Selección de Resúmenes de Menopausia

Semana del 24 al 30 de Abril 2007

 

Dr. Juan Enrique Blümel

 

 

 

Ann Epidemiol. 2007 May;17(5):342-353.

Physical Activity and Breast Cancer Risk Among Women in the Southwestern United States.

Slattery ML, Edwards S, Murtaugh MA, Sweeney C, Herrick J, Byers T, Giuliano AR, Baumgartner KB.

From the Department of Medicine, University of Utah, Salt Lake City, UT (M.L.S., S.E., M.A.M., C.S., J.H.); University of Colorado School of Medicine, Denver (T.B.); University of Arizona, Tucson (A.G. [currently at Moffitt Cancer Center, Tampa, FL]); and Department of Internal Medicine and the Cancer Research and Treatment Center Epidemiology and Cancer Prevention Program, University of New Mexico Health Science Center, Albuquerque (K.B. [currently at University of Louisville, KY]).

Physical activity may influence breast cancer risk through multiple mechanisms and at different periods in life. In this study we evaluate breast cancer risk associated with total and vigorous physical activity at ages 15, 30, and 50 years and the referent year prior to diagnosis/selection. Participants were non-Hispanic white (NHW) (1527 cases and 1601 control subjects) and Hispanic/American Indian (HAI) (798 cases and 924 controls) women. Both total and vigorous activity reduced risk of breast cancer in a dose-response manner. Among premenopausal women, only high total metabolic equivalent of the task (MET) hours of activity during the referent year was associated with reduced breast cancer risk in NHW women (odds ratio [OR] 0.62; 95% confidence interval [CI] 0.43, 0.91). Among postmenopausal women, physical activity had the greatest influence among women not recently exposed to hormones. Among these women, high total lifetime activity reduced risk of breast cancer for both NHW (OR 0.60; 95% CI 0.36, 1.02; p trend 0.01) and HAI women (OR 0.52; 95% CI 0.23, 1.16; p trend 0.07). Additionally, high total MET hours of activity at age 30 years (OR 0.56; 95% CI 0.37, 0.85) and at age 15 years (OR 0.57; 95% CI 0.38, 0.88) reduced breast cancer risk among postmenopausal NHW women not recently exposed to hormones. Among HAI women, more recent activity performed during the referent year and at age 50 appeared to have the greatest influence on breast cancer risk. Among postmenopausal NHW women. there was a significant interaction between physical activity and hormone replacement therapy (p value, 0.01), while among postmenopausal HAI women, physical activity interacted with body mass index (p value, 0.04). These data suggest that physical activity is important in reducing risk of breast cancer in both NHW and HAI women.

 

 

Curr Opin Investig Drugs. 2007 Apr;8(4):293-8. Links

A new paradigm in the treatment of osteoporosis: Wnt pathway proteins and their antagonists.

Chan A, van Bezooijen RL, Lowik CW.

Percuros BV, Plesmanlaan 1, 2333 BZ Leiden, The Netherlands. achan@percuros.com

The need to develop novel drugs that stimulate bone formation and thereby elevate bone mass (anabolics), as opposed to preventing bone loss (anti-resorptives), has opened new research areas for therapeutic intervention in the treatment of osteoporosis. One of these areas is the Wnt/beta-catenin pathway that plays an important role in regulating osteoblast proliferation and differentiation. Alterations in this pathway have been associated with bone disorders characterized by either low or high bone mass. However, as the Wnt/beta-catenin pathway is a ubiquitous mechanism not just exclusively involved in bone formation, targeting Wnts may be a challenge (eg, targeting Wnt activity may induce cancer). Nevertheless, specific pharmacological targets to influence bone formation have been identified in this pathway; these include the Wnt-lipoprotein receptor-related protein 5/6-frizzled complex and Wnt antagonists such as sclerostin. Since sclerostin expression is highly restricted to osteocytes, this specific target may be ideal for anabolic drug therapy.

 

 

BMC Public Health. 2007 Apr 26;7(1):64 [Epub ahead of print]

Vitamin D inadequacy in Belgian postmenopausal osteoporotic women.

Neuprez A, Bruyere O, Collette J, Reginster JY.

ABSTRACT: BACKGROUND: Inadequate serum vitamin D [25(OH)D] concentrations are associated with secondary hyperparathyroidism, increased bone turnover and bone loss, which increase fracture risk. The objective of this study is to assess the prevalence of inadequate serum 25(OH)D concentrations in postmenopausal Belgian women. Opinions with regard to the definition of vitamin D deficiency and adequate vitamin D status vary widely and there are no clear international agreements on what constitute adequate concentrations of vitamin D. METHODS: Assessment of 25-hydroxyvitamin D [25(OH)D] and parathyroid hormone was performed in 1195 Belgian postmenopausal women aged over 50 years. Main analysis has been performed in the whole study population and according to the previous use of vitamin D and calcium supplements. Four cut-offs of 25(OH)D inadequacy were fixed : < 80 nmol/L, <75 nmol/L, < 50 nmol/L and < 30 nmol/L. RESULTS: Mean (SD) age of the patients was 76.9 (7.5) years, body mass index was 25.7 (4.5) kg/m;2. Concentrations of 25(OH)D were 52.5 (21.4) nmol/L. In the whole study population, the prevalence of 25(OH)D inadequacy was 91.3 %, 87.5 %, 43.1 % and 15.9% when considering cut-offs of 80, 75, 50 and 30 nmol/L, respectively. Women who used vitamin D supplements, alone or combined with calcium supplements, had higher concentrations of 25(OH)D than non-users. Significant inverse correlations were found between age / serum PTH and serum 25(OH)D (r = -0.23 / r= -0.31) and also between age / serum PTH and femoral neck BMD (r= -0.29 / r=-0.15). There is a significant positive relation between age and PTH (r= 0.16), serum 25(OH)D and femoral neck BMD (r= 0.07) (P < 0.05). Vitamin D concentrations varied with the season of sampling but did not reach statistical significance (P=0.09). CONCLUSIONS: This study points out a high prevalence of vitamin D inadequacy in Belgian postmenopausal osteoporotic women, even among subjects receiving vitamin D supplements.

 

 

J Clin Endocrinol Metab. 2007 Apr 24; [Epub ahead of print]

Growth Hormone Reduces Inflammation in Postmenopausal Women with Abdominal Obesity: a 12-Month, Randomised, Placebo-Controlled Trial.

Franco C, Andersson B, Lonn L, Bengtsson BA, Svensson J, Johannsson G.

Department of Endocrinology, Department of Medicine, Department of Diagnostic Radiology, Sahlgrenska University Hospital, SE-413 45 Goteborg, Sweden.

Context: Abdominal obesity is associated with low GH secretion, elevated circulating markers of inflammation, and increased risk of CVD. Objective: To study the effect of GH treatment on inflammatory markers and vascular adhesion molecules in postmenopausal women with abdominal obesity. Design: Forty women aged 51-63 yrs received GH (0.67 mg/d) in a randomised, double-blind, placebo-controlled, 12-month trial. Measurements of inflammatory markers: highly sensitive C-reactive protein (CRP), interleukin-6 (IL-6) and amyloid polypeptideA (SAA) and markers of endothelial dysfunction: soluble E-selectin (sE-selectin), vascular adhesion molecule-1 (VCAM-1), intercellular molecule-1 (ICAM-1) and matrix metalloproteinase (MMP)-9 were performed at baseline, after 6 and 12 months of treatment. Results: After 12 months, the mean IGF SD score was 0.9 +/- 1.5 and - 0.8 +/- 0.6 in the GH and placebo groups respectively. GH treatment reduced CRP and IL-6 levels as compared with placebo (p= 0.03 and p = 0.05 respectively), whereas the markers of endothelial dysfunction were unaffected. Within the GH-treated group, a reduction was shown in CRP (4.3 +/- 4 to 3.0 +/- 3 mg/L; p < 0.05) and in IL-6 (4.4 +/- 2 to 3.3 +/- 2 ng/L; p < 0.01). In the GH-treated group, the decrease in CRP and IL-6 correlated with a reduction in visceral adipose tissueVAT (r = 0.7; p < 0.001 and r = 0.5; p < 0.05 respectively). Conclusion: GH-treatment in postmenopausal women with abdominal obesity reduced serum markers of systemic inflammation. Circulating markers of endothelial dysfunction were unaffected by treatment.

 

 

Int J Cancer. 2007 Apr 23; [Epub ahead of print

Dietary patterns, the Alternate Healthy Eating Index and plasma sex hormone concentrations in postmenopausal women.

Fung TT, Hu FB, Barbieri RL, Willett WC, Hankinson SE.

Department of Nutrition, Simmons College, Boston, MA.

To evaluate the association between overall diet and sex hormones concentrations, we collected blood from 578 postmenopausal women ages 43 and 69 years in 1989 or 1990. Food intake was measured in 1990 via a food frequency questionnaire. We calculated the Alternate Healthy Eating Index (AHEI), and dietary patterns were identified by factor analysis. The cross-sectional association between diet and estrogens, sex hormone binding globulin (SHBG) were evaluated with linear regression and adjusted for energy and other potential confounders. We found a higher AHEI score was associated with lower concentrations of estradiol, free estradiol, and higher concentrations of SHBG. The prudent pattern, with higher intakes of fruits, vegetables, and whole grains, was not associated with any sex hormones. The Western pattern, which represents higher intakes of red and processed meats, refined grains, sweets and desserts, was associated with a higher level of estradiol and lower concentrations of SHBG. Further adjustment for BMI attenuated these results except for free estradiol (5th vs. 1st quintile = 0.09 vs. 0.11 pg/mL, p for trend = 0.03). In addition, the AHEI was inversely associated with estradiol among those with BMI > 25, and Western pattern with SHBG among those with BMI < 25. In conclusion, we observed inverse associations between the AHEI score and several estrogens, and it was positively associated with plasma levels of SHBG. In contrast, the Western pattern was positively associated with estrogen levels and inversely with SHBG. However, these associations appeared to be largely accounted for by BMI.

 

 

Scand J Clin Lab Invest. 2007;67(3):257-63

High C-reactive protein levels are associated with oral hormonal menopausal therapy but not with intrauterine levonorgestrel and transdermal estradiol.

Blumenfeld Z, Boulman N, Leiba R, Siegler E, Shachar S, Linn R, Levy Y.

Reproductive Endocrinology, Department of OB/GYN.

Objective . Oral hormone replacement therapy (HRT) has been linked to increased cardiovascular (CVD) morbidity. HRT causes a sustained increase in C-reactive protein (CRP), an excellent marker of subclinical inflammation and CVD. The aim of the study was to support our hypothesis that CRP, which is synthesized in the liver, is not increased in association with transdermal/intrauterine HRT. Material and methods . A case-control study was performed in which CRP measurements in women receiving levonorgestrel intrauterine system combined with transdermal estradiol (LNG/TDE, n = 27) were followed for 9 months or longer. CRP concentrations in these women were compared with those of either oral HRT users (n = 20) or controls (n = 19). Results . No significant differences were found in CRP concentrations between the LGN/TDE and control groups (1.8+/-1.2 and 1.8+/-1.8 mg/L, respectively). However, CRP was significantly increased in the oral HRT group (5.5+/-2.9 mg/L, p<0.001). Conclusions . CRP is significantly increased by oral HRT but not by the LNG/TDE combination after 9 months of treatment. This trend may explain the preponderance of some menopausal women on HRT being at increased risk for the development of CVD. Therefore, the use of LNG/TDE is acceptable for relief of severe climacteric symptoms possibly not imposing an increased CVD risk documented upon oral HRT.

