scholarly journals Plasma Estradiol and Testosterone Levels and Ischemic Stroke in Postmenopausal Women

Stroke ◽  
2020 ◽  
Vol 51 (4) ◽  
pp. 1297-1300
Author(s):  
Jie Hu ◽  
Jennifer H. Lin ◽  
Monik C. Jiménez ◽  
JoAnn E. Manson ◽  
Susan E. Hankinson ◽  
...  
2013 ◽  
Vol 98 (7) ◽  
pp. 2967-2974 ◽  
Author(s):  
Michael E. Jones ◽  
Minouk Schoemaker ◽  
Megan Rae ◽  
Elizabeth J. Folkerd ◽  
Mitch Dowsett ◽  
...  

Context: Endogenous sex hormones are risk factors for postmenopausal breast cancer. A potential route for favorable hormonal modification is weight loss. Objective: The objective of the study was to measure change in plasma estradiol and testosterone levels in postmenopausal women in relation to change in body mass index (BMI) and plasma leptin. Setting: The setting was a cohort study of over 100 000 female volunteers from the general population, United Kingdom. Participants: The participants were a sample of 177 postmenopausal women aged over 45 years who provided blood samples during 2004–2005 and again during 2010–2011. Main Outcome Measure: Outcomes were percentage change in plasma estradiol and testosterone levels per 1 kg/m2 change in BMI and per 1 ng/mL change in plasma leptin. Results: Among women with reduction in BMI, estradiol decreased 12.7% (95% confidence interval: [6.4%, 19.5%]; P < .0001) per kg/m2 and among women with increased BMI estradiol increased 6.4% [0.2%, 12.9%] (P = .042). The corresponding figures for testosterone were 10.7% [3.0%, 19.0%] (P = .006) and 1.9% [−5.4%, 9.7%] (P = .61) per kg/m2. For women with decreases and increases in leptin, estradiol decreased by 3.6% [1.3%, 6.0%] (P = .003) per ng/mL and increased by 1.7% [−0.3%, 3.6%] (P = .094), respectively. The corresponding figures for testosterone were 4.8% [2.0%, 7.8%] (P = .009) and 0.3% [−2.0%, 2.6%] (P = .82) per ng/mL. Conclusions: In postmenopausal women, changes in BMI and plasma leptin occurring over several years are associated with changes in estradiol and testosterone levels. The results suggest that fat loss by an individual can result in substantial decreases in postmenopausal estradiol and testosterone levels and provides support for weight management to lessen breast cancer risk.


2005 ◽  
Vol 12 (2) ◽  
pp. 135-141 ◽  
Author(s):  
Ilma Simoni Brum ◽  
Poli Mara Spritzer ◽  
Franyoise Paris ◽  
Maria Augusta Maturana ◽  
Franyoise Audran ◽  
...  

2010 ◽  
Vol 28 (7) ◽  
pp. 1161-1167 ◽  
Author(s):  
Anita K. Dunbier ◽  
Helen Anderson ◽  
Zara Ghazoui ◽  
Elizabeth J. Folkerd ◽  
Roger A'Hern ◽  
...  

Purpose To determine whether plasma estradiol (E2) levels are related to gene expression in estrogen receptor (ER)–positive breast cancers in postmenopausal women. Materials and Methods Genome-wide RNA profiles were obtained from pretreatment core-cut tumor biopsies from 104 postmenopausal patients with primary ER-positive breast cancer treated with neoadjuvant anastrozole. Pretreatment plasma E2 levels were determined by highly sensitive radioimmunoassay. Genes were identified for which expression was correlated with pretreatment plasma E2 levels. Validation was performed in an independent set of 73 ER-positive breast cancers. Results The expression of many known estrogen-responsive genes and gene sets was highly significantly associated with plasma E2 levels (eg, TFF1/pS2, GREB1, PDZK1 and PGR; P < .005). Plasma E2 explained 27% of the average expression of these four average estrogen-responsive genes (ie, AvERG; r = 0.51; P < .0001), and a standardized mean of plasma E2 levels and ER transcript levels explained 37% (r, 0.61). These observations were validated in an independent set of 73 ER-positive tumors. Exploratory analysis suggested that addition of the nuclear coregulators in a multivariable analysis with ER and E2 levels might additionally improve the relationship with the AvERG. Plasma E2 and the standardized mean of E2 and ER were both significantly correlated with 2-week Ki67, a surrogate marker of clinical outcome (r = −0.179; P = .05; and r = −0.389; P = .0005, respectively). Conclusion Plasma E2 levels are significantly associated with gene expression of ER-positive breast cancers and should be considered in future genomic studies of ER-positive breast cancer. The AvERG is a new experimental tool for the study of putative estrogenic stimuli of breast cancer.


