Selección de Resúmenes de
Menopausia
Abril de 2008
Dr. Juan Enrique
Blümel, Universidad de Chile
Semana del
26 al 1 de Abril de 2008
Maturitas. 2008 Mar 26 [Epub ahead of print]
Obesity, estrone,
and coronary artery disease in postmenopausal women.
Silva TC, Barrett-Connor
E, Ramires JA, Mansur AP.
Heart Institute (InCor), University of
OBJECTIVES: The link between
obesity and endogenous estrogen with coronary artery disease (CAD) in
postmenopausal women is uncertain. In this prospective study we analyzed the
association of body mass index (BMI) and blood levels of estrone
in postmenopausal women with known CAD or with a high risk factor score for
CAD. METHODS: Participants were 251 female clinic patients aged 50-90 years who
were postmenopausal and not using estrogen therapy. Clinical and behavioral
characteristics and fasting blood for estrone and
heart disease risk factors were collected at baseline, and again at 1 and 2
years. Women were grouped according to their BMI (kg/m(2))
as normal (18.5</=BMI<25), overweight (25</=BMI<30) or obese (BMI
>/=30), and by low and high estrone levels (<15
and >/=15pg/mL, respectively). Fatal and nonfatal events were recorded for 2
years after baseline. RESULTS: Women with a low estrone
level were older, thinner, and had less hypertension, diabetes, and lower
triglyceride and glucose levels. BMI was positively associated with estrone levels, hypertension, and diabetes and inversely
associated with HDL cholesterol. There were 14 deaths, 8 attributed to CAD. The
Kaplan-Meier survival curve showed a nonsignificant
trend (p=0.074) of greater all cause mortality in women with low estrone levels (<15mL). In this model, adjusted for BMI,
age [OR=1.08; p=0.03], C-reactive protein [OR=1.24; p=0.024] and hypertension
[OR=6.22; p=0.003] were independent predictors of all cause mortality.
CONCLUSIONS: Postmenopausal women with low estrone
levels (<15pg/mL) had a trend for increased
mortality over the next 2 years. Larger, longer studies are needed.
Lancet Oncol. 2008 Apr;9(4):385-91.
Oestrogen and the colon: potential mechanisms for
cancer prevention.
Kennelly R, Kavanagh DO, Hogan AM, Winter DC.
Department of
Surgery, St Vincent's University Hospital, Dublin, Ireland.
The role of oestrogen in oncogenesis has been
examined extensively, especially in the context of breast cancer, and receptor
modulators are an integral part of targeted treatment in this disease. The role
of oestrogen signalling in
colonic carcinoma is poorly understood. Men are more susceptible than women to
colon cancer. Furthermore, hormone-replacement therapy affords an additive
protective effect for postmenopausal women, and when these women do develop
cancer, they typically have less aggressive disease. The discovery of a second oestrogen receptor (ERbeta) and
its over expression in healthy human colon coupled with reduced expression in
colon cancer suggests that this receptor might be involved. The underlying
mechanism, however, remains largely unknown. In this Review, we discuss the
various hypotheses presented in the published literature. We examine the
cellular and molecular mechanisms through which oestrogen
is purported to exert its protective influence, and we review the evidence
available to support these claims.
Osteoporos Int. 2008 Mar 29 [Epub ahead of print]
Bone mineral density at menopause does not predict breast cancer
incidence.
Trémollieres FA, Pouillès JM, Laparra J, Ribot C.
Unité Ménopause et Maladies Osseuses
et Métaboliques, Hôpital Paule de Viguier, Toulous,e France.
INTRODUCTION: This study aimed
to investigate the relationship between BMD and the risk of breast cancer (BC)
in young postmenopausal women. METHODS: As part of a clinical research program,
2,137 women who were perimenopausal or within their 5
first postmenopausal years were scanned between 1988-1990
and reviewed on average 13.1 years after their initial examination.
Ninety-eight incident BC cases were recorded throughout the follow-up. RESULTS:
Women with incident BC significantly differed from those who had never had BC
with regard to age at menarche, age of birth of 1st child, familial history of
BC and postmenopausal hormone therapy (PHT) use. There was no significant
difference between the two groups for baseline DXA of the spine. There was a
trend for BC cases for having lower femoral neck BMD compared to women without
BC. However, women with low BMD were more likely to have taken PHT by the end
of the study. In Cox multivariate analyses the relationship between BC risk and
femoral neck BMD no longer existed. CONCLUSIONS: There was no relationship
between BMD measured within the first postmenopausal years and the risk of BC,
which makes unlikely the possibility of using BMD as a predictor factor for BC
in early postmenopausal women.
Salud Publica Mex. 2008
Mar-Apr;50(2):126-35.
Physical activity and breast cancer risk in Mexican women.
Ortiz-Rodríguez SP, Torres-Mejía G, Mainero-Ratchelous F, Angeles-Llerenas A, López-Caudana AE, et al.
Centro
de Investigación en Salud Poblacional, Instituto Nacional de Salud
Pública, Cuernavaca, Morelos, México.
Objetive: To evaluate the
effect of moderate physical activity (hours per week and METs hours per week)
on the risk of breast cancer (BC) in Mexican women. Material and methods: This
is the initial stage of a case control multicentric
study based in the Federal District,
Am J Epidemiol. 2008 Mar 27 [Epub ahead of print]
Estrogen Plus Progestin Therapy and Breast
Cancer in Recently Postmenopausal Women.
