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Short-term hormone therapy improves sCD40L and endothelial function in early menopausal women: potential role of estrogen receptor polymorphisms.
Bechlioulis, A, Naka, KK, Kalantaridou, SN, Chatzikyriakidou, A, Papanikolaou, O, Kaponis, A, Vakalis, K, Vezyraki, P, Gartzonika, K, Mavridis, A, et al
Maturitas. 2012;(4):389-95
Abstract
OBJECTIVE Hormone therapy (HT) has been suggested to improve vascular function and inflammation in menopausal women, although not consistently. We aimed to investigate the effects of HT on endothelial function and inflammation, especially sCD40L, in early menopausal women, and the effect of common estrogen receptor (ER) polymorphisms on vascular responses to HT. STUDY DESIGN Eighty-four early menopausal women (<3 years in menopause) with menopausal complaints eligible for HT. Forty women received transdermal 17β-estradiol plus cyclical micronized progesterone for 3 months while 44 did not (controls). MAIN OUTCOME MEASURES Brachial artery flow-mediated dilation (FMD) and vascular inflammation markers (sICAM, sP-Selectin and sCD40L). Genetic polymorphisms of ERα (PvuII 454-397T>C and XbaI 454-351A>G) and ERβ (AluI 1730A>G) were also assessed. RESULTS The two groups did not differ at baseline. Following HT, vasomotor complaints' severity, blood pressure, LDL, sCD40L, sICAM and sP-Selectin decreased and FMD increased compared to controls (P<0.05 for all). ERβ AluI A allele presence was the most important independent predictor of HT-induced increase in FMD while ERα XbaI A allele was the only independent predictor of decrease in sCD40L. CONCLUSIONS Short-term HT in early menopausal women improved endothelial function and inflammation. Specific ER polymorphisms that were found to be main determinants of HT-induced effects on endothelium could identify subgroups of women who may benefit the most from HT.
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Longitudinal evaluation of serum leptin and bone mineral density in early postmenopausal women.
Di Carlo, C, Tommaselli, GA, Di Spiezio Sardo, A, Sammartino, A, Attianese, W, Gargano, V, Bifulco, G, Nappi, C
Menopause (New York, N.Y.). 2007;(3 Pt 1):450-4
Abstract
OBJECTIVE To evaluate total and site-specific bone mineral density (BMD) and serum leptin levels in postmenopausal women treated with a calcium supplement and in postmenopausal women receiving estrogen plus progestin therapy. DESIGN Forty-four women were randomized to receive either calcium supplementation (group A, n = 22) or transdermal 17beta-estradiol at a dose of 50 mug/day in a continuous regimen and nomegestrol at a dose of 5 mg/day for 12 days per month in a sequential regimen (group B, n = 22). All women underwent dual-energy x-ray absorptiometry determination of BMD and blood sampling in the morning at the beginning of the study and after 12 months. Leptin was determined by radioimmunoassay in all samples. RESULTS After 12 months, serum leptin levels were significantly higher in group A (control) in comparison with group B and baseline values, whereas both total and pelvic BMDs were significantly lower in group A in comparison with group B and baseline values. At baseline, a significant correlation was found between leptin levels, body mass index, and total-body BMD. After 12 months, leptin was still correlated to body mass index in both groups, but the association with BMD was lost. CONCLUSIONS This study confirms previous evidence of a significant correlation between serum leptin and BMD in early postmenopausal women. Furthermore, this correlation is lost over time during the progression of the postmenopausal period, independently from the administration of estrogen-progestin therapy. Further studies and longer follow-up periods are needed to better understand theses issues.
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Bone mineral density changes over a year in young females with schizophrenia: relationship to medication and endocrine variables.