 

 

Gynecol Endocrinol. 2007 Feb;23(2):99-104

Effects of postmenopausal hormone replacement therapy on body fat composition.

Yuksel H, Odabasi AR, Demircan S, Koseoglu K, Kizilkaya K, Onur E.

Department of Obstetrics and Gynecology, Adnan Menderes University, Faculty of Medicine. Aydin. Turkey.

Aim. To evaluate the effects of different types, regimens and administration routes of hormone replacement therapy (HRT) on body fat composition indices in postmenopausal women at increased risk of anthropometry-related cardiovascular disease (CVD). Methods. Fifty-nine postmenopausal women (aged 41-57 years, mean +/- standard deviation: 49.9 +/- 3.8 years) with body mass index (BMI) >/=25 kg/m(2) participated in this 6-month, prospective, randomized single-blind study. Subjects were assigned into three groups and received transdermal estradiol (E(2))/norethisterone acetate (NETA) (50 mug E(2) daily for 14 days followed by 50 mug E(2)/0.25 mug NETA daily for 14 days; transdermal group, n = 19), transdermal continuous E(2)/oral medroxyprogesterone acetate (MPA) (50 mug E(2)/5 mg MPA daily; transdermal/oral group, n = 19) or oral continuous E(2)/NETA (1 mg E(2)/0.5 mg NETA daily; oral group, n = 21). Anthropometric indices (body weight, height, and hip and waist circumferences) were measured, and BMI and waist-to-hip ratio (WHR) were calculated, before and after treatment. Also, the thickness of subcutaneous abdominal fat was measured by ultrasound. Depending on waist circumference (WC), the subjects were divided into two risk groups: increased-risk group with WC <88 cm (n = 32) and high-risk group with WC >/=88 cm (n = 27). Also, the effects of HRT were evaluated separately in subjects with median subcutaneous fat of <33 mm (n = 29) and those with median subcutaneous fat of >/=33 mm (n = 30). Results. Overall, all three types of HRT caused a significant decrease in both WC and subcutaneous fat (p < 0.001), and also in WHR (p < 0.05). There was no significant difference in baseline (p > 0.05) and final values (p > 0.05) between HRT groups. In each group, all types of HRT significantly decreased WC and subcutaneous fat (transdermal group: p < 0.001 and p < 0.05; transdermal/oral group: p < 0.001 and p < 0.01; oral group: p < 0.001 and p < 0.001, respectively), while body weight, BMI and WHR changed only insignificantly (p > 0.05). In the increased-risk group, body weight increased significantly (p < 0.05) while WC and subcutaneous fat decreased significantly (p < 0.001 and p < 0.001). As for the high-risk group, there was a significant decrease in WC and subcutaneous fat (p < 0.001, p < 0.001) while the remaining parameters did not change significantly. However, BMI showed a tendency to increase in the increased-risk group, while there was a decrease in all measurements in the high-risk group. Regardless of the drugs used and baseline subcutaneous fat, WC and subcutaneous fat decreased significantly at the end of the treatment (subcutaneous fat <33 mm: p < 0.001 and p < 0.01; subcutaneous fat >/=33 mm: p < 0.001 and p < 0.001, respectively). Conclusions. The three different types of HRT have comparable effects on central fat tissue in women at increased risk of anthropometry-related CVD. Indeed, the three combinations of HRT reduced fat tissue in the central part of the body. However, the overall effect of HRT was more marked in women with WC >/=88 cm and subcutaneous fat >/=33 cm. Whether HRT increases body weight depends on the body composition indices of individuals before treatment.

 

 

Climacteric. 2007 Apr;10(2):155-63

Testosterone addition during menopausal hormone therapy: effects on mammographic breast density.

Hofling M, Lundstrom E, Azavedo E, Svane G, Hirschberg AL, von Schoultz B.

Departments of Obstetrics and Gynecology.

Objective To study the effect on mammographic breast density of testosterone addition during combined estrogen/progestogen therapy in postmenopausal women. Methods A prospective, randomized, double-blind, placebo-controlled trial. A total of 99 women were given 2 mg 17beta-estradiol and 1 mg norethisterone acetate in combination with either a testosterone patch (300 mug/24 h) or a placebo patch. Mammographic breast density at baseline and after 6 months was assessed by visual classification scales and by digitized quantification. A standardized questionnaire was used to quantify subjective breast symptoms. Results Visual classifications showed an increase in mammographic density in 18-30% of the women, with no significant differences between the treatment groups. The mean increase of the area of dense breast during treatment according to digitized assessment was 7.4% in the placebo group and 5.4% in the testosterone group. Breast symptoms showed a positive association with the increase in density (r(s) = 0.34; p < 0.01). Symptoms were most pronounced at 2 months of treatment. Density, both at baseline (r(s) = -0.35; p < 0.01) and change during treatment (r(s) = -0.28; p < 0.01) showed a negative association with free testosterone levels. Conclusion The addition of testosterone does not appear to influence mammographic breast density in women concurrently treated with a common oral estrogen/progestogen regimen for a period of 6 months.

 

 

Climacteric. 2007 Apr;10(2):147-54

The influence of smoking on uterine bleeding during sequential oral hormone therapy.

Bjarnason NH, Byrjalsen I, Jorgensen HL, Christiansen C.

Center for Clinical & Basic Research. Ballerup.

Objective To study the influence of smoking on uterine bleeding patterns during sequentially administered oral hormone therapy (HT). Methods Using a post-hoc strategy, we included four sequential oral HT groups from two studies. The therapies consisted of estradiol from days 1 to 28 (estradiol or estradiol valerate) and progestogen (levonorgestrel or gestodene) on days 17-28. A total of 111 healthy, early postmenopausal women (38 smokers and 73 non-smokers) followed for 2 years were included in the analyses. Uterine bleeding data were collected from bleeding calendars. Results On the regimen containing levonorgestrel, smoking women had a cyclical bleeding significantly earlier than non-smoking women (about 2 days' difference). Moreover, smoking women had significantly longer bleeding than non-smoking women (about 1 day in difference). This was in contrast to the three regimens containing gestodene, where smoking seemed to have far less influence on uterine bleeding. Conclusions On a regimen containing levonorgestrel, smokers exhibit an earlier and longer uterine bleeding than do non-smokers. This is in contrast to regimens containing gestodene, where smoking women are less likely to differ from non-smoking women with regard to bleeding. This indicates that smoking influences progestogen metabolism, and that this influence may vary with different progestogens. Further studies are needed.

 

 

Climacteric. 2007 Apr;10(2):120-31

Ultra-low-dose estradiol and norethisterone acetate: effective menopausal symptom relief.

Panay N, Ylikorkala O, Archer DF, Gut R, Lang E.

West London Menopause and PMS Centre, Queen Charlotte's and Chelsea & Westminster Hospitals. London. UK.

Objective To evaluate the efficacy of two ultra-low-dose 17beta-estradiol plus norethisterone acetate (NETA) treatment regimens for relieving menopausal symptoms. Design A total of 577 postmenopausal women were enrolled, in three treatment groups in a double-blind, randomized, placebo-controlled study of 0.5 mg 17beta-estradiol + 0.1 mg NETA or 0.5 mg 17beta-estradiol + 0.25 mg NETA or placebo. Participants returned at weeks 4, 8, 12 and 24 for climacteric complaint evaluation based on a daily diary vasomotor symptom record. Patients were assessed by the Greene Climacteric Scale and urogenital symptoms were also evaluated. Results Treatment with ultra-low-dose 0.5 mg 17beta-estradiol + 0.1 mg NETA (0.1 Group) or 0.5 mg 17beta-estradiol + 0.25 mg NETA (0.25 Group) effectively reduced the severity and number of hot flushes within the initial weeks of therapy. Compared to placebo, a rapid, statistically significant decrease in the frequency and severity of hot flushes was achieved by week 3, followed by further improvement which continued throughout the study. There were no statistically significant differences between the active treatment arms. Conclusions The data show that both ultra-low-dose regimens are effective in reducing the severity and number of hot flushes compared to placebo, with good safety profiles.

 

 

Neuropsychol Dev Cogn B Aging Neuropsychol Cogn. 2007 May;14(3):301-28

Effects of hormone replacement therapy and aging on cognition: evidence for executive dysfunction.

Wegesin DJ, Stern Y.

G.H. Sergievsky Center, Columbia University. New York, New York. USA.

The present study was designed to explore whether the frontal lobe hypothesis of cognitive aging may be extended to describe the cognitive effects associated with estrogen use in postmenopausal women. Postmenopausal estrogen-only users, estrogen + progesterone users, and non-users (60-80 years old), as well as young, regularly cycling women (18-30 years old) completed an item and source memory task. Since source memory is thought to rely more on executive processes than item memory, we hypothesized that aging and estrogen effects would be greater for source memory than for item memory. Neuropsychological tests explored whether the effects of aging and estrogen use were revealed on other tests of frontal lobe function. Results from the experimental task revealed greater aging and estrogen effects for source memory than for item memory, and neuropsychological results revealed aging and estrogen effects on a subset of tests of executive function. Women on estrogen + progesterone therapy did not outperform non-users, suggesting that the addition of progesterone to hormone therapy may mitigate the benefits induced by estrogen use alone. Overall, findings support the hypothesis that estrogen use may temper age-related cognitive decline by helping to maintain functions subserved by the frontal lobes.

 

 

Acta Oncol. 2007;46(2):133-45.

Long-term follow-up of the randomized Stockholm trial on adjuvant tamoxifen among postmenopausal patients with early stage breast cancer.

Rutqvist LE, Johansson H;

Stockholm Breast Cancer Study Group.

Department of Oncology, Karolinska University Hospital, Sodersjukhuset, SE-118 83 Stockholm, Sweden.

The Stockholm Breast Cancer Study Group conducted a randomized trial during 1976 through 1990 comparing adjuvant tamoxifen versus control. A total of 2,738 postmenopausal women with invasive, early stage disease were randomised between tamoxifen for 2 or 5 years, or no adjuvant endocrine therapy. Among high-risk patients the treatment was given against a background of either postoperative, locoregional radiation or CMF-type chemotherapy. The median follow up was 18 years (range 11-25 years). There was a statistically significant (p =0.001) interaction between ER status and tamoxifen with no treatment benefit among receptor negatives. PgR-status had little additional predictive value. Among ER-positive patients tamoxifen reduced locoregional recurrences by 48%, contralateral breast cancers by 54%, distant metastases by 28%, and all events by 24% (p <0.001). On the other hand, there was a substantial increase of endometrial cancer associated with tamoxifen. There was no effect of tamoxifen on intercurrent mortality whereas breast cancer deaths were reduced by 31% (p <0.001) and overall mortality by 15% (p =0.01). Tamoxifen produced long-term benefits among estrogen receptor positive patients in terms of breast cancer-related events, but also an increased incidence of endometrial cancer. Despite long-term follow-up we observed no benefit with tamoxifen in terms of cardiovascular mortality.

 

 

Breast Cancer Res Treat. 2007 Apr 24; [Epub ahead of print

Decline in breast cancer incidence after decrease in utilisation of hormone replacement therapy.

Katalinic A, Rawal R.

Institute of Cancer Epidemiology, University of Lubeck, Beckergrube 43-47, 23552, Lubeck, Germany, alexander.katalinic@krebsregister-sh.de.

