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Increased reduction in bone density and skin thickness in postmenopausal women taking long-term corticosteroid therapy: a suggested role for estrogen add-back therapy.

BACKGROUND: Long-term corticosteroid therapy is complicated by osteoporosis and generalized thinning of the skin. These two complications of such therapy were routinely assessed at the Menopause Clinic of St. Luke's Hospital Medical School, University of Malta. METHODS: A cross-sectional study was performed on 64 postmenopausal women who had been taking long-term corticosteroids. Each woman had her skin thickness measured using high-resolution ultrasound (22 MHz) and her bone density measured by dual-energy X-ray absorptiometry (DEXA). These measurements were compared with those of a control group (n = 557), a group of women who had sustained osteoporotic fractures (n = 180) and a group of women taking hormone replacement therapy (HRT) (n = 399). A longitudinal study of 29 postmenopausal women taking corticosteroids was also performed. This study compared results for women who, in addition to their corticosteroids, were taking HRT and for those who were taking corticosteroids alone. RESULTS: The cross-sectional study showed that corticosteroid therapy was associated with the lowest mean skin thickness measurement (0.83 mm). Similarly, low mean bone density measurements for the lumbar spine (0.805 g/cm2) and left hip (0.715 g/cm2) were obtained for this group. The mean skin thicknesses in the control group and the HRT group were 0.93 mm and 0.935 mm, respectively, while that in the osteoporotic fracture group was 0.88 mm. The bone density of the fracture group was similar to that of the group of women taking long-term corticosteroids, with the lumbar spine having a mean density of 0.805 g/cm2 and 0.81 g/cm2, and the left hip having a density of 0.705 g/cm2 and 0.715 g/cm2, respectively. Bone densities were similar for the control group and the HRT group, and higher than that of the corticosteroid or fracture group. The lumbar spine had a mean density of 0.925 g/cm2 in the control group and 0.93 g/cm2 in the hormonally treated group. Both the treated and control groups had similar bone densities of the left hip at about 0.82 g/cm2. The small longitudinal study compared postmenopausal women on long-term corticosteroid therapy taking HRT with another group who were not taking HRT. This 4-year study revealed mean total increases in skin thickness of 6.1% and bone density of 5.5% (left hip) and 14.6% (lumbar spine) in the HRT group, since the start of the study. Conversely, the control group registered reductions over 4 years in both skin thickness (2.8%) and bone density (lumbar spine 4.5% and hip 5.0%). CONCLUSION: In postmenopausal women taking long-term corticosteroids, skin thickness and bone density were both decreased, but the addition of HRT as add-back improved the situation dramatically. Skin thickness and bone density in women taking long-term corticosteroids were comparable to those in women who had sustained osteoporotic fractures. It is therefore suggested that HRT be used as add-back therapy in postmenopausal women taking long-term corticosteroid therapy.

Absorptiometry, Photon↗

[Circadian variation of blood pressure and heart rate in normotensive pre- and postmenopausal women].

The aim of this study was to assess the effect of menopause on circadian profile of blood pressure (BP) and heart rate (HR) in the normotensive pre- and postmenopausal women. Systolic BP (SBP), diagnostic BP (DBP) and HR were monitored every 30 min for 48 hrs using noninvasive ambulatory BP monitoring in 24 premenopausal and 40 postmenopausal women. Mean 48-hours, daytime (awake), and nighttime (sleeping) SBP, DBP and HR values were analyzed by reviewing the patients' diaries, and the nocturnal reduction rate (NRR) of SBP, DBP and HR were calculated according to the following formula. NRR (%9 = [(daytime mean-nighttime mean)/daytime mean] x 100. The study subjects were then divided into two groups according to the presence (dipper) or absence (nondipper) of a significant reduction in nocturnal BP (> 10%). Mean SBP, DBP and HR measured over 48 hours were similar between the premenopausal and the postmenopausal group. The NRR of DBP and HR in the postmenopausal group were significantly smaller than those in the premenopausal group (17.1 +/- 6.0% vs. 13.5 +/- 7.0%, 241.1 +/- 6.0% vs. 19.8 +/- 9.0%: p < 0.05). There tended to be higher prevalence of nondipper in the postmenopausal (37%) than in the premenopausal group (29%).