Prentice
RL, Chlebowski RT, Stefanick ML, Manson JE, Pettinger M, Hendrix SL, Hubbell FA, et al
Division of Public
Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA.
The Women's Health Initiative
trial found a modestly increased risk of invasive breast cancer with daily
0.625-mg conjugated equine estrogens plus 2.5-mg medroxyprogesterone
acetate, with most evidence among women who had previously received postmenopausal
hormone therapy. In comparison, observational studies mostly report a larger
risk increase. To explain these patterns, the authors examined the effects of
this regimen in relation to both prior hormone therapy and time from menopause
to first use of postmenopausal hormone therapy ("gap time") in the
Women's Health Initiative trial and in a corresponding subset of the Women's
Health Initiative observational study. Postmenopausal women with a uterus
enrolled at 40
Metab Syndr Relat Disord. 2006 Spring;4(1):17-27.
The WHO and NCEP/ATPIII Definitions of the Metabolic Syndrome in
Postmenopausal Women: Are They So Different?
Piché ME, Weisnagel SJ, Corneau L, Nadeau A, Bergeron J, Lemieux S.
Institute of Nutraceuticals and Functional Foods, Laval University,
Québec (Québec), Canada., Lipid Research Center, CHUL Research
Center, Québec (Québec), Canada.
Background: The aim of this
study was to examine the metabolic risk profile in postmenopausal women
characterized by either the metabolic syndrome (MS) as defined by the World
Health Organization (WHO) or the National Cholesterol Education Program (NCEP)
Adult Treatment Panel III (ATPIII). Methods: One hundred and eight
postmenopausal women (56.9 +/- 4.2 years; 28.5 +/- 5.9 kg/m(2))
were examined. Each underwent an oral glucose tolerance test, an euglycemic-hyperinsulinemic
clamp, an assessment of body fat distribution by computed tomography, a
complete plasma lipid-lipoprotein profile, and standard measurements of
inflammatory markers. Results: The prevalence of the MS-WHO was 29.6% in our
women. Type 2 diabetes was found in 28.1% of women with the MS-WHO. Thirty-one
percent of women had the MS-ATP, from which 36.4% had type 2
diabetes. Among the 32 women identified as having MS-WHO, 25 (78.1 %)
were also identified as having the MS-ATP. On the other hand, among the 34
women identified as having MS-ATP, 24 (70.0 %) also had MS-WHO (kappa = 0.60).
When we subdivided our sample of women as having either isolated MS-WHO,
isolated MS-ATP, or combined MS-WHO and MS-ATP, we observed a more deteriorated
metabolic risk profile (higher values for visceral adipose tissue, 2-h plasma
glucose, and lower HDL-cholesterol concentrations) in women characterized by
isolated MS-ATP compared to women with isolated MS-WHO. Conclusions: These
results suggest that, in postmenopausal women, the concordance in the
identification of subjects with the MS using each of the proposed definitions
is only moderate.
Aust
N Z J Obstet Gynaecol.
2008 Apr;48(2):207-13.
Prevalence of endometrial cancer and
hyperplasia in non-symptomatic overweight and obese women.
Viola AS, Gouveia D, Andrade L, Aldrighi
JM, Viola CF, Bahamondes
L.
Obstetrics and Gynaecology, Faculty of Medical Sciences, Universidade Estadual de
Campinas, Campinas, Brazil.
Background: Obesity is a
public health problem and it is necessary to identify if non-symptomatic obese
women must be submitted to endometrial evaluation. Aims: To determine the
prevalence of endometrial hyperplasia and cancer in non-symptomatic overweight
or obese women. Methods: A cross-sectional study was carried out in 193 women
submitted to an endometrial biopsy using a Pipelle de
Cornier. The findings were classified as normal, hyperplasia or cancer, and the
results were compared to body mass index (BMI; kg/m(2)).
For the purpose of statistical analysis, women were divided into two groups:
women of reproductive age and postmenopausal women, and according to BMI as
overweight or obese. Results: The prevalence of endometrial cancer and
hyperplasia was 1.0% and 5.8% in women of reproductive age and 3.0% and 12.1%
in postmenopausal women, respectively. According to logistic regression, being
in the postmenopause increased the risk of
endometrial hyperplasia and cancer to 1.19 (95% confidence interval (CI):
0.36-3.90), while being postmenopausal and severely obese increased the odds
ratio (OR) to 1.58 (95%CI: 0.30-8.23) and being postmenopausal and morbidly
obese increased the OR to 2.72 (95%CI: 0.65-11.5). No increase in risk was
found in women of reproductive age who were either overweight or obese.
Discussion: Our results show that non-symptomatic, severe or morbidly obese
postmenopausal women have a high risk of developing endometrial hyperplasia or
cancer; however, no such risk was found for women of reproductive age.
J Natl
Cancer Inst. 2008 Mar 25 [Epub ahead of print]
Increased Risk of Recurrence After Hormone
Replacement Therapy in Breast Cancer Survivors.
Holmberg L, Iversen OE, Rudenstam CM, Hammar M, Kumpulainen E, Jaskiewicz J, Jassem J, et al
Department of
Surgical Sciences, Uppsala University, Uppsala, Sweden.
Background Hormone replacement
therapy (HT) is known to increase the risk of breast cancer in healthy women,
but its effect on breast cancer risk in breast cancer survivors is less clear.
