Effects of One-Year Adjuvant Treatment with Tamoxifen on Bone Mineral Density in Postmenopausal Breast Cancer Women

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.

2013 ◽  
Author(s):  
N Hangartner Thomas ◽  
F Short David ◽  
Gilsanz Vicente ◽  
J Kalkwarf Heidi ◽  
M Lappe Joan ◽  
...  

2018 ◽  
Vol 3 (4) ◽  
pp. 62
Author(s):  
Jose Antonio ◽  
Anya Ellerbroek ◽  
Cassandra Carson

The effects of long-term high-protein consumption (i.e., >2.2 g/kg/day) are unclear as it relates to bone mineral content. Thus, the primary endpoint of this investigation was to determine if consuming a high-protein diet for one year affected various parameters of body composition in exercise-trained women. This investigation is a follow-up to a prior 6-month study. Subjects were instructed to consume a high-protein diet (>2.2 g/kg/day) for one year. Body composition was assessed via dual-energy X-ray absorptiometry (DXA). Subjects were instructed to keep a food diary (i.e., log their food ~three days per week for a year) via the mobile app MyFitnessPal®. Furthermore, a subset of subjects had their blood analyzed (i.e., basic metabolic panel). Subjects consumed a high-protein diet for one year (mean ± SD: 2.3 ± 1.1 grams per kilogram body weight daily [g/kg/day]). There were no significant changes for any measure of body composition over the course of the year (i.e., body weight, fat mass, lean body mass, percent fat, whole body bone mineral content, whole body T-score, whole body bone mineral density, lumbar bone mineral content, lumbar bone mineral density and lumbar T-score). In addition, we found no adverse effects on kidney function. Based on this 1-year within-subjects investigation, it is evident that a diet high in protein has no adverse effects on bone mineral density or kidney function.


2011 ◽  
Vol 78 (6) ◽  
pp. 616-618 ◽  
Author(s):  
Katarzyna Wesolowska ◽  
Bozena Czarkowska-Paczek ◽  
Jerzy Przedlacki ◽  
Jacek Przybylski

Bone ◽  
2006 ◽  
Vol 38 (3) ◽  
pp. 13 ◽  
Author(s):  
Arjun L. Khandare ◽  
G. Shanker Rao ◽  
N. Balakrishna

2001 ◽  
Vol 19 (14) ◽  
pp. 3306-3311 ◽  
Author(s):  
Charles L. Shapiro ◽  
Judith Manola ◽  
Meryl Leboff

PURPOSE: We sought to evaluate the effects of chemotherapy-induced ovarian failure on bone loss and markers of skeletal turnover in a prospective longitudinal study of young women with breast cancer receiving adjuvant chemotherapy. PATIENTS AND METHODS: Forty-nine premenopausal women with stage I/II breast cancers receiving adjuvant chemotherapy were evaluated within 4 weeks of starting chemotherapy (baseline), and 6 and 12 months after starting chemotherapy with dual-energy absorptiometry and markers of skeletal turnover osteocalcin and bone-specific alkaline phosphatase. Chemotherapy-induced ovarian failure was defined as a negative pregnancy test, greater than 3 months of amenorrhea, and a follicle-stimulating hormone ≥ 30 MIU/mL at the 12-month evaluation. RESULTS: Among the 35 women who were defined as having ovarian failure, highly significant bone loss was observed in the lumbar spine by 6 months and increased further at 12 months. The median percentage decrease of bone mineral density in the spine from 0 to 6 months and 6 to 12 months was −4.0 (range, −10.4 to +1.0; P = .0001) and −3.7 (range, −10.1 to 9.2; P = .0001), respectively. In contrast, there were no significant decreases in bone mineral density in the 14 patients who retained ovarian function. Serum osteocalcin and bone specific alkaline phosphatase, markers of skeletal turnover, increased significantly in the women who developed ovarian failure. CONCLUSION: Chemotherapy-induced ovarian failure causes rapid and highly significant bone loss in the spine. This may have implications for long-term breast cancer survivors who may be at higher risk for osteopenia, and subsequently osteoporosis. Women with breast cancer who develop chemotherapy-induced ovarian failure should have their bone density monitored and treatments to attenuate bone loss should be evaluated.


2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Yasumoto Matsui ◽  
Marie Takemura ◽  
Atsushi Harada ◽  
Fujiko Ando ◽  
Hiroshi Shimokata

Bone mineral density (aBMD) is equivalent to bone mineral content (BMC) divided by area. We rechecked the significance of aBMD changes in aging by examining BMC and area separately. Subjects were 1167 community-dwelling Japanese men and women, aged 40–79 years. ABMDs of femoral neck and lumbar spine were assessed by DXA twice, at 6-year intervals. The change rates of BMC and area, as well as aBMD, were calculated and described separately by the age stratum and by sex. In the femoral neck region, aBMDs were significantly decreased in all age strata by an increase in area as well as BMC loss in the same pattern in both sexes. In the lumbar spine region, aBMDs decreased until the age of 60 in women, caused by the significant BMC decrease accompanying the small area change. Very differently in men, aBMDs increased after their 50s due to BMC increase, accompanied by an area increase. Separate analyses of BMC and area change revealed that the significance of aBMD changes in aging was very divergent among sites and between sexes. This may explain in part the dissociation of aBMD change and bone strength, suggesting that we should be more cautious when interpreting the meaning of aBMD change.


Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Vishwajeeth Pasham ◽  
Deborah Stewart ◽  
Laura Carbone ◽  
Gregory A Harshfield

Background: Previous literature has shown a strong negative effect of angiotensin II (ANGII) on bone metabolism within mouse models. Additionally, psychological stress has been associated with activation of the renin-angiotensin-aldosterone system (RAAS). Stress has also been related to lower total bone mineral density (TBMD). However, there is controversy in the literature examining the relationship between the RAAS and bone metabolism within humans and stress has not been considered as a direct link between these systems. Purpose: We aimed to examine the relationship between stress-induced RAAS activation and TBMD and total bone mineral content (TBMC). Methods: Participants were placed on a sodium controlled diet for three days. Participants then underwent two hours rest, one hour mental stressor, and two hours recovery with hourly collections of blood/urine samples. Renin, ANGII, aldosterone, TBMD and TBMC were measured. Results: This study recruited 586 adolescents (mean age 16±1.116) with 51% women and 62% African-American and 38% Caucasian. Overall, relationships were observed between ANGII and aldosterone, and TBMC and TBMD controlling for age, race, and BMI. During stress, aldosterone was related to TBMD (r=-.150, p<0.05) and ANGII was related to TBMC (r=-.156, p<0.05) and TBMD (r=-.139, p<0.05). When comparing males and females, only females demonstrated a relationship between TBMC and ANGII in response to stress (stress: r=-.229, p<0.05; post-stress: r=-.277, p<0.01) and between aldosterone and TBMC (stress: r=-.199, p<0.05) and TBMD (stress: r=-.250, p<0.01). Renin was not significantly correlated with TBMD nor TBMC in any population. Conclusion/Interpretations: These data suggest that stress-induced RAAS activation may be associated with lower TBMD and TBMC in girls. Despite small correlations, consistency across multiple measures of RAAS activation being apparent in adolescents is significant. This observation may indicate that stress activation of RAAS contributes to bone remodeling in early life.


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