Meaney, AM, O'Keane, V
Schizophrenia research. 2007;(1-3):136-43
Abstract
INTRODUCTION Hyperprolactinaemia is associated with the use of potent dopamine-2 receptor blocking anti-psychotic agents in schizophrenia and with bone loss in the general population. Significantly higher rates of reduced bone mineral density (BMD) have been identified in young pre-menopausal females with schizophrenia receiving prolactin-raising anti-psychotics compared to those receiving prolactin-sparing anti-psychotics. This prospective study compared BMD alterations over a period of 1 year in patients maintained on either prolactin-raising (e.g. risperidone, amisulpride or depot anti-psychotics) or prolactin-sparing (olanzapine) anti-psychotics. The effects of specific interventions to improve BMD were also examined in the context of whether patients were receiving either prolactin-raising or anti-psychotics or Olanzapine. METHODS Pre-menopausal females (n=38) with a diagnosis of schizophrenia, who had received exclusively either prolactin-raising (n=25) or prolactin-sparing (n=13) anti-psychotics during their treatment history, had clinical, endocrine and bone marker assessments performed at baseline and every 3 months for a period of 1 year. BMD was measured by DEXA scan at baseline and at 1-year follow-up. Patients from both groups either received specific interventions (n=16) or no interventions (n=16) to improve bone density. RESULTS There was an overall gain in lumbar BMD values in the prolactin-sparing subgroup, compared to an overall loss in the prolactin-raising subgroup (p=0.02), for the groups that received no specific interventions to improve BMD. Within the group that received specific interventions, the subgroup receiving prolactin-sparing anti-psychotics had a significant increase in lumbar (p=0.01) and hip (p=0.01) BMD over time, whereas alterations in the prolactin-raising subgroup were not significant. DISCUSSION Women taking prolactin-raising anti-psychotics and not receiving specific interventions to improve bone density had evidence of ongoing bone demineralisation over a year; whereas women taking prolactin-sparing anti-psychotics had a modest overall increase in BMD. Most clinical interventions appeared to be helpful, but were significantly more effective in those taking prolactin-sparing anti-psychotics.
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[Evaluation of the hematochemical parameters and bone mineral density of women in physiological menopause treated with hormone replacement therapy with nomegestrol acetate and surgical menopause treated with estrogen replacement. Part II].
Savoca, S, D'Agosta, S, Lombardo, G
Minerva ginecologica. 2007;(3):215-22
Abstract
AIM: The purpose of this paper was to estimate the effectiveness of the use of acetate nomegestrol in relation to indicator hematochemical parameters and bone mineral density (BMD) regarding patients in physiological menopause treated with hormone replacement therapy (HRT), compared to patients in surgical menopause treated with HRT by only administering transdermally hemi hydrate estradiol (estrogen replacement therapy, ERT). METHODS Sixty women in menopause for at least 6 months ago, aged between 40 and 55 years, were recruited. Thirty of them were given HRT with acetate nomegestrol, and 30 were given only ERT, because they were subjected to general hysterectomy with bilateral adnexectomy. The standards for inclusion were: level of FSH >or= to 30 UI beta-estradiol RESULTS Both groups at the end of treatment showed an increase in BMD level, whereas haematochemical tests were regular or at least stabilized in a large percentage of patients. CONCLUSION This research has shown the validity of HRT on BMD, underlining a more noteworthy improvement in the patients' group that used acetate nomegestrol than in those that only used estrogens.
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The phytoestrogen genistein produces acute nitric oxide-dependent dilation of human forearm vasculature with similar potency to 17beta-estradiol.
Walker, HA, Dean, TS, Sanders, TA, Jackson, G, Ritter, JM, Chowienczyk, PJ
Circulation. 2001;(2):258-62
Abstract
BACKGROUND Genistein, a phytoestrogen, may have estrogenic cardioprotective actions. We investigated whether genistein influences endothelium-dependent vasodilation in forearm vasculature of healthy human subjects and compared the effects of genistein with those of 17beta-estradiol. METHODS AND RESULTS The brachial arterial was cannulated with a 27-gauge needle for drug infusion. Forearm blood flow responses were measured with strain-gauge plethysmography. Genistein (10 to 300 nmol/min, each dose for 6 minutes) produced a dose-dependent increase in forearm blood flow from 3.4+/-0.3 to 9.6+/-1.3 mL x min(-1) x 100 mL forearm(-1) (mean+/-SEM) in men (n=9, P:<0.0001 by ANOVA). The mean forearm venous concentration of genistein during infusion of the highest dose was 1.8+/-0.3 micromol/L in 6 additional men. Genistein produced a similar increase in blood flow in premenopausal women. Daidzein, another phytoestrogen, was ineffective, but equimolar concentrations of 17beta-estradiol caused similar vasodilation to genistein. Responses to genistein and 17beta-estradiol were inhibited to the same degree by the NO synthase inhibitor N:(G)-monomethyl-L-arginine. A threshold dose of genistein potentiated the endothelium-dependent vasodilator acetylcholine but not the endothelium-independent vasodilator nitroprusside. CONCLUSIONS Genistein causes L-arginine/NO-dependent vasodilation in forearm vasculature of human subjects with similar potency to 17beta-estradiol and potentiates endothelium-dependent vasodilation to acetylcholine.