The randomized HABITS study, which compared HT for menopausal symptoms with
best management without hormones among women with previously treated breast
cancer, was stopped early due to suspicions of an increased risk of new breast
cancer events following HT. We present results after extended follow-up.
Methods HABITS was a randomized, non-placebo-controlled noninferiority
trial that aimed to be at a power of 80% to detect a 36% increase in the hazard
ratio (HR) for a new breast cancer event following HT. Cox models were used to
estimate relative risks of a breast cancer event, the maximum likelihood method
was used to calculate 95% confidence intervals (CIs), and chi(2)
tests were used to assess statistical significance, with all P values based on
two-sided tests. The absolute risk of a new breast cancer event was estimated
with the cumulative incidence function. Most patients who received HT were
prescribed continuous combined or sequential estradiol
hemihydrate and norethisterone.
Results Of the 447 women randomly assigned, 442 could
be followed for a median of 4 years. Thirty-nine of the 221 women in the HT arm
and 17 of the 221 women in the control arm experienced a new breast cancer
event (HR = 2.4, 95% CI = 1.3 to 4.2). Cumulative incidences at 5 years were
22.2% in the HT arm and 8.0% in the control arm. By the end of follow-up, six
women in the HT arm had died of breast cancer and six were alive with distant
metastases. In the control arm, five women had died of breast cancer and four
had metastatic breast cancer (P = .51, log-rank test). Conclusion After
extended follow-up, there was a clinically and statistically significant
increased risk of a new breast cancer event in survivors who took HT.
Clin Endocrinol
(Oxf). 2008 Mar 15 [Epub
ahead of print]
The majority of Danish non-toxic goitre
patients are ineligible for Levothyroxine suppressive
therapy.
Fast S, Bonnema SJ, Hegedüs L.
Department of
Endocrinology and Metabolism, Odense University Hospital, Denmark.
Objective: Levothyroxine
suppressive therapy (LT4-therapy), aimed at shrinking thyroid nodules is
controversial. Despite evidence of limited effect and long-term side effects,
questionnaire surveys indicate widespread use. Our aim was to determine, in
consecutive non-toxic goitre patients, the proportion
ineligible for LT4-therapy. Exclusion criteria were set up in agreement with
recent guidelines. Setting: Secondary/tertiary referral centre at University
Clinic. Subjects and methods: During 1997-2001, 822 patients were referred to
our endocrine unit on suspicion of non-toxic goitre.
Patients were evaluated clinically including fine needle aspiration biopsy,
thyroid scintigraphy and ultrasound. Seven-hundred
and forty-five patients (627 women and 118 men; median age 47 years, range
11-90) were potential candidates for LT4-therapy. Based on guidelines we
defined conditions where LT4-therapy is contraindicated. Exclusion criteria
included: 1) Serum TSH <1.0 mIU/l, 2)
Postmenopausal status, or males older than 60 years, 3) Thyroid volume above
100 ml, 4) Intrathoracic goitre,
5) Clinical suspicion of malignancy, 6) Dominant thyroid cyst, 7) Nondiagnostic FNA, 8) Previous ineffective LT4-therapy, 9)
Elevated serum calcitonin, 10) Osteoporosis or
cardiovascular disease. Results: 84% of patients were ineligible for
LT4-therapy. In diffuse goitre (n=35) 63%, in uninodular goitre (n=320) 77% and
in multinodular goitre
(n=390) 91% were ineligible. Main ineligibility reasons were a low serum TSH,
postmenopausal status, a large goitre or clinical
suspicion of malignancy. Conclusion: The vast majority of consecutive Danish
non-toxic goitre patients (84%) were ineligible for
LT4-therapy. Due to low efficacy and potential long-term adverse effects on the
skeleton and cardiovascular system we strongly advocate against LT4-therapy for
non-toxic goitre.
Am J Epidemiol. 2008 Mar 21 [Epub ahead of print]
Predictors of the Timing of Natural
Menopause in the Multiethnic Cohort Study.
Henderson
KD, Bernstein
L, Henderson
B, Kolonel L, Pike MC.
Department of Cancer Etiology,
City of
The timing of natural
menopause has implications for several health endpoints; in particular, it is a
risk factor for breast cancer. The authors investigated factors influencing the
timing of natural menopause among 95,704 women with a mean age of 59.7 years
(10th-90th percentile range, 47.0-71.0) in five racial/ethnic groups in the
Multiethnic Cohort Study, including non-Latina Whites, Japanese Americans,
African Americans, Native Hawai'ians, and Latinas.
The authors investigated whether race/ethnicity and several lifestyle and
reproductive characteristics were associated with the timing of natural
menopause. Race/ethnicity was a significant independent predictor of the timing
of natural menopause. Other factors, including smoking, age at menarche,
parity, and body mass index, did not significantly alter the
race/ethnicity-specific hazard ratios. Relative to non-Latina Whites, natural
menopause occurred earlier among Latinas (US-born Latinas: hazard ratio (HR) =
1.10, 95% confidence interval (CI): 1.07, 1.14; non-US-born Latinas: HR = 1.25,
95% CI: 1.21, 1.30) and later among Japanese Americans (HR = 0.93, 95% CI:
0.90, 0.95). These results support the hypothesis that the timing of natural
menopause is driven by a combination of genetic, reproductive, and lifestyle
factors.
Maturitas. 2008 Mar 20 [Epub ahead of print]
Effects of estradiol
and norethisterone on lipids, insulin resistance and
carotid flow.