Adult↗

Evaluation of the changes in serum lipid profile and ferritin concentrations in relation to body ascorbic acid status in healthy pre- and postmenopausal women.

The aim of this work was to study the relationship between body ascorbic acid (AA) status and serum lipid profile and ferritin concentrations in healthy pre- and postmenopausal women. The mean leukocyte and plasma ascorbate values in postmenopausal women were found to be significantly low but within acceptable ranges as compared to premenopausal women. According to these results, plasma and leukocyte AA concentrations decreased after the cessation of ovarian hormone production. In addition, significant increases in total cholesterol, triglyceride and LDL-cholesterol but a significant decrease in HDL-cholesterol were observed in postmenopausal women as compared to premenopausal women. A close positive relationship was found between plasma and leukocyte AA and body iron status in postmenopausal women. The findings were prominent especially in the subgroup of postmenopausal women with low body AA status. Thus, it is concluded that women having low body AA concentrations might have a predisposition for iron depletion.

Adult↗

The role of body mass index in the relative risk of developing premenopausal versus postmenopausal breast cancer.

Many women in industrialized countries are overweight. Excess body fat is associated with excess morbidity and mortality from atherosclerosis and diabetes. In some cases, overweight/obesity also is implicated with increased incidence of breast cancer, but the results of these studies are not consistent. Human breast cancer is usually distinguished as either premenopausal or postmenopausal. In this review, we focus on literature that presents body mass index (BMI, weight/height2) ranges and identifies menstrual status. The majority of the relevant prospective studies support an inverse relationship between BMI and the relative risk (RR) of developing premenopausal breast cancer. In contrast, a positive relationship between BMI and the RR of developing postmenopausal breast cancer is reported in only half of all prospective studies on this topic. Those studies that do not show a positive RR, in general, have used younger postmenopausal women, and their body weights were obtained prior to menopause. Many case-control studies also report an inverse association between BMI and the RR of developing premenopausal breast cancer, and a positive association between BMI and the RR of developing postmenopausal breast cancer. Other studies do not find these associations, but a number of these studies have used small sample sizes and, for the postmenopausal subjects, have represented populations with low obesity and/or breast cancer rates. Other factors that might play a role in breast cancer development, such as body fat distribution, weight at earlier ages, and weight gain, are also addressed, as well as the effect of obesity in breast cancer prognosis. In addition, limited data available for animal studies related to this topic, as well as potential mechanisms by which body fat may play a role in breast cancer development, are discussed. Finally, the need for better animal models in which to perform controlled dietary and/or drug intervention studies to test rigorously the proposed mechanisms by which body fat may contribute to breast cancer development is addressed.

Animals↗

Does postmenopausal estrogen administration increase the risk of breast cancer? Contributions of animal, biochemical, and clinical investigative studies to a resolution of the controversy.

Despite nearly six decades of epidemiological studies, meta-analyses, and reviews, there is still considerable controversy in the literature about the question, does postmenopausal estrogen administration increase the risk of breast cancer? In an effort to resolve the controversy, a number of animal, biochemical, and clinical investigative studies in this field have been reviewed. The following summary formulation is proposed: 1. Administration of estrogen is inherently capable of promoting the growth of breast cancer, and therefore of increasing the incidence of clinical breast cancer. 2. Human response to estrogen is like that of the low-cancer-incidence strains of mice studied by Lacassagne, in that large doses and prolonged administration are required to induce clinical breast cancer. 3. The blood levels of estradiol produced by the usual doses of postmenopausal estrogen are relatively low, equivalent to those of the follicular phase of the menstrual cycle. These levels may be near the threshold for producing breast-cancer-promoting effects; therefore, the tumor response will vary greatly in different populations, depending on genetic susceptibility factors: a. The prevalence of a family history of premenopausal breast cancer in a first-degree relative. b. The prevalence of abnormal BRCA1, BRCA2, and p53 genes. c. The prevalence of increased 16 alpha-hydroxylation of estradiol. d. The prevalence of smokers who are slow acetylators. 4. Consumption of alcohol (5 grams or more daily) along with the postmenopausal estrogen administration results in elevation of blood estradiol levels to values equivalent to those of the periovulatory peak of the menstrual cycle, which may be well above the threshold for producing breast-cancer-promoting effects in all women. The risk for cancer will therefore be uniformly increased in women who use alcohol and take estrogen. 5. Increased risk of breast cancer from postmenopausal estrogen administration can be eliminated by taking two synergistic steps: a. Eliminating alcohol consumption, or at least keeping it well below an average of 5 grams daily (equivalent to 2/3 ounce of whiskey or 3 ounces of wine). b. Diminishing the capacity to 16 alpha-hydroxylate estradiol, either through pharmacological agents such as indole-3-carbinol or through increased consumption of cruciferous vegetables. It is concluded that despite the inherent ability of postmenopausal estrogen therapy to increase the risk of breast cancer in theory, the increased risk can be eliminated in practice by minimizing or eliminating consumption of alcohol and ingesting pharmacological or dietary agents that reduce the 16 alpha-hydroxylation of estradiol.