Hormone replacement therapy (HRT) has been implicated as a risk factor for breast cancer and the use of HRT has decreased substantially in general population over the last years. Recently, there are first indications that breast cancer incidence has started declining. We examined recent breast cancer incidence and actual data on HRT utilisation in Schleswig-Holstein, Germany, to find out population based evidence on decreasing breast cancer incidence and its possible relationship with reduced HRT usage. Breast cancer incidence is taken from the population based cancer registry of Schleswig-Holstein. HRT data was extracted from a cohort of 102,000 women taking part in a quality assurance project in breast cancer diagnosis for the years 2001-2005. The annual percentage change in incidence of breast cancer and HRT utilisation was measured by linear regression. There is a linear decline in HRT utilisation among less than 50 years group, 50-69 years group and all age group women between the years 2001 and 2005. Breast cancer incidence decreased between the years 2001 and 2005 for more than 50 years old and all age group, but not in the younger than 50 years women. The decline of breast cancer incidence started about two years after the HRT decline. Breast cancer incidence decline and decreased HRT utilisation showed a high correlation. A drastic change in age-incidence relationship in breast cancer has taken place, the change is likely to continue and in future it has to be monitored closely with HRT use and other possible explanations.

 

 

Menopause Int. 2007 Mar;13(1):44-5.

Management of premature menopause.

Writing Group for the British Menopause Society Council.

There has been some confusion among women and health professionals since the publication of the Women's Health Initiative and Million Women studies about the management of premature ovarian failure (POF). Both studies were undertaken in women aged 50 and over, and cannot be extrapolated to their younger counterparts, who would normally be producing their endogenous estrogen, since they have functioning ovaries. Estrogen-based replacement therapy is the main stay of treatment for women with POF and is recommended at least until the average age of natural menopause (52 years in the UK). This view is endorsed by regulatory bodies such as the Committee on Safety of Medicines (now the Commission on Human Medicines) in the UK. No evidence shows that estrogen replacement increases the risk of breast cancer to a level greater than that found in normally menstruating women, and women with POF do not need to start mammographic screening early unless other risk factors are present, such as family history.

Semana del 17 al 23 de Abril 2007

Dr. Juan Enrique Blümel

 

Menopause. 2007 Apr 13; [Epub ahead of print]

The role of local vaginal estrogen for treatment of vaginal atrophy in postmenopausal women: 2007 position statement of The North American Menopause Society.

OBJECTIVE:: To create an evidence-based position statement published by The North American Menopause Society (NAMS) on the role of local vaginal estrogen therapy (ET) for the treatment of vaginal atrophy in postmenopausal women. DESIGN:: NAMS followed the general principles established for evidence-based guidelines to create this document. A panel of clinicians and researchers acknowledged to be experts in the field of genitourinary disease was enlisted to review, synthesize, and interpret the current evidence on vaginal ET for vaginal atrophy, develop conclusions, and make recommendations. Their advice was used to assist the NAMS Board of Trustees in publishing this position statement. RESULTS:: Randomized controlled trials, albeit limited, have shown that low-dose, local vaginal estrogen delivery is effective and well tolerated for treating vaginal atrophy. All of the low-dose vaginal estrogen products approved in the United States for treatment of vaginal atrophy are equally effective at the doses recommended in labeling. CONCLUSIONS:: The choice of therapy should be guided by clinical experience and patient preference. Progestogen is generally not indicated when low-dose estrogen is administered locally for vaginal atrophy. Data are insufficient to recommend annual endometrial surveillance in asymptomatic women using vaginal ET. Vaginal ET should be continued for women as long as distressful symptoms remain. For women treated for non-hormone-dependent cancer, management of vaginal atrophy is similar to that for women without a cancer history. For women with a history of hormone-dependent cancer, management recommendations are dependent upon each woman's preference in consultation with her oncologist.

 

N Engl J Med. 2007 Apr 19;356(16):1670-4

The decrease in breast-cancer incidence in 2003 in the United States.

Ravdin PM, Cronin KA, Howlader N, Berg CD, Chlebowski RT, Feuer EJ, Edwards BK, Berry DA.

Department of Biostatistics, M.D. Anderson Cancer Center, Houston, USA.

An initial analysis of data from the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) registries shows that the age-adjusted incidence rate of breast cancer in women in the United States fell sharply (by 6.7%) in 2003, as compared with the rate in 2002. Data from 2004 showed a leveling off relative to the 2003 rate, with little additional decrease. Regression analysis showed that the decrease began in mid-2002 and had begun to level off by mid-2003. A comparison of incidence rates in 2001 with those in 2004 (omitting the years in which the incidence was changing) showed that the decrease in annual age-adjusted incidence was 8.6% (95% confidence interval [CI], 6.8 to 10.4). The decrease was evident only in women who were 50 years of age or older and was more evident in cancers that were estrogen-receptor-positive than in those that were estrogen-receptor-negative. The decrease in breast-cancer incidence seems to be temporally related to the first report of the Women's Health Initiative and the ensuing drop in the use of hormone-replacement therapy among postmenopausal women in the United States. The contributions of other causes to the change in incidence seem less likely to have played a major role but have not been excluded.

 

Cancer Causes Control. 2007 Apr 16; [Epub ahead of print]

Alcohol consumption, cigarette smoking, and endometrial cancer risk: results from the Netherlands Cohort Study.

Loerbroks A, Schouten LJ, Goldbohm RA, van den Brandt PA.

Department of Epidemiology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands, lj.schouten@epid.unimaas.nl.

OBJECTIVE: To examine the association between alcohol consumption, cigarette smoking, and endometrial cancer. METHODS: In 1986, the Netherlands Cohort Study was initiated. A self-administered questionnaire on dietary habits and other cancer risk factors was completed by 62,573 women. Follow-up for cancer was established by record linkage to the Netherlands Cancer Registry. RESULTS: After 11.3-years of follow-up, 280 incident endometrial cancer cases were available for analyses. In multivariate analysis, the rate ratio (RR) for alcohol users versus non-users was 1.06 (95% Confidence Interval (95% CI) = 0.78-1.43). There were neither dose-dependent trends nor associations with different types of beverages. The RR for former and current smokers versus never-smokers was 0.83 (95% CI = 0.58-1.20) and 0.59 (95% CI = 0.40-0.88), respectively. These estimates did not change significantly when body mass index (BMI) and age at menopause were added to the models. CONCLUSIONS: There is no association between alcohol consumption and endometrial cancer. Current smoking is associated with a reduced risk of endometrial cancer. This association is neither mediated by BMI nor by age at menopause.

 

Menopause. 2007 Apr 13; [Epub ahead of print]

Estrogen effects on arteries vary with stage of reproductive life and extent of subclinical atherosclerosis progression.

Clarkson TB.

From the Comparative Medicine Clinical Research Center, Wake Forest University School of Medicine, Winston-Salem, NC.

ABSTRACT: The past several years have been marked by confusion and controversy concerning whether estrogens are cardioprotective. The issue is of utmost public health importance because coronary heart disease (CHD) remains the leading cause of death among postmenopausal women. Fortunately, a unifying hypothesis has emerged that reproductive stage is a major determinant of the effect of estrogens on atherosclerosis progression, complications, and plaque vulnerability. PREMENOPAUSAL YEARS:: Premenopausal atherosclerosis progression seems to be an important determinant of postmenopausal atherosclerosis and thus the risk for CHD. Clearly, plasma lipids/lipoproteins influence this progression; however, estradiol deficiency seems to be the major modulator. Both monkeys and women with premenopausal estrogen deficiency develop premature atherosclerosis, an effect that can be prevented in both species by estrogen-containing oral contraceptives. PERIMENOPAUSAL/EARLY POSTMENOPAUSAL YEARS:: During this stage, there are robust estrogen benefits. Monkeys given estrogens immediately after surgical menopause have a 70% inhibition in coronary atherosclerosis progression. Estrogen treatment prevented progression of atherosclerosis of women in the Estrogen in the Prevention of Atherosclerosis Trial. A meta-analysis of women younger than 60 years given hormone therapy had reduced total mortality (relative risk = 0.61, 95% CI: 0.39-0.95). LATE POSTMENOPAUSAL YEARS:: This stage is one in which there are no or possible deleterious estrogen effects. Monkeys lose CHD benefits of estrogens when treatment is delayed. The increase in CHD events associated with initiating hormone therapy 10 or more years after menopause seems to be related to up-regulation of the plaque inflammatory processes and plaque instability and may be down-regulated by statin pretreatment.

 

Bone. 2007 May;40(5 Suppl 1):S5-8. Epub 2007 Feb 17

Strontium ranelate: New insights into its dual mode of action.

Marie PJ.

INSERM U606 and University Paris 7, Lariboisiere Hospital, 2 rue Ambroise Pare, 75475 Paris cedex 10, France.

Strontium ranelate is a newly developed drug that acts as an effective antiosteoporotic therapy in postmenopausal women with osteoporosis. In contrast to other available treatments for osteoporosis, strontium ranelate induces opposite effects on bone resorption and formation. Preclinical studies showed that this dual effect results in increased bone mass and improved bone microarchitecture and strength in intact rodents, and in prevention of bone loss in osteopenic animals. Histomorphometric analysis of unpaired iliac crest bone biopsies in postmenopausal osteoporotic patients treated with strontium ranelate for 3 years showed that the drug increased bone formation, assessed by both the mineralization rate and osteoblast surface, and tended to decrease the osteoclast surface, compared with the placebo group. Three-dimensional micro-computed tomography analysis of the bone biopsies consistently showed a higher number of trabeculae, decreased trabecular separation, and an increase in cortical thickness, which provides evidence for a better trabecular and cortical bone microarchitecture in treated patients compared with the placebo group. Some mechanisms that underlie the beneficial effects of strontium ranelate on bone metabolism and strength have now been identified. In vitro analyses showed that strontium activates the calcium-sensing receptor. We, however, showed that strontium ranelate activates cell replication and downstream ERK1/2 signaling in osteoblasts from calcium-sensing receptor-null mice, indicating that, in addition to the calcium-sensing receptor, another receptor could mediate the effect of strontium ranelate on osteoblastic cell replication. Other in vitro studies showed that strontium ranelate can activate the osteogenic differentiation of bone marrow stromal cells by activating cyclo-oxygenase 2 (COX-2)-mediated prostaglandin E(2) production. Finally, recent data indicate that strontium ranelate can upregulate osteoprotegerin (OPG) and decrease receptor activator of nuclear factor kappa B (RANK) ligand expression in human osteoblastic cells, suggesting that strontium ranelate may reduce bone resorption by modulating the RANK/RANK-ligand/OPG system, which is essential for osteoclastogenesis. These recent data provide new insights into the mechanism of action of strontium ranelate and give biochemical support to cell physiology which explain the opposite effects of strontium ranelate on bone formation and resorption.

 

Clin Endocrinol (Oxf). 2007 Apr 15

Menopausal hormone therapy and gallbladder disease: the Study of Health in Pomerania (SHIP).

Schwarz S, Volzke H, Baumeister SE, Hampe J, Doren M.

Charite- Universitatsmedizin Berlin, Campus Benjamin Franklin, Clinical Research Centre of Women's Health, Berlin, Germany.