Fernandes
CE, Pompei LM, Machado RB, Ferreira
JA, Melo NR, Peixoto S.
ABC School of
Medicine, São Paulo, Brazil.
OBJECTIVES: To evaluate the
lipid profile, insulin resistance and vasomotricity,
and the interaction between these factors, in postmenopausal women receiving
hormone therapy. METHODS: A prospective, randomized, double-blind study was
carried out in which 77 postmenopausal women received one of the three
treatment regimens: (A) 2mg oral micronized estradiol
(E(2)) (n=25); (B) 2mg oral E(2)+1mg oral norethisterone acetate (NETA) (n=28); or C) placebo (n=24),
daily for 6 months. Evaluations were carried out at baseline and at the end of
treatment on lipid and lipoprotein profiles, homeostasis model assessment of
insulin resistance (HOMA-IR) and pulsatility index
(PI) of the internal carotid artery by Doppler ultrasonography.
RESULTS: Mean increases of 15.6% and 2.4% and a reduction of 6.4% in
high-density lipoprotein (HDL) levels were found for the E(2),
E(2)+NETA and placebo groups, respectively. Reductions of 9.5% and 3.7% and an
increase of 12.1% in low-density lipoprotein (LDL), and reductions of 20.0% and
3.8% and an increase of 28.8% in the LDL:HDL ratio were found for the E(2),
E(2)+NETA and placebo groups, respectively (p<
Semana del
19 al 25 de Marzo de 2008
Obesity
(Silver Spring). 2008 Feb 28 [Epub ahead of print
Contribution of the Lean Body Mass to Insulin Resistance in
Postmenopausal Women With Visceral Obesity: A Monet
Study.
Brochu M, Mathieu ME, Karelis AD, Doucet E, Lavoie ME, Garrel D, Rabasa-Lhoret
R.
1Faculty of
Physical Education and Sports, University of Sherbrooke, Sherbrooke, Quebec,
Canada.
Some insulin-resistant obese
postmenopausal (PM) women are characterized by an android body fat distribution
type and higher levels of lean body mass (LBM) compared to insulin-sensitive
obese PM women. This study investigates the independent contribution of LBM to
the detrimental effect of visceral fat (VF) levels on the metabolic profile.
One hundred and three PM women (age: 58.0 +/- 4.9 years) were studied and
categorized in four groups on the basis of their VF (higher vs. lower) and lean
BMI (LBMI = LBM (kg)/height (m (2)); higher vs. lower). Measures included:
fasting lipids, glucose homeostasis (by euglycemic/hyperinsulinemic clamp
technique and 2-h oral glucose tolerance test (OGTT)), C-reactive protein (CRP)
levels, fat distribution (by computed tomography (CT) scan), and body
composition (by dual-energy X-ray absorptiometry). Women in the higher
VF/higher LBMI group had lower glucose disposal and higher plasma insulin
levels compared to the other groups. They also had higher plasma CRP levels
than the women in the lower VF/lower LBMI group. VF was independently
associated with insulin levels, measures of glucose disposal, and CRP levels (P
< 0.05). LBMI was also independently associated with insulin levels, glucose
disposal, and CRP levels (P < 0.05). Finally, significant interactions were
observed between LBMI and VF levels for insulin levels during the OGTT and measures
of glucose disposal (P < 0.05). In conclusion, VF and LBMI are both
independently associated with alterations in glucose homeostasis and CRP
levels. The contribution of VF to insulin resistance seems to be exacerbated by
increased LBM in PM women.
J Womens
Health (Larchmt). 2008 Mar 17 [Epub
ahead of print]
Coronary Heart Disease Risk and Bone
Mineral Density among U.S. Women and Men.
ABSTRACT Aims: Low bone
mineral density (BMD) has been shown to predict cardiovascular disease (CVD)
and coronary heart disease (CHD) mortality in both women and men. The purpose
of the current study was to determine whether a CHD risk assessment tool might
be useful for identifying persons likely to have low BMD in a multiethnic
population of women and men. Methods: Cross-sectional data for 3881 women and
men aged 50-74 years without overt CHD or stroke from the Third National Health
and Nutrition Examination Survey (NHANES III) were used to explore the
relationship between BMD and 10-year CHD risk, as estimated using the
Framingham CHD risk prediction algorithm, in gender-stratified multiple
logistic regression models. Results: When compared with women who had a <10%
CHD risk, women with a 10%-19% CHD risk were 45% more likely and those with a
>/=20% CHD risk were 73% more likely to have low BMD. Similar increases in
low BMD risk were not detected in men. Conclusions: In the
BJOG. 2008 Mar 19 [Epub ahead of print
Differential impact of conventional and
low-dose oral hormone therapy, tibolone and raloxifene on mammographic breast
density, assessed by an automated quantitative method.
Eilertsen AL, Karssemeijer N, Skaane P, Qvigstad E, Sandset PM.
Department of
Haematology and Faculty Division, Ullevål University Hospital Trust,
Oslo, Norway.
Objective To
evaluate impact of different postmenopausal hormone therapy (HT) regimens and
raloxifene on mammographic breast density. Design Open,
randomised, comparative clinical trial. Setting Women were recruited
through local newspapers and posters. They were examined at the Departments of
Haematology, Gynaecology, and Radiology in a
Cancer Epidemiol
Biomarkers Prev. 2008 Mar;17(3):655-60
Postmenopausal Hormone Therapy and Lung
Cancer Risk in the Cancer Prevention Study II Nutrition Cohort.