Alcohol Drinking↗

Experimental mouse model of hormonal therapy effects on the postmenopausal mammary gland.

Menopausal hormone therapy, in particular estrogen plus progestin therapy, has been associated with increased breast cancer risk. In order to understand the basis for increased breast cancer risk, more information is needed about the effects of menopausal hormone therapies on the breast. In this review we describe studies carried out in a mouse model of early vs. late postmenopausal states. We investigated the effects of 1) estrogen alone, 2) combined continuous estrogen + progestin, 3) systemically vs. locally administered estrogen and progestin, and 4) the effect of pregnancy on the response to hormonal therapies. We analysed the effects on mammary gland morphology and proliferation. Estrogen therapy started in late postmenopause caused a greater proliferative response than when started in early postmenopause. In parous, late postmenopausal mice the greater proliferative response to estrogen was not observed. Overall, the greatest proliferative response was observed with combined continuous estrogen + progestin hormone therapy and did not differ significantly in early vs. late nulliparous or parous postmenopausal mice. Both estrogen and progestin were found to act directly on the mammary gland rather than through systemically mediated effects. The possible implications of these findings for menopausal hormone therapy in women and breast cancer risk are discussed.

Animals↗

Effect of long-term hormone therapy on telomere length in postmenopausal women.

Telomeres undergo attrition with each cell division, and telomere length is associated with age-related diseases and mortality in the elderly. Estrogen can influence the attrition of telomeres by diverse mechanisms. This is a retrospective case control study that investigated the influence of long-term hormone therapy (HT) on telomere length in postmenopausal women. We recruited 130 postmenopausal women from 55 to 69 years of age for this study, and divided them into two groups. The first group included 65 women who had been on estrogen and progesterone therapy for more than five years (HT group). The other group was composed of 65 women matched in age to the HT group who had never had HT (non- HT group). The relative ratios of telomere length of study subjects to a reference DNA from a healthy young female were measured using quantitative PCR. Plasma levels of lipid profiles, total antioxidant status (TAS), C-reactive proteins (CRP), fasting glucose levels, and estradiol levels were measured. Age at menopause, vitamin use, and exercise, alcohol, and cigarette smoking histories were also assessed in a questionnaire. Mean duration (+/- SD) of HT was 8.4 +/- 2.3 years. Prevalence of vitamin use and regular exercise were higher in the HT group than in the non-HT group (p < 0.01). Relative telomere length ratios in the HT group were significantly greater than those in the non-HT group (p < 0.01). HT was significantly correlated with the relative telomere length ratio in multivariate analysis when potential confounding variables were controlled for (p < 0.05). In conclusion, telomere lengths were longer in postmenopausal women who had a history of long-term HT than in postmenopausal women without HT. Long-term HT in postmenopausal women may alleviate telomere attrition.

Aged↗

[Influencing factors on quality of life in pre- and postmenopausal women].

