Endogenous estrogen levels, bone mineral density and estrogen receptor status in breast cancer

2005 ◽  
Vol 89 (2) ◽  
pp. 213-213
Author(s):  
Kadri Altundag ◽  
Ozden Altundag ◽  
Mehmet Gunduz
2016 ◽  
Vol 12 (3) ◽  
pp. 119-122
Author(s):  
Zeynep Erdogan Iyigun ◽  
Kezban Nur Pilanci ◽  
Fatmagul Kusku Cabuk ◽  
Serkan Ilgun ◽  
Cetin Ordu ◽  
...  

2011 ◽  
Vol 96 (2) ◽  
pp. 308-319 ◽  
Author(s):  
R. J. Santen

abstract Context: Two common strategies are used to treat estrogen receptor-positive breast cancer in women: tamoxifen to inhibit estrogen action, and aromatase inhibitors (AIs) to block estrogen biosynthesis. Recent data suggest that AIs are more effective than tamoxifen in the adjuvant and advanced disease settings and are now being more commonly used. Tamoxifen, as a selective estrogen receptor modulator, exerts estrogenic effects to preserve bone, whereas the AIs profoundly lower estrogen levels and cause bone loss. Recent comparative studies of these agents provide extensive data on fracture rates, bone mineral density, and markers of bone formation and resorption. Objective: The aim of the study was to review the mechanistic effects of estrogen on bone and clinical data regarding bone density, bone turnover markers, and fracture rates in women with breast cancer taking tamoxifen or AIs. Evidence Acquisition and Synthesis: Data presented reflect a review of the literature and data integration from the perspective of the author's knowledge of the field. Results: Tamoxifen increases bone density and reduces fractures in postmenopausal women with breast cancer, whereas AIs increase rate of fracture, accelerate loss of bone mineral density, and enhance levels of markers of bone formation and resorption. Bisphosphonates and denosumab counteract the effects of the AIs on bone. Guidelines for management of AI-induced bone loss are available from several sources, but a simple algorithm guides decision making most effectively. Conclusions: Endocrine therapy for postmenopausal women with breast cancer exerts substantial effects on bone, and guidelines are available to assist in the management of bone-related problems.


Maturitas ◽  
2007 ◽  
Vol 57 (3) ◽  
pp. 221-225 ◽  
Author(s):  
Tsutomu Douchi ◽  
Yukie Yonehara ◽  
Shoichiro Kosha ◽  
Ichiro Iwamoto ◽  
Yoshiaki Rai ◽  
...  

2017 ◽  
Vol 13 (18) ◽  
pp. 1
Author(s):  
Nana Khachidze ◽  
Elene Giorgadze ◽  
Marina Tsagareli ◽  
Nino Dolidze ◽  
Tea Sulikashvvili

Background and Aim: Aromatase inhibitors (AIs) and selective estrogen receptor modulators (SERMs) are important components of adjuvant endocrine therapy in postmenopausal women with estrogen receptor positive breast cancer. The aim of our study was to assess the effect of AIs and SERMs on bone mineral density (BMD) in Caucasian postmenopausal women with breast cancer. Patients and Methods: 118 postmenopausal Caucasian women were enrolled in the study. 60 patients were receiving AIs and 58 patients – SERMs-Tamoxifen. Patients were also divided into two sub groups: 1) patients with more than 3 years of last menstrual period (LMP) and 2) patients with less than 3 years of last menstrual period. Results: Among Aromatase inhibitors treated patients, there was a decrease in median BMD from baseline to 5 years in lumbar spine and total hip compared with the Tamoxifen group. No patients with normal BMD at baseline became osteoporotic at 5 years. Conclusion: Aromatase inhibitors are associated with accelerated bone loss over the 5-year treatment period. In postmenopausal women, treatment with tamoxifen is associated with preservation of the bone mineral density of the lumbar spine.


2013 ◽  
Author(s):  
Sonia Munoz Gil ◽  
Tomas Mut Dolera ◽  
Belen C Garrido Lopez ◽  
M D Torregrosa Maicas ◽  
R Girones Sarrio ◽  
...  

2020 ◽  
Author(s):  
Lungwani Muungo

Although it is well established that estrogen deficiencycauses osteoporosis among the postmenopausalwomen, the involvement of estrogen receptor (ER) in itspathogenesis still remains uncertain. In the presentstudy, we have generated rats harboring a dominantnegative ERa, which inhibits the actions of not only ERabut also recently identified ERb. Contrary to our expectation,the bone mineral density (BMD) of the resultingtransgenic female rats was maintained at the same levelwith that of the wild-type littermates when sham-operated.In addition, ovariectomy-induced bone loss wasobserved almost equally in both groups. Strikingly, however,the BMD of the transgenic female rats, after ovariectomized,remained decreased even if 17b-estradiol(E2) was administrated, whereas, in contrast, the decreaseof littermate BMD was completely prevented byE2. Moreover, bone histomorphometrical analysis ofovariectomized transgenic rats revealed that the higherrates of bone turnover still remained after treatmentwith E2. These results demonstrate that the preventionfrom the ovariectomy-induced bone loss by estrogen ismediated by ER pathways and that the maintenanceof BMD before ovariectomy might be compensatedby other mechanisms distinct from ERa and ERbpathways.


1996 ◽  
Vol 82 (1) ◽  
pp. 65-67 ◽  
Author(s):  
Sandro Barni ◽  
Paolo Lissoni ◽  
Gabriele Tancini ◽  
Antonio Ardizzoia ◽  
Marina Cazzaniga

In this study, the authors have analyzed the possible effects of one-year adjuvant treatment with tamoxifen on bone mineral density in postmenopausal breast cancer women. Bone mineral content was studied by photon absorptiometry (I-125), whereas bone balance was analyzed indirectly by serum PTH, osteocalcin, calcitonin, calcium and alkaline phosphatase levels. Bone mineral content and serum bone-related substances were measured before starting treatment and after one year. Results were analyzed using Student's t test for paired data. No difference was found between the two measurements for bone mineral content, PTH, calcitonin, calcium and alkaline phosphatase levels. Measurements at entry and after one year of treatment showed a statistically significant difference ( P < 0.001) only for osteocalcin. In accordance with other authors, we can conclude that treatment with tamoxifen does not cause an increase in menopausal bone resorption. The finding that osteocalcin levels decreased after one year of therapy with tamoxifen is interesting, but further studies are necessary to clarify the role of such levels in predicting a turnover of bone balance towards osteoblastic activity.


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