Objective Several studies suggest that oral menopausal hormone therapy (MHT) is associated with an increased risk of gallbladder disease. It has been hypothesized that nonoral MHT may reduce the risk of cholelithiasis. The objective of the present study was to analyse the association between (1) use of life-time MHT (ever use) and gallbladder disease and (2) nonoral use of MHT and gallbladder disease. Design Cross-sectional study using population-based data from the Study of Health in Pomerania (SHIP). Population The study population included 994 postmenopausal women, aged 40-79 years. The subgroup of current oral and nonoral MHT users comprised 139 women. Methods and measurements Sociodemographic, medical and reproductive characteristics were based on computer-assisted personal interviews, and selected laboratory parameters were analysed. Gallbladder disease was defined by either a prior history of cholecystectomy or the presence of current sonographically diagnosed gallstones. Data analyses consisted of descriptive, bivariable and multivariable procedures. We performed Poisson regression with Huber/White standard errors to investigate the association between ever use, current nonoral use of MHT and gallbladder disease. Results We found no significant association between ever use of MHT and gallbladder disease and sonographically diagnosed gallstones in fully adjusted analyses. Women who used MHT had a significantly higher risk for cholecystectomy compared to nonusers. There was no association between nonoral use of MHT and gallbladder disease. Conclusions Our analyses do not lend support to the hypothesis that use of MHT is associated with gallbladder disease.

 

J Clin Endocrinol Metab. 2007 Apr 17; [Epub ahead of print

Addition of monofluorophosphate to estrogen therapy in postmenopausal osteoporosis - a randomized controlled trial.

Reid IR, Cundy T, Grey AB, Horne A, Clearwater J, Ames R, Orr-Walker BJ, Wu F, Evans MC, Gamble GD, King A.

Department of Medicine, University of Auckland, Auckland, New Zealand; Pathology Laboratory, Middlemore Hospital, Auckland, New Zealand.

Introduction: Treatment of osteoporosis with high-dose fluoride alone does not reduce fracture risk. We hypothesized that the anti-fracture efficacy of fluoride could be optimized by its use in low doses combined with an antiresorptive agent. Experimental Subjects: 80 women with postmenopausal osteoporosis who had been taking estrogen for >/=1 year. Methods: Subjects were randomized to receive monofluorophosphate (fluoride content of 20 mg/day) or placebo over 4 years in a double-blind trial. Results and Discussion: There were progressive increases in lumbar spine bone density (BMD) over the duration of the study (MFP 22%, placebo 6%, P<0.0001). In the trabecular bone of L3, these increases were even greater (MFP 49%, placebo 2.5%, P<0.0001). In the proximal femur there were smaller but significant treatment effects (P=0.015). Total body scans and their subregions also showed significantly greater increases in the MFP group. Bone formation markers increased significantly in the MFP group at year 1. Hyperosteoidosis was present in biopsies from 5 of 7 MFP subjects, with osteomalacia in 2 of 7. The hazards ratio for vertebral fractures was 0.20 (95% confidence interval 0.05-1.30) and the incidence rate ratio was 0.12 (95% confidence interval, 0.06-0.23, P<0.01). The hazards ratio for non-vertebral fractures was 3.3 (95% CI 0.8-12.0). We conclude that fluoride 20 mg/day produces substantial increases in BMD, but still interferes with bone mineralization. This indicates that most previous studies with this ion have used toxic doses, and that much lower doses should be assessed to find a safe dose window for the use of this powerful anabolic agent.

 

Rev Endocr Metab Disord. 2007 Apr 14; [Epub ahead of print

SERMs for the treatment and prevention of breast cancer.

Swaby RF, Sharma CG, Jordan VC.

Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA, 19111-2497, USA, v.craig.jordan@fccc.edu.

Tamoxifen and raloxifene are both selective estrogen receptor modulators (SERMs). The medicines can block estrogen mediated breast cancer growth and development but will also maintain bone density in postmenopausal women and lower circulating cholesterol. Tamoxifen has remained the antihormonal therapy of choice for the treatment of ER positive breast cancer for the last 30 years. However, although adjuvant tamoxifen produces profound increases in disease-free and overall survival in patients with ER positive breast cancer, concerns about drug resistance, blood clots and endometrial cancer have resulted in a change to the use of aromatase inhibitors for the treatment of postmenopausal women. Nevertheless, tamoxifen remains the antihormonal treatment of choice for premenopausal women with ER positive breast cancer and for risk reduction in premenopausal women who are at high risk for developing breast cancer. The risk of endometrial cancer and thromboembolic disorders during tamoxifen therapy is not elevated in premenopausal women. It is important to note that aromatase inhibitors or raloxifene should not be used in premenopausal women. Raloxifene is used to prevent osteoporosis in postmenopausal women and, unlike tamoxifen, does not increase the risk of endometrial cancer. However, raloxifene does reduce breast cancer risk by 50-70% in both low risk and high risk postmenopausal women. Comparisons of raloxifene with tamoxifen show equal efficacy as a chemopreventive for breast cancer but there is a reduction in thromboembolic disorders, fewer endometrial cancers, hysterectomies, cataracts and cataract surgeries in women taking raloxifene. Overall, SERMs continue to fulfill their promise as appropriate medicines that target specific populations for the treatment and prevention of breast cancer.

 

Endocrinology. 2007 Apr 19; [Epub ahead of print]

The endogenous estradiol metabolite 2-methoxyestradiol reduces atherosclerotic lesion formation in female ApoE-deficient mice.

Bourghardt J, Bergstrom G, Krettek A, Sjoberg S, Boren J, Tivesten A.

The Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy at Goteborg University, Sahlgrenska University Hospital, SE-413 45 Goteborg, Sweden.

Estradiol, the major endogenous estrogen, reduces experimental atherosclerosis and metabolizes to 2-methoxyestradiol in vascular cells. Currently undergoing evaluation in clinical cancer trials, 2-methoxyestradiol potently inhibits cell proliferation independently of the classical estrogen receptors. This study examined whether 2-methoxyestradiol affects atherosclerosis development in female mice. Apolipoprotein E-deficient mice, a well-established mouse model of atherosclerosis, were ovariectomized and treated through slow release pellets with placebo; 17beta-estradiol (6 microg/day); or 2-methoxyestradiol (6.66 microg/day (ME low) or 66.6 microg/day (ME high)). After 90 days, body weight gain decreased and uterine weight increased in the ME high but not in the ME low group. En face analysis showed that the fractional area of the aorta covered by atherosclerotic lesions decreased in the ME high (52%) but not in the ME low group. Total serum cholesterol levels decreased in the high and low dose ME groups (19%, P < 0.05 and 21%, P = 0.062, respectively). Estradiol treatment reduced the fractional atherosclerotic lesion area (85%) and decreased cholesterol levels (42%). In conclusion, our study shows for the first time that 2-methoxyestradiol reduces atherosclerotic lesion formation in vivo. The anti-atherogenic activity of an estradiol metabolite lacking estrogen receptor activating capacity may argue that trials on cardiovascular effects of hormone replacement therapy should use estradiol rather than other estrogens. Future research should define the role of 2-methoxyestradiol as a mediator of the anti-atherosclerotic actions of estradiol. Furthermore, evaluation of the effects of 2-methoxyestradiol on cardiovascular disease endpoints in ongoing clinical trials is of great interest.

 

J Natl Med Assoc. 2007 Apr;99(4):412-8

History of fractures as predictor of subsequent hip and nonhip fractures among older Mexican Americans.

Ojo F, Al Snih S, Ray LA, Raji MA, Markides KS.

Osteoporosis Clinic in the Division of Geriatrics, Internal Medicine Department, Sealy Center on Aging, The University of Texas Medical Branch, Galveston 77555-0460, USA. folojo@utmb.edu

OBJECTIVE: To examine the association between previous fracture and risk of new hip and nonhip fractures over a seven-year period among older Mexican Americans. METHOD: Data used are from the Hispanic Established Population for the Epidemiological Study of the Elderly (H-EPESE) (1993-2001). Measures included history of previous fracture (hip fracture only, a nonhip fracture, hip and nonhip fractures, and no fractures), sociodemographic factors, smoking status, medical conditions (arthritis, diabetes, stroke and cancer), activities of daily living disability, and high depressive symptoms. Cox proportional regression model was used to estimate the seven-year incidence of fractures. RESULTS: Of the 2,589 subjects, 42 reported a hip fracture, 328 reported a nonhip fracture, and 2,219 did not report a fracture at baseline. After controlling for all covariates, the hazard ratio (HR) of new hip fracture at seven-year follow-up was 6.48 (95% CI: 3.26-12.97) for subjects with only hip fracture at baseline and 1.96 (95% CI: 1.22-3.16) for subjects with nonhip fracture at baseline. The HR of new nonhip fracture was 1.90 (95% CI: 0.96-3.77) for subjects with only hip fracture at baseline and 2.62 (95% CI: 1.95-3.52) for subjects with nonhip fracture at baseline. CONCLUSIONS: A previous history of fractures in older Mexican Americans is the strongest predictor of recurrent fractures at hip and nonhip sites, independent of other health measures. Our findings of recurrent fractures suggest the need for more aggressive detection and adequate treatment of osteoporosis- and fall-related factors in this population.

 

PLoS ONE. 2007 Apr 18;2:e377

Established risk factors account for most of the racial differences in cardiovascular disease mortality.

Henderson SO, Haiman CA, Wilkens LR, Kolonel LN, Wan P, Pike MC.

Department of Preventive Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, California, United States of America.

BACKGROUND: Cardiovascular disease (CVD) mortality varies across racial and ethnic groups in the U.S., and the extent that known risk factors can explain the differences has not been extensively explored. METHODS: We examined the risk of dying from acute myocardial infarction (AMI) and other heart disease (OHD) among 139,406 African-American (AA), Native Hawaiian (NH), Japanese-American (JA), Latino and White men and women initially free from cardiovascular disease followed prospectively between 1993-1996 and 2003 in the Multiethnic Cohort Study (MEC). During this period, 946 deaths from AMI and 2,323 deaths from OHD were observed. Relative risks of AMI and OHD mortality were calculated accounting for established CVD risk factors: body mass index (BMI), hypertension, diabetes, smoking, alcohol consumption, amount of vigorous physical activity, educational level, diet and, for women, type and age at menopause and hormone replacement therapy (HRT) use. RESULTS: Established CVD risk factors explained much of the observed racial and ethnic differences in risk of AMI and OHD mortality. After adjustment, NH men and women had greater risks of OHD than Whites (69% excess, P<0.001 and 62% excess, P = 0.003, respectively), and AA women had greater risks of AMI (48% excess, P = 0.01) and OHD (35% excess, P = 0.007). JA men had lower risks of AMI (51% deficit, P<0.001) and OHD (27% deficit, P = 0.001), as did JA women (AMI, 37% deficit, P = 0.03; OHD, 40% deficit, P = 0.001). Latinos had underlying lower risk of AMI death (26% deficit in men and 35% in women, P = 0.03). CONCLUSION: Known risk factors explain the majority of racial and ethnic differences in mortality due to AMI and OHD. The unexplained excess in NH and AA and the deficits in JA suggest the presence of unmeasured determinants for cardiovascular mortality that are distributed unequally across these populations.

 

Carcinogenesis. 2007 Apr 17; [Epub ahead of print

Diabetes and risk of breast cancer in Asian-American women.

Wu AH, Yu MC, Tseng CC, Stanczyk FZ, Pike MC.

