatty acid compositions of serum phospholipids of the samples were determined and compared by one-way analysis of variance. RESULTS: In comparison with the Greenlanders, baseline Canadian women had 73% and 46% less EPA (20:5omega-3) and DHA (22:6omega-3), respectively, and 32% and 91% more linoleic acid (LA; 18:2omega-6) and arachidonic acid (AA; 20:4omega-6), respectively. The omega-3 supplementation in Canadian women increased DHA and decreased LA levels to approach those in Greenland Inuit and raised EPA levels to surpass (45% higher) those in Greenland women (P < 0.0001). In contrast, AA was only moderately lowered (by 16% overall) such that AA levels remained 62% higher in the supplemented Canadians than in the Greenlanders (P < 0.0001). CONCLUSIONS: Short-term EPA plus DHA supplementation of postmenopausal North American women can mimic the high EPA and DHA levels and lower LA levels in corresponding Inuit women but not the markedly lower levels of AA. The present findings also support the hypothesis of genetically decreased Delta5-desaturase potential in the Greenland Inuit compared with Canadian postmenopausal women.

Arachidonic Acid↗

PubMed2006

Tuboovarian abscesses in postmenopausal women.

OBJECTIVE: To compare the clinical features of tuboovarian abscess (TOA) in pre- and postmenopausal women. MATERIALS AND METHODS: Between January 1992 and December 2000, all patients with surgically documented TOA at National Taiwan University Hospital were enrolled into this retrospective study. Salient information with respect to the history, current illnesses, risk factors, physical findings, laboratory data, surgeries and postoperative complications was obtained from medical records. RESULTS: Of 74 patients with TOA, nine were postmenopausal women. Compared with the premenopausal group, postmenopausal patients were significantly more likely to have contributing medical disorders (p < 0.001) and concomitant pelvic malignant tumors (p = 0.037). CONCLUSION: Thorough investigation for concomitant pelvic malignant tumors and meticulous medical care should be provided for postmenopausal women with TOA.

Abdominal Pain↗

PubMed2006

Expression of estrogen receptors alfa and beta mRNA and alkaline phosphatase in the differentiation of osteoblasts from elderly postmenopausal women: comparison with osteoblasts from osteosarcoma cell lines.

OBJECTIVE: To evaluate the expression of estrogen receptors (ER) alpha and beta, and activity of alkaline phosphatase during differentiation of primary osteoblast cells (hOB) from aged postmenopausal women and human osteosarcoma cell lines (HOS, MG63). MATERIALS AND METHODS: Osteoblast cultures were prepared from the upper femur of postmenopausal patients (age, 60-74 years) and HOS. At the indicated times (days 5, 10, 15, 20, and 25), alkaline phosphatase activity and expression of ERalpha and ERbeta mRNA were evaluated. RESULTS: In both cultures of primary hOB and HOS, alkaline phosphatase activity decreased at the osteoblast proliferation stage, whereas it subsequently increased at the matrix maturation stage. ER beta mRNA was strongly expressed in HOS on day 15 and remained at high levels of transcription through to day 25 (matrix maturation phase), whereas ERalpha mRNA was barely detectable during osteoblast differentiation. In hOB, transcription of ERalpha mRNA was much stronger than that of ERbeta mRNA. CONCLUSION: The presence of ERalpha and ERbeta mRNA in osteoblasts supports the involvement of estrogen in human bone formation. The developmental expression of alkaline phosphatase was not correlated to ER mRNA expression during osteoblast differentiation. ER isoforms may have different functions or interact with each other during osteoblast differentiation. Since the expression of ER isoforms is different between postmenopausal women and osteosarcoma cell lines, characteristics of osteosarcoma cell lines may not be suitable as a model for the evaluation of estrogen effects on postmenopausal osteoporosis.

Aged↗

PubMed2003

Effect of medroxyprogesterone on inspiratory flow shapes during sleep in postmenopausal women.

We previously showed that medroxyprogesterone acetate (MPA) effectively decreases the arterial CO(2) levels in postmenopausal women with partial upper airway obstruction. The aim of the present study was to analyze the effects of MPA on the inspiratory flow shapes during sleep. Eight postmenopausal women with hypoxemia and partial upper airway obstruction during sleep (patients) received MPA 60 mg daily for 14 days. Four matched postmenopausal women without MPA treatment served as controls. Sleep and nasal pressure were recorded on each visit. Each breath was analyzed for duration, volume and inspiratory flow shape class. MPA shortened inspiration and prolonged expiration. The inspiratory volumes increased consistently in all flow shape classes. The inspiratory shapes with single late peak were transformed to those with double peak. MPA also decreased shapes with mid-peak or mid-plateau. MPA did not have an effect on sleep. Sleep modified the flow shape distribution only in patients but in a similar fashion in stages S2, SWS and REM. The results suggest that postmenopausal women present with a significant proportion breaths with poor initial inspiratory flow, which is reversed with MPA-induced respiratory stimulation.

Female↗

PubMed2003

Effect of simvastatin treatment on bone mineral density and bone turnover in hypercholesterolemic postmenopausal women: a 1-year longitudinal study.

Although several studies have reported a lower risk of osteoporotic fracture in hypercholesterolemic patients treated with statins, so far longitudinal studies on the effects of statins on bone are lacking. The aim of the present study was to evaluate bone mineral density (BMD) and bone turnover changes induced by 1-year simvastatin treatment on postmenopausal women. Thirty consecutive postmenopausal hypercholesterolemic women (61.2 +/- 4.9 years) were treated for 12 months with 40 mg/day simvastatin and 30 normocholesterolemic age-matched postmenopausal women provided control data. In all subjects, at baseline and at 3-month intervals, serum lipids, calcium, phosphate, total and bone alkaline phosphatase (Bone-ALP), and carboxy-terminal fragment of type I collagen (CTx) were measured in a fasting blood sample. At baseline and after 6 and 12 months BMD was measured at lumbar spine (BMD-LS) and at femur (BMD-Ftot) and at femoral neck (BMD-Fn) by DXA. In the simvastatin-treated group Bone-ALP showed a significant increase (P < 0.05) with respect to baseline from the sixth month, whereas serum CTx showed a weak and nonsignificant increase over the study period. In treated women BMD-LS, BMD-Fn, and BMD-Ftot increased respectively by 1.1, 0.9, and 0.4% at Month 6; and by 2.8, 1.0, and 0.8% at Month 12. In controls BMD-LS, BMD-Fn, and BMD-Ftot at the end of the study period decreased by 1.6, 1.4, and 1.2%, respectively. The difference between controls and simvastatin-treated patients was significant (P < 0.05) for both BMD-LS and BMD-Fn only at Month 12. In conclusion our results, although obtained from a small sample of postmenopausal hypercholesterolemic women, suggest a probable positive effect of simvastatin on bone formation and BMD.

Aged↗