Rodriguez
C, Spencer Feigelson H, Deka A, Patel AV, Jacobs EJ, Thun MJ, Calle EE.
Epidemiology and Surveillance
Research, American Cancer Society, National Home Office, Northwest,
BACKGROUND: Studies of
postmenopausal hormone therapy and lung cancer incidence have reported
positive, negative, and null associations. Most of these studies, however, have
had limited ability to control rigorously for cigarette smoking or to examine
risk separately by smoking status. METHODS: We examined the association between
postmenopausal hormone therapy and lung cancer incidence by smoking status
among 72,772 women in the Cancer Prevention Study II Nutrition Cohort.
Proportional hazards modeling was used to calculate rate ratios (RR). RESULTS:
During follow-up from 1992 to 2003, we identified 659 cases of incident lung
cancer. Current use of any postmenopausal hormone therapy was significantly
associated with decreased risk of incident lung cancer [multivariate RR, 0.76;
95% confidence interval (95% CI), 0.62-0.92]. Similar risk estimates were
observed for unopposed estrogen use (RR, 0.76; 95% CI, 0.60-0.94) and for
estrogen plus progestin (RR, 0.76; 95% CI, 0.57-1.01). Risk associated with current
use of postmenopausal hormone therapy was decreased among never smokers (RR,
0.56; 95% CI, 0.33-0.95) as well as current smokers (RR, 0.76; 95% CI,
0.55-1.05) and former smokers (RR, 0.76; 95% CI, 0.58-0.99). Former hormone use
was not associated with lung cancer. No trend with duration of hormone use was
detected. CONCLUSION: These results support the hypothesis that postmenopausal
hormone therapy is associated with reduced risk of lung cancer, although the
absence of a dose-response relationship weakens the evidence for causality.
J Clin Endocrinol Metab. 2008 Mar 18 [Epub ahead of print
Randomized Trial of Once-Weekly PTH(1-84) on
Bone Mineral Density and Remodeling.
Black DM, Bouxsein
ML, Palermo L, McGowan JA, Newitt D, Rosen E, Majumdar S, Rosen CJ; for the
PTH Once-Weekly Research (POWR) group.
Context: Daily parathyroid
hormone (PTH) administration increases bone mineral density (BMD) and reduces
fracture risk. However, cost and compliance significantly limit clinical use.
Objective: To determine whether less frequent PTH administration increases
lumbar spine BMD Design: Double-blind, randomized placebo-controlled trial
Participants: 50 postmenopausal women ages 45-70 with femoral neck BMD T-score
between -1.0 and -2.0 Setting: St. Joseph Hospital, Bangor, Maine Intervention:
Subcutaneous injections of daily PTH(1-84) (100 microg) or placebo for one
month, followed by weekly injections (PTH or placebo) for 11 months Outcomes:
Change in lumbar spine DXA areal BMD (aBMD, Primary). Secondary outcomes
included volumetric BMD (vBMD) at spine and hip by QCT, trabecular bone
microarchitecture by MRI of distal radius, and biochemical bone turnover
markers. Results: At 12 months, lumbar spine aBMD increased 2.1% in PTH-treated
women compared to placebo (p=0.03). Vertebral trabecular vBMD increased 3.8% in
PTH-treated women compared to placebo group (p=0.08). PTH-treated women also
had higher distal radial trabecular bone volume, number, and thickness compared
to placebo-treated women (p<0.04). After one month of daily PTH, PINP was
markedly increased compared to placebo (p<0.0001) and a difference
persisted, although lessened, throughout the study. Bone resorption indices
were unchanged in PTH-treated women and were reduced in placebo group.
Conclusion: Once-weekly PTH after one month of daily treatment increases spine
BMD, radial trabecular bone and bone formation markers in postmenopausal women.
These results suggest that less frequent alternatives to daily PTH dosing for
two years could be effective. Further studies are required to define the
optimal frequency of PTH administration.
Appl Physiol Nutr Metab. 2008 Apr;33(2):309-14.
Relationship between the metabolic syndrome and physical activity energy
expenditure: a MONET study.
Karelis AD, Lavoie ME, Messier V, Mignault D, Garrel D, Prud'homme D, Rabasa-Lhoret R.
The purpose of this
cross-sectional study was to examine the association between the metabolic
syndrome (MetS) and physical activity energy expenditure (PAEE) in overweight
and obese sedentary postmenopausal women. The study population consisted of 137
overweight and obese sedentary postmenopausal women (age, 57.7 +/- 4.8 years;
BMI, 32.4 +/-
Menopause. 2008 Mar 14 [Epub ahead of print]
Associations of circulating adiponectin with estradiol and monocyte chemotactic protein-
Miyatani Y, Yasui T, Uemura H, Yamada M, Matsuzaki T, Kuwahara A, Tsuchiya N, Yuzurihara M, Kase Y, Irahara M.
Departments of
Obstetrics and Gynecology, Tsumura Central Research
Institute, Ibaraki-ken, Japan.