PURPOSE: This study was to investigate the factors influencing quality of life and difference of quality of life in a postmenopausal group compared to premenopausal women. METHOD: The subjects consisted of 213 women from 40 to 64 years old. The data were collected from June 1, 2003 to June 31, 2004 using structured questionnaires which included questions relating to demographic and obstetric background and 4 scales(climacteric symptoms scale, marital satisfaction scale, sex-role attitude scale, quality of life scale). RESULT: Comparing pre- and postmenopausal women, significant statistical differences were demonstrated in climacteric symptoms and sex-role attitude. However, quality of life was not different between pre- and postmenopausal women. In premenopausal women, marital satisfaction(32.7%) and educational level(8.0%) were significant predictors to explain quality of life. Marital satisfaction(12.9%) was significant predictor to explain quality of life in postmenopausal women. CONCLUSION: No difference of quality in life between pre- and postmenopausal women provides information for changing traditional approaches of menopause according to physiological changes as illness. In addition the study showed that it is necessary to use marital satisfaction information when developing nursing interventions to promote the quality of life.

Adult↗

Prepregnancy exposure to cigarette smoking and subsequent risk of postmenopausal breast cancer.

OBJECTIVE: To examine the association of cigarette smoking before first pregnancy with risk of postmenopausal breast cancer in a large population-based cohort. PATIENTS AND METHODS: The Iowa Women's Health Study is a prospective cohort study of 55- to 69-year-old women at baseline in 1986. In January 1986, a questionnaire was mailed to 99,826 postmenopausal women to Identify risk factors for cancer and other chronic diseases; 41,836 women responded (42.7% response rate). The primary analyses examined the associations among smoking, parity, age at first birth, and postmenopausal breast cancer. RESULTS: Of the 37,105 women in the cohort at risk, 7095 (19%) and 4186 (11%) initiated smoking before and after first pregnancy, respectively, and 2017 breast cancers were identified before December 31, 1999. Compared with parous women who never smoked, women who began smoking after their first full-term pregnancy were not at increased risk of postmenopausal breast cancer (multivariate-adjusted risk ratio, 1.03; 95% confidence interval, 0.88-1.21). However, women who began smoking before their first pregnancy had a slightly elevated risk of breast cancer (risk ratio, 1.21; 95% confidence Interval, 1.07-1.37). Results were not attenuated by adjustment for age at first pregnancy or number of live births. CONCLUSION: These data suggest that cigarette smoking is associated with a slightly greater risk of postmenopausal breast cancer for women who started smoking before their first full-term pregnancy.

Age Factors↗

Postmenopausal hormone use and risk for colorectal cancer and adenoma.

BACKGROUND: Accumulating evidence suggests that postmenopausal hormone use may decrease the risk for colorectal cancer. OBJECTIVE: To examine the relation of postmenopausal hormone therapy to colorectal adenoma and cancer. DESIGN: Prospective cohort and nested case-control studies. SETTING: Nurses' Health Study, a study of registered nurses recruited from 11 U.S. states. PARTICIPANTS: 59 002 postmenopausal participants in the Nurses' Health Study. MEASUREMENTS: Self-reported data on hormone use and cases of distal colorectal adenoma and colorectal cancer obtained from biennial questionnaires completed from 1980 to 1994. Cases of colorectal adenoma and cancer were confirmed by medical record review. RESULTS: 470 women developed colorectal cancer, and 838 developed distal colorectal adenomas. Current use of postmenopausal hormones was associated with a decreased risk for colorectal cancer (relative risk [RR], 0.65 [95% CI, 0.50 to 0.83]). This association was attenuated in past users (RR, 0.84 [CI, 0.67 to 1.05]) and disappeared 5 years after hormone use was discontinued (RR, 0.92 [CI, 0.70 to 1.21]). Longer duration of current use did not afford greater protection (RR with > or =5 years of use, 0.72 [CI, 0.53 to 0.96]). Even after exclusion of women who reported having screening sigmoidoscopy, the relative risk for colorectal cancer seen with current hormone use was 0.64 (CI, 0.49 to 0.82). This suggests that the apparent protection is unlikely to be due to more intensive screening among hormone users. Current users also had a lower risk for large (> or =1 cm) adenomas than did women who had never used hormones (RR, 0.74 [CI, 0.55 to 0.99]), although no overall material association was seen between colorectal adenoma and current hormone use (RR, 0.91 [CI,0.77 to 1.08]). CONCLUSIONS: The risk for colorectal cancer was decreased among women currently receiving postmenopausal hormone therapy, but the apparent reduction substantially diminished upon cessation of therapy. Hormone use was inversely associated with large colorectal adenomas but not small ones.