Affiliations of authors: A.H.Wu, C.C. Tseng, M.C. Pike, Department of Preventive Medicine; F.Z. Stanczyk, Department of Obstetrics and Gynecology, University of Southern California Keck School of Medicine, Los Angeles, California 90089. M.C. Yu, The Cancer Center, University of Minnesota, Minneapolis, MN 55455.

The role of diabetes in the etiology of breast cancer in Asian-Americans is not known. We investigated the relation between diabetes and breast cancer risk in a population-based case-control study in Los Angeles County that included 1,248 Asian American women with incident, histologically confirmed breast cancer and 1,148 control women, who were frequency matched to cases on age, Asian ethnicity and neighborhood of residence. The relation between history of diabetes and serum concentrations of estrogens, androgens and sex hormone-binding globulin (SHBG) was investigated in 212 postmenopausal control women. A history of diabetes was statistically significantly associated with breast cancer risk (odds ratio (OR)=1.68, 95% confidence interval (CI)=1.15-2.47) after adjusting for reproductive and other factors. This increased risk was unchanged after further adjustment for body mass index (BMI) and waist-hip ratio (WHR). We found a stronger diabetes-breast cancer association in women with lower BMI (<=22.7) (adjusted OR= 3.50, P=0.011) than those with higher BMI (>22.7) (adjusted OR=1.39, P=0.23) but this difference in ORs was not statistically significant. Our results also show that the diabetes-breast cancer association was observed only in low/intermediate soy consumers (OR=2.48, P=0.0008) but not among high soy consumers (OR=0.75, P=0.41) (P interaction =0.014). Controls who were diabetic showed significantly lower SHBG (20%) (P=0.02) but higher free testosterone levels (26%) (P=0.08) than women without such a history after adjusting for BMI and WHR. Our results support the hypothesis that diabetes may have a role in the development of breast cancer, influencing risk via both sex hormone and insulin pathways.

 

BMC Public Health. 2007 Apr 17;7(1):56 [Epub ahead of print

Changes of the prescription of hormone therapy in menopausal women: An observational study in Taiwan.

Huang WF, Tsai YW, Hsiao FY, Liu WC.

ABSTRACT: BACKGROUND: The prescribing of hormone therapy to menopausal women has been changed since the publication of 2002 Womens Health Initiative (WHI) report. This study evaluates the impact of WHI study results on the prescription of menopausal hormone therapy (MHT) to treat menopause-related symptoms in Taiwan. METHODS: This retrospective study participant data were collected from women interviewed in 2001 Taiwans National Health Interview Survey (NHIS) and the National Health Insurance (NHI) outpatient claims for women being treated for menopause-related symptoms. We compared prescriptions made for MHI to women seeking outpatient treatment for menopause-related symptoms before and after the publication of the 2002 WHI to study its effect of prescription behavior in Taiwan. There was one dichotomous outcome variable, which was whether MHT was prescribed or not in an outpatient visit to treat menopause-related symptoms. RESULTS: Our study included 504 women 45 years old or above whose outpatient visits for menopause-related symptoms were covered by National Health Insurance in 2002. In total, these 504 women made 2549 outpatient visits to be treated for these symptoms. The proportion of outpatient visits in which MHT was prescribed dropped from 83.0% (n=1,155) before WHI to 73.0% (n=844) after WHI. We found a decrease in likelihood that women would be prescribe MHT for menopause-related symptoms after the release of the WHI report (OR=0.36, 95%CI=0.25 to 0.52, p<0.05). Gynecologists and obstetricians more likely to prescribe MHT than physicians with other medical specialties (5.34; 95%CI=3.45 to 8.26, p<0.05). Women with college level educations or higher were became less likely to be prescribed MHT (Model 2; OR 0.30; 95% CI 0.11-0.83), and academic medical centers became less likely to prescribe MHT than other medical care institutions (Model 3; OR 0.15; 95% CI 0.34-0.63). CONCLUSIONS: The WHI report caused a substantial decline in the use of MHT to treat menopause-related symptoms in Taiwan. It was found to exert most of its influence in patients with higher educations, physicians with specialties other than gynecologists and obstetricians, and academic medical centers.

 

Am J Med Sci. 2007 Apr;333(4):208-214

Interrelationship Between Insulin Resistance and Menopause on the Metabolic Syndrome and Its Individual Component Among Nondiabetic Women in the Kinmen Study.

Lin KC, Tsai ST, Kuo SC, Tsay SL, Chou P.

From the Department of Nursing, National Taipei College of Nursing, Taipei, Taiwan (kcl, slt); the Department of Medicine, Veterans General Hospital-Taipei, Taipei, Taiwan (stt); Graduate Institute of Nurse-Midwifery, National Taipei College of Nursing, Taipei, Taiwan (sck); and Community Medicine Research Center, Institute of Public Health, National Yang-Ming University, Taipei, Taiwan (pc).

BACKGROUND:: The literature to date is not clear as to whether any interactive effect exists between insulin resistance and menopause on the metabolic syndrome and its individual components. We explored this issue in 4107 homogeneous, nondiabetic Chinese women in the Kinmen Study. METHODS:: Overnight fasting blood samples were drawn for glucose, insulin, lipid, and other biochemical measurements. Demographic and clinical variables including body mass index, waist circumference, and blood pressure were measured and documented during face-to-face interviews with structured questionnaires. Menstrual history was used to define menopause as the absence of menses for 12 consecutive months. RESULTS:: Approximately 16% of premenopausal women (390/2423) were insulin-resistant. After adjustment for age, body mass index, lifestyle, and diet, both menopause and insulin resistance were independently and significantly correlated with metabolic syndrome. For each component of the metabolic syndrome, besides the main effect, the interaction (insulin resistance x menopause) had significant correlation with systolic blood pressure, diastolic blood pressure, and waist circumference. CONCLUSIONS:: Both insulin resistance and menopause have significant effects on metabolic syndrome independent of age and obesity. In premenopausal and nondiabetic women, various degrees of insulin resistance exist. The synergistic contribution of insulin resistance and menopause to components of the metabolic syndrome were observed with systolic blood pressure, diastolic blood pressure, and waist circumference. This requires further study.

 

Semana del 10 al 16 de Abril 2007

 

Dr. Juan Enrique Blümel

 

 

Calcif Tissue Int. 2007 Apr 13; [Epub ahead of print]

Relationship between Vascular Calcification and Bone Mineral Density in the Old-Order Amish.

Shen H, Bielak LF, Streeten EA, Ryan KA, Rumberger JA, Sheedy PF 2nd, Shuldiner AR, Peyser PA, Mitchell BD.

Division of Endocrinology, Diabetes, and Nutrition, Department of Medicine, University of Maryland, 660 W. Redwood Street, Room 492, Baltimore, MD, 21201, USA, bmitchel@medicine.umaryland.edu.

Vascular calcification and osteoporosis are common age-related processes that are influenced by both genetic and nongenetic factors. Whether common genes underlie these processes is not known. We measured coronary artery calcification (CAC), aortic calcification (AC), and bone mineral density (BMD) in 682 men and women from large Old-Order Amish families. We assessed the heritabilities of these traits and then evaluated, using variance decomposition procedures, whether variation in the traits was influenced by a common set of genes (i.e., pleiotropy). Significant heritabilities were detected for BMD of the femoral neck and spine (0.65, 0.63) and CAC and AC (0.43, 0.42). Mean BMD did not differ significantly across quartiles of either CAC or AC in either sex. In neither the total group nor any single subgroup (men, women, postmenopausal women) did any of the genetic or environmental correlations between BMD and vascular calcification achieve statistical significance. However, subjects with a history of cardiovascular disease (CVD) events had significantly lower BMD at the femoral neck compared to subjects who reported no prior history of CVD (age-, sex-, body mass index-, and family structure-adjusted P = 0.003). We detected no evidence for shared genes affecting the joint distribution of bone and vascular calcification. However, our results do reveal a lower BMD in subjects with a prior history of CVD in the Old-Order Amish.

 

 

Endocr Rev. 2007 Apr 12; [Epub ahead of print]

Novel perspectives for progesterone in HRT, with special reference to the nervous system.

Schumacher M, Guennoun R, Ghoumari A, Massaad C, Robert F, El-Etr M, Akwa Y, Rajkowski K, Baulieu EE.

INSERM UMR 788 and University Paris-Sud 11, 80, rue du General Leclerc, 94276 Kremlin-Bicetre, France.

The utility and safety of postmenopausal hormone replacement therapy (HRT) has recently been put into question by large clinical trials. Their outcome has been extensively commented upon, but discussions have mainly been limited to the effects of estrogens. In fact, progestagens are generally only considered with respect to their usefulness in preventing estrogen stimulation of uterine hyperplasia and malignancy. In addition, various risks have been attributed to progestagens, and their omission from HRT has been considered, but this may be to underestimate their potential benefits and therapeutic promises. A major reason for the controversial reputation of progestagens is that they are generally considered as a single class. Moreover, the term progesterone is often used as a generic one for the different types of both natural and synthetic progestagens. This is not appropriate, as natural progesterone has properties very distinct from the synthetic progestins. Within the nervous system, the neuroprotective and promyelinating effects of progesterone are promising not only for preventing, but also for reversing, age-dependent changes and dysfunctions. There is indeed strong evidence that the aging nervous system remains at least to some extent sensitive to these beneficial effects of progesterone. The actions of progesterone in peripheral target tissues including breast, blood vessels and bones are less well understood, but there is evidence for its beneficial effects. The variety of signaling mechanisms of progesterone offers exciting possibilities for the development of more selective, efficient and safe progestagens. The recognition that progesterone is synthesized by neurons and glial cells requires a re-evaluation of hormonal aging.

 

 

Int J Gynecol Cancer. 2007 Apr 8;

The relation between age, time since menopause, and endometrial cancer in women with postmenopausal bleeding.

van Doorn HC, Opmeer BC, Jitze Duk M, Kruitwagen RF, Dijkhuizen FP, Mol BW.

Department of Obstetrics and Gynaecology, University Medical Centre Utrecht, Utrecht, The Netherlands.

The objective is to assess among women with postmenopausal bleeding the relationship of age and time since menopause on one hand and the presence of endometrial cancer and atypical hyperplasia on the other hand. In a multicenter prospective cohort study, 614 women presenting with postmenopausal bleeding were included. Women underwent transvaginal sonography and, in cases where the endometrial thickness was >4 mm, endometrial sampling. Splines were used to assess the association between each of the continuous variables and (pre)malignancy of the endometrium. Subsequently, univariate and multivariate analysis were performed. The average age for women without (pre)malignancy was 61.7 years (SD 9.8). As malignant and premalignant cases were found to have similar age, these subgroups were merged in the analyses. Age was an independent predictor of (pre)malignancy. In women younger than 55 years, the odds ratio was 1.9 (95% CI: 1.1-3.3) for each year under 55 years of age and 1.03 (95% CI: 1.00-1.06) for each year over 55 years of age. The risk of (pre)malignancy of the endometrium was 4.9% in women less than 3 years postmenopausal versus 19.7% in women more than 20 years postmenopausal. However, in a multivariate analysis only age contributed to the prediction of risk. This study demonstrates that, in postmenopausal women with vaginal bleeding, the risk of (pre)malignancy of the endometrium is low in women under 50 years of age, increases considerably until 55 years of age, and rises only modestly with further advancing age. Future studies should explore whether these findings can be incorporated in the diagnostic work-up of women with postmenopausal bleeding.

 

 

Drug Metab Dispos. 2007 Apr 9; [Epub ahead of print]

Selective tissue distribution of tibolone metabolites in mature ovariectomized female cynomolgus monkeys after multiple doses of tibolone.