OBJECTIVE::
The aim of the present study was to clarify the association of serum adiponectin concentrations with serum 17beta-estradiol
concentrations in pre-, peri-, and postmenopausal
women. In addition, the associations of serum adiponectin
with serum concentrations of proinflammatory and
anti-inflammatory cytokines were examined in women during the menopausal
transition. DESIGN:: A total of 197 women were
enrolled in this study: 33 premenopausal women, 80 perimenopausal
women, and 84 postmenopausal women. Serum adiponectin
concentration was measured by an enzyme-linked immunosorbent
assay. Serum concentrations of the proinflammatory
cytokines interleukin (IL)-1beta, IL-6, and tumor
necrosis factor alpha, anti-inflammatory cytokine IL-10, and the chemokines IL-8, macrophage inflammatory protein-1beta and monocyte chemotactic protein-1
were measured by using a multiplexed human cytokine assay. RESULTS:: Serum adiponectin concentration
showed a significant negative correlation with serum estradiol
concentration (r = -0.400, P = 0.001) in postmenopausal women but not in pre-
and perimenopausal women, and this correlation was
significant after adjustment for age and body mass index. Serum adiponectin concentration also showed a significant
negative correlation with serum monocyte chemotactic protein-1 concentration (r = -0.244, P= 0.05)
in postmenopausal women. CONCLUSION:: An increase in adiponectin level due to a decrease in estradiol
results in a reduction in monocyte chemotactic protein-1 level in postmenopausal women,
suggesting that adiponectin may be associated with a
protective role against insulin resistance and atherosclerosis, which occur in
the postmenopausal stage.
Semana del
5 al 11 de Marzo de 2008
Acta Cytol. 2008 Jan-Feb;52(1):8-13.Links
Osteopenia and osteoporosis can be Predicted
from Pap test.
Repse-Fokter
A, Fokter SK.
Department of Pathomorphology and Cytology, Celje General Hospital, Celje,
Slovenia. alenka.repse-
OBJECTIVE:
To determine sensitivity and specificity of Pap tests for osteopenia
and osteoporosis using bone
mineral
density (BMD) with dual x-ray absorptiometry (DXA) as
the reference standard. STUDY DESIGN: DXA measurement was performed on 136
routine Pap smears. Results of DXA measurement were expressed in T-scores,
indicating degree of deviation compared to a young adult population of same age
and gender. Smears were grouped into atrophic and mature cell patterns. Using a
stereologic analysis, mean areas of squamous cells, their nuclei and their cytoplasm were
estimated. RESULTS: There was significant positive correlation between cell
area and T-score (p < 0.001), as well as between cytoplasm area and T-score
(p < 0.001). There was no significant relationship between nucleus area and
T-score (p > 0.05). Mean T-scores of patients with atrophic cells were
significantly lower than mean T-scores of patients with mature cell patterns (p
< 0.001). The group including patients with atrophic or mature cells had a sensitivity
of 61.4% and specificity of 86.4%, with positive predictive value of 95.9% in
detecting patients with osteopenia or osteoporosis.
CONCLUSION: Women with atrophic smear pattern are susceptible to osteopenia or osteoporosis; many cases could be detected
with routine Pap test without additional costs.
Neurodegener Dis. 2008;5(3-4):257-60. Epub
2008 Mar 6.
The
long-term effects of oophorectomy on cognitive and
motor aging are age dependent.
Rocca WA,
Grossardt BR, Maraganore DM.
Division of Epidemiology, Mayo Clinic College of Medicine, Rochester,
Minn., USA.
Background:
The evidence for a neuroprotective effect of estrogen
in women remains controversial. Objective: We studied the long-term risk of parkinsonism and of cognitive impairment or dementia in
women who underwent oophorectomy before menopause.
Methods: We conducted a historical cohort study among all women residing in
Women
were followed for a median of 25-30 years. Parkinsonism was assessed using
screening and examination, through a medical records- linkage system, and
through death certificates. Cognitive status was assessed using a structured
questionnaire via a direct or proxy telephone interview. Results: The risk of parkinsonism and of cognitive impairment or dementia
increased following oophorectomy. In particular, we
observed significant linear trends of increasing risk for either outcome with
younger age at oophorectomy. Conclusion: Our
findings, combined with previous laboratory and epidemiologic findings, suggest
that estrogen may have an age-dependent neuroprotective
effect.
Int J
Fertil Womens Med. 2007 Mar-Jun;52(2-3):93-6.
Climacteric
symptom control after the addition of low-dose esterified
conjugated estrogens to raloxifene standard doses.
Carranza-Lira
S, Gooch AL, Saldivar N, Osterwalder MS.
Gynecologic Endocrinology Department
Hospital de Ginecología y Obstetricia Luis Castelazo
Ayala, DF México.
INTRODUCTION:
Hormone therapy (HT) is one the best options for climacteric symptom control;
however when women are switched to raloxifene, after
several years of HT, they restart with symptoms. OBJECTIVE: To evaluate the
effect of the addition of low-dose esterified
conjugated estrogens to the conventional dose of raloxifene
in the control of climacteric symptoms. MATERIALS AND METHODS: 14 healthy
postmenopausal patients were studied.
Climacteric
symptoms were evaluated at baseline and 3 months after the beginning of
treatment by the Kupperman's index (KI) and by the
sum of the symptom evaluations carried out with an analog visual scale called
SUMEVA. In all the anthropometric variables were documented, as well as time
since menopause and endometrial thickness. At random they were distributed in
some of the following groups: I) Raloxifene 60 mg/day
(n=7) and II) Raloxifene 60 mg/day plus esterified conjugated estrogens 0.312 mg/day (n=7). STATISTICAL
ANALYSIS: Differences among the groups, as well as those among baseline and
those at the end of treatment, were determined by student's t test for
independent samples and paired samples respectively. RESULTS: There were no
differences in anthropometric variables, nor in the
time since menopause. After three months of treatment the libido alterations
vertigo and vaginal dryness were significantly greater in group I. In group II
a significant decrease in hot flushes, insomnia, nervousness, vaginal dryness,
KI, and SUMEVA were found, as was a significant increase in endometrial
thickness. CONCLUSION: The treatment that is proposed in this study can
constitute a temporary alternative during the period
of
transition from HT to raloxifene.