Adenoma↗

A prospective, observational study of postmenopausal hormone therapy and primary prevention of cardiovascular disease.

BACKGROUND: Most primary prevention studies have found that long-term users of postmenopausal hormone therapy are at lower risk for coronary events, but numerous questions remain. An adverse influence of hormone therapy on cardiovascular risk has been suggested during the initial year of use; however, few data are available on short-term hormone therapy. In addition, the cardiovascular effects of daily doses of oral conjugated estrogen lower than 0.625 mg are unknown, and few studies have examined estrogen plus progestin in this regard. OBJECTIVE: To investigate duration, dose, and type of postmenopausal hormone therapy and primary prevention of cardiovascular disease. DESIGN: Prospective, observational cohort study. SETTING: Nurses' Health Study, with follow-up from 1976 to 1996. PATIENTS: 70 533 postmenopausal women, in whom 1258 major coronary events (nonfatal myocardial infarction or fatal coronary disease) and 767 strokes were identified. MEASUREMENTS: Details of postmenopausal hormone use were ascertained by using biennial questionnaires. Cardiovascular disease was established by using a questionnaire and was confirmed by medical record review. Logistic regression models were used to calculate relative risks and 95% CIs, adjusted for confounders. RESULTS: When all cardiovascular risk factors were considered, the risk for major coronary events was lower among current users of hormone therapy, including short-term users, compared with never-users (relative risk, 0.61 [95% CI, 0.52 to 0.71]). Among women taking oral conjugated estrogen, the risk for coronary events was similarly reduced in those currently taking 0.625 mg daily (relative risk, 0.54 [CI, 0.44 to 0.67]) and those taking 0.3 mg daily (relative risk, 0.58 [CI, 0. 37 to 0.92]) compared with never-users. However, the risk for stroke was statistically significantly increased among women taking 0.625 mg or more of oral conjugated estrogen daily (relative risk, 1.35 [CI, 1.08 to 1.68] for 0.625 mg/d and 1.63 [CI, 1.18 to 2.26] for >/=1.25 mg/d) and those taking estrogen plus progestin (relative risk, 1.45 [CI, 1.10 to 1.92]). Overall, little relation was observed between combination hormone therapy and risk for cardiovascular disease (major coronary heart disease plus stroke) (relative risk, 0.91 [CI, 0.75 to 1.11]). CONCLUSIONS: Postmenopausal hormone use appears to decrease risk for major coronary events in women without previous heart disease. Furthermore, 0.3 mg of oral conjugated estrogen daily is associated with a reduction similar to that seen with the standard dose of 0.625 mg. However, estrogen at daily doses of 0.625 mg or greater and in combination with progestin may increase risk for stroke.

Adult↗

Effect of estrogen plus progestin on risk for biliary tract surgery in postmenopausal women with coronary artery disease. The Heart and Estrogen/progestin Replacement Study.

BACKGROUND: Animal and observational epidemiologic studies have reported that estrogens may increase the risk for gallstones. No major clinical trials have examined the effect of estrogen plus progestin therapy in postmenopausal women on the risk for biliary tract surgery. OBJECTIVE: To determine the effect of estrogen plus progestin on the risk for biliary tract surgery in postmenopausal women with known coronary artery disease. DESIGN: Randomized, double-blind placebo-controlled trial of postmenopausal hormone therapy for coronary heart disease. SETTING: 20 U.S. clinical centers. PARTICIPANTS: 2253 postmenopausal women with a gallbladder, 44 to 79 years of age at baseline, in the Heart and Estrogen/progestin Replacement Study (HERS). INTERVENTION: Conjugated equine estrogens, 0.625 mg, plus medroxyprogesterone acetate, 2.5 mg, daily in one tablet or identical placebo. MEASUREMENTS: Documented biliary tract surgery. RESULTS: A total of 147 women (7%) were hospitalized for biliary tract surgery in HERS. Treatment with estrogen plus progestin resulted in a marginally significant 38% increase in the relative risk for biliary tract surgery (P = 0.05). A small absolute difference in risk suggested that for every 185 women treated with estrogen plus progestin, one additional woman had biliary tract surgery per year. After adjustment for baseline and in-study statin use, the association was attenuated further (P = 0.09). After adjustment for treatment assignment and other variables, increased body mass index, fibric acid use, and a history of nonsurgical gallbladder disease were associated with an increased risk for biliary tract surgery, whereas statin use was associated with a decreased risk (for each comparison, P < 0.05). CONCLUSION: Estrogen plus progestin therapy among postmenopausal women with known coronary disease resulted in a marginally significant increase in the risk for biliary tract surgery.