Verheul HA, van Iersel ML, Delbressine LP, Kloosterboer HJ.Organon.

Tibolone is a selective tissue estrogenic activity regulator (STEAR). In postmenopausal women, it acts as an estrogen on brain, vagina and bone, but not on endometrium and breast. Despite ample supporting in vitro data for tissue selective actions, confirmative tissue levels of tibolone metabolites are not available. Therefore, we analyzed tibolone and metabolites in plasma and tissues from six ovariectomized cynomolgus monkeys that received tibolone (0.5 mg/kg/day by gavage) for 36 days and were necropsied at 1, 1.25, 2.25, 4, 6 and 24 hours after the final dose. The plasma and tissue levels of active, non-sulfated (tibolone, 3alpha-hydroxytibolone, 3beta-hydroxytibolone, Delta(4)-tibolone), mono-sulfated (3alpha-sulfate,17beta-hydroxytibolone, 3beta-sulfate,17beta-hydroxytibolone) and di-sulfated (3alpha,17beta-di-sulfated-tibolone, 3beta,17betaS-di-sulfated-tibolone) metabolites were measured by validated gas chromatography with mass spectrometry and liquid chromatography with tandem mass spectrometry. Detection limits were 0.1-0.5 ng/mL (plasma) and 0.5-2 ng/g (tissues). In brain tissues, estrogenic 3alpha-hydroxytibolone was predominant with 3-8 times higher levels than in plasma; levels of sulfated metabolites were low. In vaginal tissues, major non-sulfated metabolites were 3alpha-hydroxytibolone and the androgenic/progestagenic Delta(4)-tibolone; di-sulfated metabolites were predominant. Remarkably high levels of mono-sulfated metabolites were found in the proximal vagina. In endometrium, myometrium and mammary glands, levels of 3-hydroxymetabolites were low and those of sulfated metabolites high (about 98% di-sulfated). Delta(4)-tibolone/3-hydroxytibolone ratios were 2-3 in endometrium, about equal in breast and proximal vagina, and 0.1 in plasma and brain. It is concluded that tibolone metabolites show a unique tissue-specific distribution pattern explaining the tissue effects in monkeys and the clinical effects in postmenopausal women.

 

 

Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):740-6

Age at Menarche and Menopause and Breast Cancer Risk in the International BRCA1/2 Carrier Cohort Study.

Chang-Claude J, Andrieu N, Rookus M, Brohet R, Antoniou AC, Peock S, Davidson R, Izatt L, Cole T, Nogues C, Luporsi E, Huiart L, Hoogerbrugge N, Van Leeuwen FE, Osorio A, Eyfjord J, Radice P, Goldgar DE, Easton DF.

Division of Cancer Epidemiology, German Cancer Research Center, Im Neuenheimer Feld 280 69120 Heidelberg, Germany. j.chang-claude@dkfz-heidelberg.de.

BACKGROUND: Early menarche and late menopause are important risk factors for breast cancer, but their effects on breast cancer risk in BRCA1 and BRCA2 carriers are unknown. METHODS: We assessed breast cancer risk in a large series of 1,187 BRCA1 and 414 BRCA2 carriers from the International BRCA1/2 Carrier Cohort Study. Rate ratios were estimated using a weighted Cox-regression approach. RESULTS: Breast cancer risk was not significantly related to age at menopause {hazard ratio [HR] for menopause below age 35 years, 0.60 [95% confidence interval (95% CI), 0.25-1.44]; 35 to 40 years, 1.15 [0.65-2.04]; 45 to 54 years, 1.02 [0.65-1.60]; >/=55 years, 1.12 [0.12-5.02], as compared with premenopausal women}. However, there was some suggestion of a reduction in risk after menopause in BRCA2 carriers. There was some evidence of a protective effect of oophorectomy (HR, 0.56; 95% CI, 0.29-1.09) and a significant trend of decreasing risk with increasing time since oophorectomy, but no apparent effect of natural menopause. There was no association between age at menarche and breast cancer risk, nor any apparent association with the estimated total duration of breast mitotic activity. CONCLUSIONS: These results are consistent with other observations suggesting a protective effect of oophorectomy, similar in relative effect to that in the general population. The absence of an effect of age at natural menopause is, however, not consistent with findings in the general population and may reflect the different natural history of the disease in carriers.

 

 

Maturitas 20 April 2007; Volume 56, Issue 4, , Pages 368-374

Relationship between adolescent amenorrhea and climacteric osteoporosis

Tamás Csermely, László Halvax, Miklós Vizer, István Drozgyik, Péter Tamás, Péter Göcze, István Szabó, Sára Jeges and András Szilágyi

Department of Obstetrics and Gynecology, University of Pécs, Faculty of Medicine, H-7624 Pécs, Édesanyák útja 17, Hungary; Department of Biostatistics and Health Informatics of Faculty of Health Sciences, University of Pécs, Hungary.

Objectives: The relationship between climacteric osteoporosis and disturbances in menstrual cycle during adolescence was examined. Methods: Seven hundred and seventy-one questionnaires were shared out among women visiting the outpatient department for climacteric complaints for the first time between 2001 and 2004. Questions revealed the age, age at menarche and menopause, the regularity or irregularity of menstrual cycle during adolescence and adult ages. The bone mineral density was examined using the Dual Energy X-ray Absorptiometry (DEXA) method on the lumbar spine. Results: Six hundred and thirty-five of the 771 questionnaires were suitable for analysis. Osteoporosis was observed in 30.1% of the cases. Age, age at the menarche or at the menopause did not alter in the subgroups with or without osteoporosis. The incidence and severity of osteoporosis were significantly higher in patients reporting secondary amenorrhea during adolescent ages (42.1%; average BMD of the lumbar spine 71.6 ± 3.9), as compared to the patients with normal cycle (30.4%; average BMD of the lumbar spine 84.8 ± 7.8). No correlation between the occurrence of osteoporosis and the frequency of menstrual cycle during adulthood was observed. Conclusions: Secondary amenorrhea during the years of adolescence might play a role in the development of more severe osteoporosis in menopause.

 

 

Maturitas  Volume 56, Issue 4, 20 April 2007, Pages 436-446

Use of hormone replacement therapy (HRT) among women aged 45–64 years in the German EPIC-cohorts

Gabriele Nagel, Petra H Lahmann, Mandy Schulz, Heiner Boeing and Jakob Linseisen.

Division of Clinical Epidemiology, German Cancer Research Centre, Heidelberg, Germany. Department of Epidemiology, University Ulm, Ulm, Germany. German Institute of Human Nutrition, Potsdam-Rehbücke, Nuthetal, Germany
Objective: To describe the prevalence and to assess type and indicators of hormone replacement therapy (HRT) use in the two German EPIC-cohorts. Methods: Approximately 30,000 women predominantly aged 35–65 years were recruited in EPIC-Heidelberg and EPIC-Potsdam between 1994 and 1998. Information on diet and lifestyle, medical history and use of hormone therapy was collected at recruitment. Prevalence and type of HRT-regime was described and logistic regression models used to examine correlates of HRT-use. Results: Among women aged 45–64 years, 37.9% in
Heidelberg and 35.8% in Potsdam were current HRT users. Among current users without bilateral oophorectomy, 40.5% in Heidelberg and 23.7% in Potsdam used HRT for at least 5 years. Most women in Heidelberg were taking cyclic combined or estrogen monotherapy, whereas in Potsdam both continuous combined and cyclic combined therapies were most frequently used. In both centres, older age, ever use of oral contraceptives, and alcohol consumption were indicators for both current and ever HRT-use. HRT-use was less frequent in obese women as compared to women with lower BMI. In Potsdam, but not in Heidelberg, higher education and current smoking were associated with HRT-use. Conclusion: In both German EPIC-cohorts, the prevalence of medication with HRT is high compared to other European countries. Types of exogenous hormones used differed by centre. Various reproductive and lifestyle characteristics were identified as correlates of HRT-use.

 

 

Maturitas.2007.02.011. Available online 26 March 2007

Breast cancer: Are oestrogen metabolites carcinogenic?

Alfred O. Mueck, and Harald Seeger

University Women's Hospital of Tuebingen, Tuebingen, Germany

The World Health Organization (WHO) classified oestrogens as carcinogenic in humans. One of the main arguments has been that oestrogens not only can promote cancers but also may initiate mutations caused by certain oestrogen metabolites. Indeed there is evidence that they can have biological properties even at very low concentrations which can exceed manifold those of their parent substance. Highly sophisticated laboratory methods will allow us to understand oestrogenic effects as a net effect of the corresponding metabolite pattern. Current research focuses on the possible carcinogenic properties of 4-hydroxyoestrogens and 16-alpha-hydroxyoestrone, but also on the anticancerogenic effects particularly of 2-methoxyoestradiol. Thus, potential toxic secondary metabolites like 4-quinones can be eliminated, e.g. by methylation. 2-methoxyoestradiol is a potent antiproliferative and antiangiogenic metabolite, and is currently tested in patients with refractory metastatic breast cancer. Observational trials have demonstrated that the ratio of 2- to 16-alpha-hydroxyoestrone is decreased in women with breast cancer. We have been able to demonstrate that oestradiol metabolism during HRT can be influenced by administration route, possibly also by certain progestogens. In in vitro and animal experiments certain oestrogen metabolites indeed can act as carcinogens. However, since for the formation of these metabolites the appearance of very special conditions is a prerequisite and also various protective mechanisms are present, this might only contribute to breast carcinogenesis in very rare cases. However, the clinical relevance remains unclear and it appears to be important to ascertain this issue.

 

 

Maturitas. Article in Press. Available online 21 March 2007.

WHI risks: Any relevance to menopause management?

Henry G. Burger

Prince Henry's Institute & Jean Hailes Foundation For Women's Health, Clayton, Victoria, Australia

Two randomised controlled trials of hormone therapy (HT) were conducted within the US Women's Health Initiative. Both were chronic disease prevention trials, undertaken to determine whether HT reduced cardiovascular risk and increased breast cancer risk. Because the majority of subjects in both trials were asymptomatic and many years postmenopausal, and because substantial numbers had received HT prior to recruitment to the trials, care must be taken in drawing conclusions that the observed risks are applicable to women for whom HT is conventionally prescribed. Each of the reported risks must be examined critically to determine its likely applicability to symptomatic women treated for two to three years to relieve symptoms, but sometimes for substantially longer periods. Further, the risks reported in each of the two trials must be considered separately. Concerning cardiovascular disease, many subjects in the trials were at increased baseline risk because of their age, body mass index, smoking status, blood pressure and years since menopause, in contrast to the usual situation for symptomatic perimenopausal women. Therefore the reported overall cardiovascular risks in WHI, in both treatment arms, should be regarded as irrelevant to menopause management. In contrast, breast cancer risk is relevant, providing that proper note is taken of the fact that there was no increased risk after five years of combined hormone therapy in non-prior HT users and there was a tendency to a decreased risk in oestrogen only treated individuals. Other risks are analysed similarly.

 

Semana del 3 al 9 de Abril 2007

Dr. Juan Enrique Blümel

 

JAMA. 2007 Apr 4;297(13):1465-77.

Postmenopausal hormone therapy and risk of cardiovascular disease by age and years since menopause.

Rossouw JE, Prentice RL, Manson JE, Wu L, Barad D, Barnabei VM, Ko M, LaCroix AZ, Margolis KL, Stefanick ML.