2009 ◽  
Vol 10 (4) ◽  
pp. 650-654 ◽  
Author(s):  
Simerjot K. Jassal ◽  
Elizabeth Barrett-Connor ◽  
Sharon L. Edelstein

2006 ◽  
Vol 2 ◽  
pp. S635-S635
Author(s):  
Vasileios T. Papaliagkas ◽  
Magda Tsolaki ◽  
Philip Grammaticos ◽  
Chrysanthi Karanasou ◽  
Vassilios Balaris ◽  
...  

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Danxia Yu ◽  
Xiao-Ou Shu ◽  
Honglan Li ◽  
Gong Yang ◽  
Qiuyin Cai ◽  
...  

Background: Postmenopausal hormone therapy has been shown to increase stroke risk. It is unclear whether high exposure to pytoestrogens, such as soy isoflavones, may confer the same risk of stroke. Objective: To examine associations of urinary isoflavonoids, which reflect isoflavones intake, absorption, and metabolism, with risk of ischemic stroke in postmenopausal Chinese women. Design: A nested case-control study. Method: We identified 1438 incident cases of ischemic stroke druing 1997-2010 and individually matched them to 1438 controls on age, date and time of sample collection, time since last meal, and recent use of antibiotics. All subjects were postmenopausal women who had never used hormone therapy and had no history of CVD or cancer at baseline. Seven isoflavonoids were measured by LC-MS and standardized by urinary creatinine. Results: We found no significant difference between case-control pairs in mean levels of total or individual urinary isoflavonoids, including 3 parent compounds (daidzein, genistein, and glycitein) and 4 metabolites derived from intestinal bacteria (dihydrogenistein, dihydrodaidzein, O-desmethylangolensin, and equol). Multivariate analyses revealed that women in the highest quintile of equol concentration had a lower risk of ischemic stroke (OR=0.77, 95%CI=0.60-0.98). Analyses stratified by equol producing status showed a significant inverse association between isoflavone bacterial metabolites and stroke risk in equol producers (31.8% of the study population, OR=0.40 across extreme quartiles, 95%CI=0.18-0.87, Ptrend=0.002), but no association in equol non-producers. Conclusion: Overall, this large prospective study suggests that urinary isoflavonoids are not associated with risk of ischemic stroke in postmenopausal Chinese women. High level of bacteria-derived metabolites of isoflavones, however, was associated with a reduced risk in equol producers, suggesting a possible interaction between gut microbiome and soy foods in the pathogenesis of ischemic stroke.


2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 10614-10614
Author(s):  
M. Mundia ◽  
M. F. Ali

10614 Background: Aromatse Inhibitors are a class of drugs that inhibit tumor growth in hormone receptor positive breast cancers in postmenopausal women. They exert their action by inhibiting the enzyme aromatse involved in the last step in conversion of Androgens to estrogens. They are currently used extensively in both advanced and adjuvant treatments. Methods: Clinical Charts of postmenopausal women, with estrogen receptor positive breast cancer, receiving the non-steroidal aromatse inhibitor, Anastrazole 1 mg daily at a community oncology practice were evaluated for androgenic effect of the drug. Review included presence of clinical Hirsutism and serum testosterone levels. Results: There were 33 women, receiving Anastrazole, 29 for adjuvant therapy, and 4 for metastatic disease. Age 51–77years (median: 63 years), Duration of Anastrazole therapy 6 months to 42 months (median: 18 months), There was no Clinical evidence of hirsutism noted. Serum testosterone levels varied from 9 ng/ml to 58 ng/ml. (Normal range: 14–76 ng/ml) in 32 women. 1 woman had a serum testosterone level of 86 ng/ml with no clinical hirsutism. The most common side effect of Anastrazole was arthralgias, seen in three women. Conclusions: Anastrozole 1 mg daily does not appear to cause any clinical androgenic effect, or elevation of serum testosterone levels. No significant financial relationships to disclose.


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