Adult↗

Cost-effectiveness of alendronate therapy for osteopenic postmenopausal women.

BACKGROUND: Treatment guidelines recommend drug treatment to prevent fractures for some postmenopausal women who have low bone mass (osteopenia) but do not have osteoporosis or a history of clinical fractures. OBJECTIVE: To estimate the societal costs and health benefits of alendronate drug treatment to prevent fractures in postmenopausal women with osteopenia. DESIGN: Markov model with 8 health states: no fracture, post-distal forearm fracture, post-clinical vertebral fracture, post-radiographic (but clinically inapparent) vertebral fracture, post-hip fracture, post-hip and vertebral fractures, post-other fracture, and death. DATA SOURCES: Population-based studies of age-specific fracture rates and costs, prospectively measured estimates of disutility after fractures, and the Fracture Intervention Trial of alendronate versus placebo to prevent fracture. TARGET POPULATION: Postmenopausal women 55 to 75 years of age with femoral neck T-scores between -1.5 and -2.4. TIME HORIZON: Lifetime. PERSPECTIVE: Societal. INTERVENTIONS: Five years of alendronate therapy or no drug treatment. OUTCOME MEASURES: Costs, quality-adjusted life-years, and incremental cost-effectiveness ratios. RESULTS OF BASE-CASE ANALYSIS: For women with no additional fracture risk factors, the cost per quality-adjusted life-year gained ranged from 70,000 dollars to 332,000 dollars, depending on age and femoral neck bone density. RESULTS OF SENSITIVITY ANALYSES: Results were sensitive to changes in fracture risk reduction attributable to alendronate and alendronate cost. LIMITATIONS: Results apply only to postmenopausal white women residing in the United States. CONCLUSION: Alendronate therapy for postmenopausal women with femoral neck T-scores better than -2.5 and no history of clinical fractures or other bone mineral density-independent risk factors for fracture is not cost-effective, assuming U.S. costs of alendronate and currently available estimates of alendronate efficacy in osteopenic women.

Aged↗

Endometrial and myometrial thickness and uterine blood flow in postmenopausal women: the influence of hormonal replacement therapy and age.

The aim of our study was to assess the age and hormonal influence on endometrial and myometrial thickness and uterine blood flow in postmenopausal women. One hundred and nine healthy postmenopausal women were examined by transvaginal ultrasonography and color Doppler ultrasonography. Twenty women (18.4%) were under continuous HRT for at least 1 year. In all patients, full thickness of the endometrium and half thickness of the myometrium was measured. Pulsed Doppler waveforms were used to calculate the RI for the left and right uterine arteries. Endometrium thickness in the groups without HRT did not change as the years of postmenopause progressed. This was also true for myometrial thickness. The resistance to blood flow in the uterine arteries remained the same as the postmenopause progressed, but with each 5 year analysis, the ability to see the uterine arteries decreased. The duration of the therapy did not affect the measured parameters. The thickness of the endometrium was larger in the groups with HRT in comparison with all groups without HRT (P < 0.01). Myometrial thickness and uterine blood flow are not affected and did not show any significant influence from HRT. In conclusion, continuous HRT significantly influences the thickness of the postmenopausal endometrium but not of the myometrium or the uterine artery blood flow.

Aged↗

Endometrial sonographic findings in asymptomatic, hypertensive postmenopausal women.