Women's Health Initiative Branch, National Heart, Lung, and Blood Institute, Bethesda, Md 20892, USA.

CONTEXT: The timing of initiation of hormone therapy may influence its effect on cardiovascular disease. OBJECTIVE: To explore whether the effects of hormone therapy on risk of cardiovascular disease vary by age or years since menopause began. DESIGN, SETTING, AND PARTICIPANTS: Secondary analysis of the Women's Health Initiative (WHI) randomized controlled trials of hormone therapy in which 10,739 postmenopausal women who had undergone a hysterectomy were randomized to conjugated equine estrogens (CEE) or placebo and 16,608 postmenopausal women who had not had a hysterectomy were randomized to CEE plus medroxyprogesterone acetate (CEE + MPA) or placebo. Women aged 50 to 79 years were recruited to the study from 40 US clinical centers between September 1993 and October 1998. MAIN OUTCOME MEASURES: Statistical test for trend of the effect of hormone therapy on coronary heart disease (CHD) and stroke across categories of age and years since menopause in the combined trials. RESULTS: In the combined trials, there were 396 cases of CHD and 327 cases of stroke in the hormone therapy group vs 379 cases of CHD and 239 cases of stroke in the placebo group. For women with less than 10 years since menopause began, the hazard ratio (HR) for CHD was 0.76 (95% confidence interval [CI], 0.50-1.16); 10 to 19 years, 1.10 (95% CI, 0.84-1.45); and 20 or more years, 1.28 (95% CI, 1.03-1.58) (P for trend = .02). The estimated absolute excess risk for CHD for women within 10 years of menopause was -6 per 10,000 person-years; for women 10 to 19 years since menopause began, 4 per 10,000 person-years; and for women 20 or more years from menopause onset, 17 per 10,000 person-years. For the age group of 50 to 59 years, the HR for CHD was 0.93 (95% CI, 0.65-1.33) and the absolute excess risk was -2 per 10,000 person-years; 60 to 69 years, 0.98 (95% CI, 0.79-1.21) and -1 per 10,000 person-years; and 70 to 79 years, 1.26 (95% CI, 1.00-1.59) and 19 per 10,000 person-years (P for trend = .16). Hormone therapy increased the risk of stroke (HR, 1.32; 95% CI, 1.12-1.56). Risk did not vary significantly by age or time since menopause. There was a nonsignificant tendency for the effects of hormone therapy on total mortality to be more favorable in younger than older women (HR of 0.70 for 50-59 years; 1.05 for 60-69 years, and 1.14 for 70-79 years; P for trend = .06). CONCLUSIONS: Women who initiated hormone therapy closer to menopause tended to have reduced CHD risk compared with the increase in CHD risk among women more distant from menopause, but this trend test did not meet our criterion for statistical significance. A similar nonsignificant trend was observed for total mortality but the risk of stroke was elevated regardless of years since menopause. These data should be considered in regard to the short-term treatment of menopausal symptoms.

 

MedGenMed. 2006;8(3):40.

Should symptomatic menopausal women be offered hormone therapy?

Lobo RA, Belisle S, Creasman WT, Frankel NR, Goodman NF, Hall JE, Ivey SL, Kingsberg S, Langer R, Lehman R, McArthur DB, Montgomery-Rice V, Notelovitz M, Packin GS, Rebar RW, Rousseau M, Schenken RS, Schneider DL, Sherif K, Wysocki S.

Columbia University, Columbia University Medical Center, New York, NY, USA.

Many physicians remain uncertain about prescribing hormone therapy for symptomatic women at the onset of menopause. The American Society for Reproductive Medicine (ASRM) convened a multidisciplinary group of healthcare providers to discuss the efficacy and risks of hormone therapy for symptomatic women, and to determine whether it would be appropriate to treat women at the onset of menopause who were complaining of menopausal symptoms. MAJOR FINDINGS: Numerous controlled clinical trials consistently demonstrate that hormone therapy, administered via oral, transdermal, or vaginal routes, is the most effective treatment for vasomotor symptoms. Topical vaginal formulations of hormone therapy should be preferred when prescribing solely for the treatment of symptoms of vulvar and vaginal atrophy. Data from the Women's Health Initiative indicate that the overall attributable risk of invasive breast cancer in women receiving estrogen plus progestin was 8 more cases per 10,000 women-years. No increased risk for invasive breast cancer was detected for women who never used hormone therapy in the past or for those receiving estrogen only. Hormone therapy is not effective for the treatment of cardiovascular disease and that the risk of cardiovascular disease with hormone therapy is principally in older women who are considerably postmenopause. CONCLUSIONS: Healthy symptomatic women should be offered the option of hormone therapy for menopausal symptoms. Symptom relief with hormone therapy for many younger women (at the onset of menopause) with menopausal symptoms outweighs the risks and may provide an overall improvement in quality of life. Hormone therapy should be individualized for symptomatic women. This involves tailoring the regimen and dose to individual needs.

 

FASEB J. 2007 Apr 5; [Epub ahead of print]

Disruption of androgen receptor signaling by synthetic progestins may increase risk of developing breast cancer.

Birrell SN, Butler LM, Harris JM, Buchanan G, Tilley WD.

*Dame Roma Mitchell Cancer Research Laboratories, The University of Adelaide, Hanson Institute, Adelaide, South Australia, Australia; andSchool of Life Science, Queensland University of Technology, Brisbane, Queensland, Australia.

There is now considerable evidence that using a combination of synthetic progestins and estrogens in hormone replacement therapy (HRT) increases the risk of breast cancer compared with estrogen alone. Furthermore, the World Health Organization has recently cited combination contraceptives, which contain synthetic progestins, as potentially carcinogenic to humans, particularly for increased breast cancer risk. Given the above observations and the current trend toward progestin-only contraception, it is important that we have a comprehensive understanding of how progestins act in the millions of women worldwide who regularly take these medications. While synthetic progestins, such as medroxyprogesterone acetate (MPA), which are currently used in both HRT and oral contraceptives were designed to act exclusively through the progesterone receptor, it is clear from both clinical and experimental settings that their effects may be mediated, in part, by binding to the androgen receptor (AR). Disruption of androgen action by synthetic progestins may have serious deleterious side effects in the breast, where the balance between estrogen signaling and androgen signaling plays a critical role in breast homeostasis. Here, we review the role of androgen signaling in the normal breast and in breast cancer and present new data demonstrating that androgen receptor function can be perturbed by low doses of MPA, similar to doses achieved in serum of women taking HRT. We propose that the observed excess of breast malignancies associated with combined HRT may be explained, in part, by synthetic progestins such as MPA acting as endocrine disruptors to negate the protective effects of androgen signaling in the breast. Understanding the role of androgen signaling in the breast and how this is modulated by synthetic progestins is necessary to determine how combined HRT alters breast cancer risk, and to inform the development of optimal preventive and treatment strategies for this disease.

 

Bone. 2007 Mar 1; [Epub ahead of print]

Effects of statins on bone mineral density: A meta-analysis of clinical studies.

Uzzan B, Cohen R, Nicolas P, Cucherat M, Perret GY.

AP-HP, Laboratoire de Pharmacologie, Hopital Avicenne, 125 route de Stalingrad, 93009-Bobigny, France et Universite Paris-XIII, France.

CONTEXT: Statins inhibit HMG-CoA reductase, preventing synthesis of mevalonate but also of isoprenoids, which affect osteoclast activity. Amino-bisphosphonates share this effect. In vitro and in vivo, statins show convincing anabolic and anti-resorptive bone effects. However, in a clinical meta-analysis (MA), they did not prevent hip fractures. OBJECTIVE AND DESIGN: Our meta-analysis studied the impact of statins on bone mineral density (BMD) at various sites and compared the effects of lipophilic and more hydrophilic statins. DATA SOURCES: Our PubMed and Embase queries using two keywords (statins, BMD) were updated to October 2006. DATA COLLECTION: Two readers independently collected BMDs from studies. DATA SYNTHESIS: Twenty-one studies, mostly observational (three randomized controlled trials and one pseudo-randomized study), were assessed. Two studies were excluded (no control groups). Three studies could not be analyzed. The sixteen studies analyzed mainly included postmenopausal osteopenic women (2971 patients under statins). Statins significantly increased BMD at total hip (TH) and femoral neck (FN). Effect sizes (ESs) were modest: 0.21 at TH (95% confidence interval [CI]: 0.16-0.25) and 0.20 at FN (CI: 0.08-0.28). Among women, statins acted similarly (ES: 0.20 for TH and 0.18 for FN; CI: 0.14-0.25 and 0.06-0.31 respectively); lipophilic statins (simvastatin, lovastatin) almost entirely caused this effect, at both TH (ES: 0.20; CI: 0.15-0.26) and FN (ES: 0.22; CI: 0.06-0.37). CONCLUSION: Our findings of modest but statistically significant beneficial effects of statins on hip BMD should promote large double-blind randomized controlled trials on their bone effects, in view of their major beneficial cardiovascular effects with excellent safety profile.

 

Br J Cancer. 2007 Apr 9;96(7):1139-46.

Meat consumption and risk of breast cancer in the UK Women's Cohort Study.

Taylor EF, Burley VJ, Greenwood DC, Cade JE.

1Nutritional Epidemiology Group, 30-32 Hyde Terrace, University of Leeds, Leeds, LS2 9LN, UK.

We performed a survival analysis to assess the effect of meat consumption and meat type on the risk of breast cancer in the UK Women's Cohort Study. Between 1995 and 1998 a cohort of 35 372 women was recruited, aged between 35 and 69 years with a wide range of dietary intakes, assessed by a 217-item food frequency questionnaire. Hazard ratios (HRs) were estimated using Cox regression adjusted for known confounders. High consumption of total meat compared with none was associated with premenopausal breast cancer, HR= 1.20 (95% CI: 0.86-1.68), and high non-processed meat intake compared with none, HR=1.20 (95% CI: 0.86-1.68). Larger effect sizes were found in postmenopausal women for all meat types, with significant associations with total, processed and red meat consumption. Processed meat showed the strongest HR= 1.64 (95% CI: 1.14-2.37) for high consumption compared with none. Women, both pre- and postmenopausal, who consumed the most meat had the highest risk of breast cancer.

 

Eur J Cancer Prev. 2007 Jun;16(3):232-242.

Hormonal interventions to prevent hormonal cancers: breast and prostate cancers.

Dunn BK, Ford LG.

Basic Prevention Science Research Group National Cancer Institute, Division of Cancer Prevention, Bethesda, Maryland.

In 1998, the concept of breast cancer prevention became a reality with the approval of tamoxifen to reduce the risk of developing breast cancer in women at increased risk for the disease. This approval was based on decades of research on selective estrogen receptor modulators providing an understanding of the role of the estrogen receptor in breast cell growth, and an appreciation of the carcinogenic process. Although results from the Breast Cancer Prevention Trial demonstrated a 49% reduction in breast cancer in women at increased risk, there were associated toxicities related to the estrogenic effects of tamoxifen; that is, deep vein thrombosis, pulmonary embolism, and endometrial cancer. In an effort to improve its benefit-risk profile, tamoxifen is now being compared with raloxifene, a selective estrogen receptor modulator approved for the treatment and prevention of osteoporosis. This equivalency prevention Study of Tamoxifen and Raloxifene completed accrual of 19 747 high-risk postmenopausal women in November 2004. Meanwhile, another class of estrogen-directed drugs, the aromatase inhibitors, have shown efficacy in breast cancer adjuvant trials, spawning a number of prevention trials that have recently been initiated. As with breast cancer the hormonal contribution to prostate carcinogenesis was the basis for the Prostate Cancer Prevention Trial which showed that finasteride, an androgen antagonist, reduces the incidence of prostate cancer compared to placebo.