Steroids. 2008 Jan 18 [Epub ahead of print]
Vascular cell signaling by membrane estrogen receptors.
Kim
KH, Moriarty K, Bender JR.
Division
of Cardiovascular Medicine and Departments of Internal Medicine and Immunobiology, the Raymond and Beverly Sackler
Foundation Cardiovascular Laboratory, Yale University School of Medicine, New
Haven, USA.
The
definition of estrogen's actions has expanded from transcriptional regulation
to the rapid, membrane-initiated activation of numerous signal transduction
cascades. Multiple biological effects of estrogen have been shown in numerous
animals, cellular and molecular studies, which support the favorable effects of
estrogen on vascular structure, function, and cell signaling. Work from several
laboratories has shown that these effects are mediated by distinct forms of
estrogen receptor (ER) alpha. This includes estrogen-stimulated rapid
activation of endothelial nitric oxide synthase (eNOS), resulting in the elaboration of the athero-protective, angiogenesis-promoting product nitric
oxide (NO). We have described the expression of ER46, an N-terminus truncated isoform of the ERalpha, in human
endothelial cells (EC), and its critical role in membrane-initiated, rapid
responses to 17beta-estradiol (E2). We have
proposed an
ER46-centered, eNOS activating molecular complex in
human EC caveolar membranes, containing c-Src, phosphatidylinositol
3-kinase (PI3K), Akt and eNOS.
Our previous studies support estrogen-induced rapid eNOS
activation via a sequential c-Src/PI3K/Akt cascade in EC. In this review, we
describe estrogen-induced, rapid, non-genomic actions in endothelium, driven by
c-Src-ER46-caveolin-1 interactions, with consequent activation of eNOS. Amidst ongoing controversies in hormone replacement
therapy, these molecular and cellular data, defining favorable estrogenic
effects on the endothelium, provide a strong impetus to resolve these clinical
questions.
Fertil Steril. 2008 Mar 4 [Epub ahead of print]
Effect of ovarian hormones on serum adiponectin and
resistin concentrations.
Chalvatzas N, Dafopoulos K, Kosmas
G, Kallitsaris A, Pournaras
S, Messinis IE.
Departments of Obstetrics and Gynecology, University of Thessalia, Larissa,
Greece.
OBJECTIVE:
To investigate the effect of ovarian hormones on adiponectin and resistin
levels in women. DESIGN:
Experimental study. SETTING: University hospital. PATIENT(S): Thirteen normally cycling women
(
J Clin Oncol. 2008 Mar 10;26(8):1260-8.
Use of different postmenopausal hormone therapies and
risk of histology- and hormone receptor-defined invasive breast cancer.
Fournier
A, Fabre A, Mesrine S, Boutron-Ruault MC, Berrino F, Clavel-Chapelon F.
Institut
National de
PURPOSE:
We previously found that the risk of invasive breast cancer varied according to
the progestagen
component of
combined postmenopausal hormone therapy (CHT): progesterone, dydrogesterone, or
other
progestagens. We conducted the present study to assess how these CHTs were associated
with histology- and
hormone
receptor-defined breast cancer. PATIENTS AND METHODS: We used data from the
French E3N cohort study, with 80,391 postmenopausal women followed for a mean
duration of 8.1 years; 2,265 histologically confirmed invasive breast cancers
were identified through biennial self-administered questionnaires completed from
1990 to2002. The relative risks (RRs) were estimated using Cox proportional
hazards models. RESULTS: Compared withpostmenopausal hormone therapy (HT)
never-use, ever-use of estrogen+progesterone was not significantlyassociated
with the risk of any breast cancer subtype, but increasing duration of
estrogen+progesterone wasassociated with increasing risks of lobular (P = .06)
and estrogen receptor-positive/progesterone receptor-negative(ER+/PR-; P =
.02). Estrogen+dydrogesterone was associated with a
significant increase in risk of lobular carcinoma(RR,
1.7; 95% CI, 1.1 to 2.6). Estrogen+other progestagens was associated with significant increases in
risk of ductal and lobular carcinomas (RR, 1.6; 95%
CI, 1.3 to 1.8; and 2.0; 95% CI, 1.5 to 2.7, respectively), of ER+/PR+ and ER
+/PR-
carcinomas (RR, 1.8; 95% CI, 1.5 to 2.1; and 2.6; 95% CI, 1.9 to 3.5,
respectively), but not of ER-/PR+ or ER-/PR- carcinomas (RR, 1.0; 95% CI, 0.5
to 2.1; and 1.4; 95% CI, 0.9 to 2.0, respectively). CONCLUSION: The increase in
risk of breast cancer observed with the use of CHTs other than estrogen+progesterone and estrogen+dydrogesterone
seems to apply preferentially to ER+ carcinomas, especially those ER+/PR-, and
to affect both
ductal and lobular carcinomas.
J Clin Endocrinol Metab. 2008 Mar 4 [Epub ahead
of print]
Does Osteoprotegerin or RANKL Mediate the Association Between
Bone and Coronary Artery Calcification?