PURPOSE: In this retrospective study, the sonographically measured endometrial thickness in asymptomatic, hypertensive postmenopausal women was compared with that in normotensive postmenopausal women. METHODS: We reviewed clinical and sonographic data on 511 consecutive, unselected, asymptomatic postmenopausal women who attended our hospital for routine gynecologic examinations during a 6-month period. Two hundred nineteen patients (mean age, 60.2 years; age range, 49-81 years) were included in the study. Reasons for exclusion were: clinical data about hypertension were not available (n = 159); the patient had received or was receiving hormonal treatment (n = 78); the patient had undergone a hysterectomy (n = 25); and endometrial thickness could not be determined (n = 30). All patients had been examined using transvaginal or transabdominal sonography. Endometrial thickness was measured at the level of its maximum thickness in the uterine sagittal plane. RESULTS: Fifty-six (26%) of 219 patients were hypertensive. Of these 56 patients, 41 (73%) were receiving drug treatment. The mean endometrial thickness in the hypertensive patients receiving treatment [6.2 mm; 95% confidence interval (CI), 5.1-7.4 mm] was significantly greater than in both the untreated, hypertensive patients (4.3 mm; 95% CI, 3.1-5. 5 mm) (p = 0.008) and the normotensive patients (3.6 mm; 95% CI, 3. 4-3.8 mm) (p < 0.0001). Endometrial thickness was equal to or greater than 5 mm in 59% of the hypertensive patients receiving drug treatment compared with 40% of the untreated, hypertensive patients and 18% of the normotensive patients (p < 0.001). An endometrial stripe was sonographically detected in 22% of the hypertensive patients undergoing treatment, 7% of the hypertensive patients undergoing no treatment, and 1% of the normotensive patients (p < 0. 0001). CONCLUSIONS: Our data indicate that endometrial thickness, which can be determined sonographically, is frequently greater in asymptomatic, hypertensive postmenopausal women receiving antihypertensive drugs than in untreated hypertensive and normotensive patients. This conclusion could have clinical relevance when interpreting endometrial sonographic findings in asymptomatic, hypertensive postmenopausal patients.

Adrenergic beta-Antagonists↗

[Transvaginal sonography of the postmenopausal endometrium].

INTRODUCTION: The most frequent symptom suggesting endometrial pathology is uterine bleeding. Each postmenopausal uterine bleeding requires fraction explorative curettage and histopathologic examination of the material obtained from the cervical canal and uterine cavity. The aim of this study was to estimate the efficacy of ultrasonography as a non-invasive method in detection of endometrial pathology in postmenopausal women, and to find out whether its more frequent use could safely decrease the number of curettages in detection of these conditions. MATERIAL AND METHODS: A prospective investigation has been performed in postmenopausal women not menstruating for more than a year, and who reported to the Department of Obstetrics and Gynaecology in Novi Sad for uterine bleeding during 1996 and 1997. Each woman underwent ultrasonographic examination by vaginal probe of 5 MHz and fraction curettage, whereas the samples from cervical canal (if obtained) and from uterine cavity were sent to histopathologic examination to the Institute of Pathology in Novi Sad. Standard statistical methods have been used for the analysis of the results. Validity of the applied ultrasonographic method in detecting endometrial pathology has been estimated by calculation of its sensitivity and specificity. RESULTS: A satisfactory visualisation of the endometrium has been obtained in all 35 examined cases. The thinnest endometrium was 1 mm wide and the thickest one was--25 mm. The fraction curettage has been used to obtain material from the cervix in 2 cases and from the uterine cavity in 35 cases. In our patients with uterine bleeding, who were in the postmenopause for 13 years on average, endometrial atrophy was recorded in 17.14%, endometrial polyp in 11.43%, endometrial hyperplasia in 22.86%, endometrial adenocarcinoma in 42.86% and uterine sarcoma in 5.71%. There were 2 false negative ultrasonographic findings (2 cases of endometrial hyperplasia) and sonographic thickness less than standard versus 2 false positive cases (endometrium thicker than the limit value, 7 and 14 mm, with no real pathology) which showed that the sensitivity of the investigated method was 93.10% and the specificity was 66.66%, if the limit value for the thickness of endometrium was 3 mm. DISCUSSION: Ultrasonographic thickness of endometrium means maximum double thickness in longitudinal plane, i.e. the distance of the opposite bordering surfaces of endometrium and myometrium. The procedure of measurements of endometrial thickness is simple in most cases. Most authors agree that there is a positive correlation between the thickness of endometrium and its pathological conditions. The most often used limit values are 3 and 4 mm. Higher limit values of endometrial thickness increase the sensitivity of the method even to 100%, but negatively affect its specificity making this method inadequate as a screening method for endometrial carcinoma. Many authors insist on introducing other criteria for evaluation of the endometrium i.e. for taking its thickness as the only criterion. Ultrasonography does not provide a completely safe differentiation between benign hyperplasia and endometrial carcinoma. CONCLUSION: The transvaginal sonography is an efficient and acceptable, noninvasive method for early detection of endometrial pathology in postmenopausal women. The thickened endometrium during menopause is the most significant ultrasonographic criterion implicating its pathology. The vaginosonographically measured thickness of 3 mm and less, gives a relatively safe prediction of endometrial atrophy, whereas the thickness above 3 mm requires explorative curettage and histopathologic examination of the endometrium, no matter if the woman has or has not uterine bleeding. (ABSTRACT TRUNCATED)