 

Menopause. 2007 Mar 23; [Epub ahead of print]

Mammographic density in a multiethnic cohort.

Habel LA, Capra AM, Oestreicher N, Greendale GA, Cauley JA, Bromberger J, Crandall CJ, Gold EB, Modugno F, Salane M, Quesenberry C, Sternfeld B.

Division of Research, Kaiser Permanente, Oakland, CA; David Geffen School of Medicine at UCLA, Los Angeles, CA; University of Pittsburgh, Pittsburgh, Pittsburgh, PA; University of California, Davis, CA; and MSW Consulting, Bloomfield Hills, MI.

OBJECTIVES:: To compare mammographic density among premenopausal and early perimenopausal women from four racial/ethnic groups and to examine density and acculturation among Japanese and Chinese women. DESIGN:: The study included 391 white, 60 African American, 171 Japanese, and 179 Chinese participants in the Study of Women's Health Across the Nation, a multisite study of US women transitioning through menopause. Mammograms done when women were premenopausal or early perimenopausal were assessed for area of dense breast tissue and the percent of the breast occupied by dense tissue (percent density). Information on race/ethnicity, acculturation, and other factors was obtained from standardized instruments. Multiple linear regression modeling was used to examine the association between race/ethnicity or acculturation and density measures. RESULTS:: Age-adjusted mean percent density was highest for Chinese (52%) and lowest for African American (34%) women. After additional adjustment for body mass index, menopause status, age at first birth, breast-feeding duration, waist circumference, and smoking, African Americans had the highest mean percent density (51%) and Japanese women had the lowest (39%). In contrast, the area of dense tissue was highest for African Americans and similar for white, Japanese, and Chinese women. Less acculturated Chinese and Japanese women tended to have a larger area of density and a higher percent density. CONCLUSIONS:: Neither the age-adjusted nor fully adjusted results for percent density or area of dense tissue reflected current differences in breast cancer incidence rates among similarly aged African American, Japanese, Chinese, and white women. In addition, mammographic density was higher in less acculturated Asian women.

 

Clin Orthop Relat Res. 2007 Mar 29; [Epub ahead of print]

Prior Fractures Are Common in Patients With Subsequent Hip Fractures.

Edwards BJ, Bunta AD, Simonelli C, Bolander M, Fitzpatrick LA.

Northwestern University, Chicago, IL; daggerHealthEast System, St. Paul, MN.

Treating osteoporosisin patients with prior fractures potentially results in a 50% reduction of risk of future fractures. We retrospectively reviewed 632 patients with incident hip fractures to evaluate (1) the prevalence of prior fractures in incident hip fractures, (2) whether prior fractures led to an increase in the treatment of osteoporosis, and (3) the cost utility of osteoporosis treatment after a prior fracture. The patients were treated at three hospitals from January 2000 to June 2001 and 514 (80%) were women. A minimal trauma fracture was defined as a fracture resulting from a fall while standing or walking or falling from a height less than 4 feet. Two hundred eighty-two patients (45%) with incident hip fractures described a prior minimal trauma fracture. Osteoporosis was diagnosed in 43 (13%) women and three (5%) men. In 107 cases (17%), the incident hip fracture was the second hip fracture. A prior minimal trauma fracture did not increase treatment for osteoporosis. Presuming a 50% reduction in fracture risk with medications, treating the 282 patients with prior minimal trauma fracture would have resulted in a savings of $3.5 million.Level of Evidence: Level III, therapeutic Study. See the Guidelines for Authors for a complete description of levels of evidence.

 

Med Sci Sports Exerc. 2007 Apr;39(4):587-92.

Exercise training-induced changes in coagulation factors in older adults.

Lockard MM, Gopinathannair R, Paton CM, Phares DA, Hagberg JM.

Department of Kinesiology, University of Maryland, College Park, MD.

The coagulation cascade plays a critical role in the development of cardiovascular disease (CVD). Elevated plasma prothrombin fragment 1 + 2 (F1 + 2) and factor VIII antigen (FVIII:Ag) levels have been associated with a hypercoagulable state, enhancing the risk for vascular thrombotic events. Aerobic training is known to reduce CVD risk, and an improved coagulation profile may contribute to this reduction. PURPOSE:: To analyze the effect of 6 months of standardized aerobic exercise training on resting F1 + 2 and FVIII:Ag levels in men and postmenopausal women aged 50-75 while accounting for several possibly confounding factors. MATERIALS AND METHODS:: Sedentary men (N = 16) and women (N = 31) underwent supervised aerobic training 3 d.wk for 6 months while maintaining the American Heart Association step 1 diet. Baseline and final testing included measurement of F1 + 2, FVIII:Ag, plasma lipoprotein-lipid levels, body composition, and V O2max. RESULTS:: When adjusted for baseline values and changes in diastolic blood pressure with training, F1 + 2 was found to decrease significantly with exercise training from 1.493 +/- 0.058 to 1.422 +/- 0.059 nM (P = 0.014). FVIII:Ag levels were found to increase significantly with training when adjusted for baseline values, from 152.5 +/- 6.7% of standard at baseline to 156.0 +/- 6.1% of standard at final testing (P = 0.005). Training-induced changes in coagulation markers were independent of changes in blood lipids, aerobic capacity, and body composition. CONCLUSIONS:: These results indicate that endurance training has a significant impact on the coagulation cascade, reducing coagulation activity in the common pathway and thrombin formation at rest while increasing the activation potential of the intrinsic pathway.

 

Menopause. 2007 Mar 19; [Epub ahead of print]

Development and preliminary validation of the Menopause Symptoms Treatment Satisfaction Questionnaire (MS-TSQ).

Hill CD, Fehnel SE, Bobula JD, Yu H, McLeod LD.

RTI Health Solutions Park, NC; and 2Wyeth Research, Research Triangle Collegeville, PA.

OBJECTIVE:: The Menopause Symptoms Treatment Satisfaction Questionnaire, an eight-item questionnaire with a 4-week recall period, was developed to assess women's satisfaction with treatment for symptoms associated with menopause. We describe the development and initial testing of the scale. DESIGN:: Following standard instrument-development procedures, focus groups were conducted with menopausal women experiencing hot flushes to generate potential constructs. Multiple items were drafted to address each construct. An iterative process of cognitive testing, item revision, and item reduction was followed to identify the most appropriate items and optimal response scales. The psychometric validation of the questionnaire used data collected through a multicenter, randomized, double-blind, placebo-controlled study including 543 postmenopausal women. Psychometric analyses were conducted to explore potential item reduction and to address questionnaire scaling and scoring. Internal consistency reliability, construct validity, and discriminant validity of the new scale were also examined. RESULTS:: The questionnaire includes items addressing the control of daytime and nighttime hot flushes; effects of treatment on sleep, mood, libido, and cognition; medication tolerability; and overall satisfaction. Correlation analyses indicated that the items are related to each other without being overly redundant and that the item set is best described using a one-factor model. The subsequent scale score demonstrated sound internal consistency reliability, strong construct validity, and good discriminant validity. CONCLUSIONS:: The results of the development and initial validation are favorable. It is expected that the questionnaire will prove to be a worthwhile tool for assessing women's satisfaction with treatment for menopausal symptoms.

 

Obstet Gynecol. 2007 Apr;109(4):823-30.

Ineffectiveness of sertraline for treatment of menopausal hot flushes: a randomized controlled trial.

Grady D, Cohen B, Tice J, Kristof M, Olyaie A, Sawaya GF.

University of California, San Francisco; and San Francisco VA Medical Center, San Francisco, California.

OBJECTIVE: To estimate the effect of the selective serotonin reuptake inhibitor sertraline on hot flush frequency and severity in perimenopausal and postmenopausal women. METHODS: We performed a randomized, blinded, placebo-controlled trial in women aged 40 to 60 years with 14 or more hot flushes per week (N=99). Women were randomly assigned initially to daily oral sertraline (50 mg) or identical placebo for 2 weeks. If no substantial side effects were noted, the dose was increased to two tablets daily (100 mg sertraline or placebo) and continued for an additional 4 weeks. Hot flush frequency and severity were recorded on a daily diary. Hot flush score was calculated as frequency multiplied by severity. Participants also completed questionnaires addressing quality of life, menopausal symptoms, sleep quality, sexual function, mood, and side effects. RESULTS: After 6 weeks of treatment, hot flush frequency decreased similarly in both the placebo (38%) and sertraline (39%) groups (P=.94). Mean hot flush scores also decreased similarly in both groups (41% and 42%, respectively, P=.86). Compared with placebo, women in the sertraline group were more likely to report gastrointestinal complaints, dry mouth, and dizziness. Treatment with sertraline also resulted in greater worsening of scores on the Medical Outcomes Study (MOS) Short Form 36 standardized physical component and the global Female Sexual Function Index. Results were similar in women at least 80% adherent to study medication. CONCLUSION: Treatment with sertraline did not improve hot flush frequency or severity in generally healthy perimenopausal and postmenopausal women, but was associated with bothersome side effects.

 

JAMA. 2007 Feb 28;297(8):842-57.

Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis.

Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C.

The Cochrane Hepato-Biliary Group, Copenhagen Trial Unit, Center for Clinical Intervention Research, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. goranb@junis.ni.ac.yu

CONTEXT: Antioxidant supplements are used for prevention of several diseases. OBJECTIVE: To assess the effect of antioxidant supplements on mortality in randomized primary and secondary prevention trials. DATA SOURCES AND TRIAL SELECTION: We searched electronic databases and bibliographies published by October 2005. All randomized trials involving adults comparing beta carotene, vitamin A, vitamin C (ascorbic acid), vitamin E, and selenium either singly or combined vs placebo or vs no intervention were included in our analysis. Randomization, blinding, and follow-up were considered markers of bias in the included trials. The effect of antioxidant supplements on all-cause mortality was analyzed with random-effects meta-analyses and reported as relative risk (RR) with 95% confidence intervals (CIs). Meta-regression was used to assess the effect of covariates across the trials. DATA EXTRACTION: We included 68 randomized trials with 232 606 participants (385 publications). DATA SYNTHESIS: When all low- and high-bias risk trials of antioxidant supplements were pooled together there was no significant effect on mortality (RR, 1.02; 95% CI, 0.98-1.06). Multivariate meta-regression analyses showed that low-bias risk trials (RR, 1.16; 95% CI, 1.05-1.29) and selenium (RR, 0.998; 95% CI, 0.997-0.9995) were significantly associated with mortality. In 47 low-bias trials with 180 938 participants, the antioxidant supplements significantly increased mortality (RR, 1.05; 95% CI, 1.02-1.08). In low-bias risk trials, after exclusion of selenium trials, beta carotene (RR, 1.07; 95% CI, 1.02-1.11), vitamin A (RR, 1.16; 95% CI, 1.10-1.24), and vitamin E (RR, 1.04; 95% CI, 1.01-1.07), singly or combined, significantly increased mortality. Vitamin C and selenium had no significant effect on mortality. CONCLUSIONS: Treatment with beta carotene, vitamin A, and vitamin E may increase mortality. The potential roles of vitamin C and selenium on mortality need further study.