Division
of Pharmacy Practice,
postmenopausal
women (aged 58-81 years) taking ET who had hip and spine BMD assessed by
dual-energy x-ray absorptiometry and CAC measured by
electron-beam computed tomography in 1998-2002, and serum RANKL and OPG levels
measured in samples collected in 1997-1999. Total CAC score was dichotomized as
"none/minimal" (</=10) versus "some" (>10). Results:
OPG serum levels were higher in women who had some CAC compared to those who
had none/minimal (126.8+/-1.08 vs. 102.9+/-1.07 pg/ml, respectively, p=0.03);
these differences became nonsignificant after
adjustment for age and other risk factors (p=0.51). A one standard deviation
increase in hip BMD was associated with significantly lower odds of having CAC
> 10 (OR=0.52; 95% CI: 0.29-0.93) independent of age,fat-free
mass, HDL cholesterol, current smoking, and use of cholesterol-lowering
medications. Other skeletal sites demonstrated a similar pattern. Addition of
RANKL and/or OPG to the model had minimal effect on the magnitudeor
statistical significance of the BMD-CAC association. Additionally, a test of
interaction indicated that RANKL andOPG are not
significant effect modifiers. Conclusions: Serum OPG and RANKL do not account
for the observe dassociation between bone and coronary
artery calcification among postmenopausal women using hormone therapy.
J Clin Endocrinol Metab. 2008 Mar 4 [Epub ahead
of print]
Effects
in Postmenopausal Women of Estradiol and Medroxyprogesterone Alone and Combined on Resistance Artery
Function and Endothelial Morphology and Movement.
Kublickiene K, Fu XD, Svedas E, Landgren
BM, Genazzani AR, Simoncini
T.
Department
of Clinical Science, Intervention and Technology, Section for Obstetrics and
Gynecology, KarolinskaInstitute, Karolinska
University Hospital-Huddinge campus, 14186 Stockholm, Sweden; Molecular and
Cellular Gynecological Endocrinology Laboratory (MCGEL), Department of
Reproductive Medicine and Child Development, University of Pisa, 56100, Pisa,
Italy.
Context:
Endothelial dysfunction in resistance arteries after menopause is important for
the development of highblood pressure and
cardiovascular disease. Objective: To study the effects of different hormone
replacement therapies (HRT) on the function and morphology of isolated
resistance arteries, and to look for their mechanisticbasis.
Design and setting: A randomized, placebo-controlled double-blind study in a
University hospital, along with laboratory-based studies. Patients and
interventions: We isolated resistance arteries in subcutaneous biopsies from 55
postmenopausal women before and after 3 months of therapy with estradiol (E2), medroxyprogesterone
acetate(MPA), E2 + MPA or placebo. In addition, we
studied isolated human endothelial cells. Main Outcome Measuresand
Results: Artery flow-mediated dilatation was augmented after treatment with E2
or E2+MPA, whereas MPA orplacebo had no effect.
Pressure-induced myogenic tone was reduced by E2 +
MPA, while it was unchanged in theother groups.
Scanning microscopy showed that E2 improved endothelial cell morphology and
decreased signs ofendothelial apoptosis, but the
addition of MPA impaired these events. E2, MPA or the combination all increased
theexpression and phosphorylation
of the actin-binding protein, moesin
and of the focal adhesion complex controller, focal adhesion kinase and induced the rearrangement of cytoskeletal
actin and vinculin fibers.
All treatments promoted endothelial cell horizontal migration, with E2 inducing
the strongest effect. Conclusions: This study file:///C|/Documents%20and%20Settings/HBLTJEFELABORATORIO/Mis%20documentos/080311.htm
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suggests that
HRT with estrogens or in combination with MPA may benefit the function of resistance
arteries and may preserve the morphological integrity of endothelial cells by
regulatory actions on the cytoskeleton.
Am J Obstet Gynecol. 2008 Mar;198(3):265.e1-7.
The
effect of ultralow-dose transdermal estradiol on sexual function in
postmenopausal women.
Huang
A, Yaffe K, Vittinghoff E, Kuppermann M, Addis I, Hanes V, Quan
J, Grady D.
Department
of Medicine, University of California San Francisco School of Medicine, San
Francisco, CA, USA. OBJECTIVE: This study was undertaken to examine the effect
of ultralow-dose transdermal estradiol
on sexual function in postmenopausal women. STUDY DESIGN: Analysis of data from
a multicenter, randomized, doubleblind,placebo-controlled
trial of a 0.014 mg/day transdermal estradiol patch in 417 women aged 60 to 80 years.Sexual function was assessed by self-administered
questionnaires at baseline and 4, 12, and 24 months. A lineareffects
model was used to assess treatment effects using data from all on-study
assessments. RESULTS: Womenrandomly assigned to estradiol had a 4.3 point greater improvement in the
vaginal pain/dryness domain relative toplacebo (95%
CI = 0.3-8.4, P = .04). No significant differences in frequency of sexual
activity or other sexualfunction domains (desire,
satisfaction, problems, or orgasm) were observed between treatment groups (P
> or = .10(or all). CONCLUSIONS: Ultralow-dose estradiol
resulted in modest improvement in sexual function related tovaginal
pain and dryness, but not in other domains of sexual function.file:///C|/Documents%20and%20Settings/HBLTJEFELABORATORIO/Mis%20documentos/080311.htm
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