Aged↗

Clinical significance of atypical glandular cells of undetermined significance in postmenopausal women.

BACKGROUND: Glandular atypia in Papanicolaou (Pap) smears from postmenopausal women is encountered frequently. This finding can be the result of artifactual alterations such as drying artifacts and inflammatory changes or may represent a squamous or glandular, preneoplastic or neoplastic process. Therefore, it is important to determine the clinical implication of a diagnosis of atypical glandular cells of undetermined significance (AGUS) in postmenopausal patients. METHODS: A total of 30,036 Pap smears were obtained from postmenopausal women between 1995 and 1997. Among these smears, 154 (0.51%) had a diagnosis of AGUS. Follow-up was available for 133 patients (86.4%); 110 patients (82.7%) had histologic follow-up (including cervical biopsy, endocervical [EC] curettage, and/or endometrial [EM] biopsy) and 23 patients (17.3%) had repeat smears. RESULTS: Thirty-six of 110 patients (32.7%) were found to have a clinically significant lesion (defined as a preneoplastic or neoplastic, glandular or squamous lesion) on subsequent histologic follow-up. Nineteen patients (53%) had glandular lesions (15 EM adenocarcinoma [ACA] cases, 2 EC ACA cases, 1 EC adenocarcinoma is situ case, and 1 EM hyperplasia case). Seventeen patients (47%) had a squamous intraepithelial lesion (SIL) (6 cases of low-grade SIL, 9 cases of high-grade [HGIL], and 2 cases of squamous cell carcinoma). Among those patients with repeat Pap smears, five patients had persistent AGUS/atypical squamous cells of undetermined significance and one patient had an SIL. CONCLUSIONS: The incidence of AGUS among postmenopausal patients was similar to that of the general population (0.51% vs. 0.56%; P > 0.05). A significant percentage of these patients were found to have a clinically significant lesion on subsequent follow-up. Furthermore, a majority of these lesions were ACA (53%) or HGSIL (26%). The findings of the current study strongly suggest the need for the close follow-up of postmenopausal patients with a diagnosis of AGUS. Cancer (Cancer Cytopathol)

Adult↗

Prevalence of hormone replacement therapy and antidepressant use in peri- and postmenopausal women.

OBJECTIVE: To examine the prevalence of hormone replacement therapy (HRT) and antidepressant use in peri- and postmenopausal women. DESIGN: Prevalence survey. SUBJECTS: Peri- and postmenopausal outpatients (N = 253) at five medical clinics. METHODS: Participants completed a 47-item questionnaire requesting information on mood changes associated with menstruation, childbirth, oral contraceptive use, and menopause. Peri- and postmenopausal participants were asked to rate the severity of dysphoric symptoms experienced during the menopausal transition and to specify whether HRT, antianxiety medication, or antidepressant medication relieved the symptoms. RESULTS: Forty percent of respondents experienced more severe depression than anticipated during menopause, but only 8% were treated with antidepressants. Forty-six percent of respondents were treated with HRT. CONCLUSIONS: The data suggest that antidepressant and antianxiety medications are more helpful than HRT in relieving peri- and postmenopausal depression or anxiety. However, most women managed the mood changes associated with menopause without psychopharmacologic intervention. This is consistent with other reports on the transitory nature of peri- and postmenopausal depression for most women.

Adult↗