Ovarian Failure After Adjuvant Chemotherapy Is Associated With Rapid Bone Loss in Women With Early-Stage Breast Cancer

2001 ◽  
Vol 19 (14) ◽  
pp. 3306-3311 ◽  
Author(s):  
Charles L. Shapiro ◽  
Judith Manola ◽  
Meryl Leboff
Keyword(s):  
Breast Cancer ◽  
Bone Mineral Density ◽  
Alkaline Phosphatase ◽  
Adjuvant Chemotherapy ◽  
Bone Loss ◽  
Bone Mineral ◽  
Ovarian Failure ◽  
Mineral Density ◽  
Specific Alkaline Phosphatase ◽  
Bone Specific Alkaline Phosphatase

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.

Changes in bone mineral density and bone-specific alkaline phosphatase in ovariectomized ewes

Bone ◽  
1995 ◽  
Vol 17 (4) ◽  
pp. S395-S402 ◽  
Author(s):  
A.S. Turner ◽  
M. Alvis ◽  
W. Myers ◽  
M.L. Stevens ◽  
M.W. Lundy
Keyword(s):  
Bone Mineral Density ◽  
Alkaline Phosphatase ◽  
Bone Mineral ◽  
Mineral Density ◽  
Specific Alkaline Phosphatase ◽  
Bone Specific Alkaline Phosphatase

scholarly journals Decreased Nitric Oxide Levels and Bone Turnover in Amenorrheic Athletes with Spinal Osteopenia1

1998 ◽  
Vol 83 (9) ◽  
pp. 3056-3061 ◽  
Author(s):  
E. Stacey ◽  
P. Korkia ◽  
M. V. J. Hukkanen ◽  
J. M. Polak ◽  
O. M. Rutherford
Keyword(s):  
Nitric Oxide ◽  
Bone Mineral Density ◽  
Alkaline Phosphatase ◽  
Bone Turnover ◽  
Postmenopausal Women ◽  
Bone Mineral ◽  
No Production ◽  
Mineral Density ◽  
Specific Alkaline Phosphatase ◽  
Bone Specific Alkaline Phosphatase

Amenorrheic athletes have been likened to postmenopausal women, with low estrogen levels and osteopenia. It has been suggested that estrogen exerts its antiresorptive actions on bone via a nitric oxide (NO)-dependent mechanism. This study investigated whether the mechanism of bone loss in amenorrheic athletes is similar to that of postmenopausal women with reduced NO levels and high bone turnover. Eleven amenorrheic athletes, 15 eumenorrheic athletes, and 10 sedentary controls were studied. Spine and hip bone mineral density was measured using dual-energy x-ray absorptiometry. Bone turnover was assessed by biochemical markers of formation (osteocalcin and bone-specific alkaline phosphatase) and resorption (deoxypyridinoline). NO metabolites were measured from 24-h urine samples using a chemiluminescence assay. Spine, but not hip, bone mineral density was reduced in the amenorrheic group, compared with the eumenorrheic (P = 0.0001) and control (P = 0.04) groups. Osteocalcin, bone-specific alkaline phosphatase, and deoxypyridinoline were similar in all groups. NO metabolites were lower in the amenorrheic group, compared with controls (P = 0.035), despite a higher dietary intake of nitrates. Unlike postmenopausal women, amenorrheic athletes do not have raised bone turnover but do have reduced NO metabolites and spinal osteopenia. The results show, however, that reduced NO production is a common denominator in both conditions and further support the importance of NO in estrogen-mediated protection of skeletal mass and strength.

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
Keyword(s):  
Breast Cancer ◽  
Bone Mineral Density ◽  
Alkaline Phosphatase ◽  
Bone Mineral Content ◽  
Bone Mineral ◽  
Adjuvant Treatment ◽  
Mineral Content ◽  
Postmenopausal Breast Cancer ◽  
Mineral Density ◽  
One Year

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.

scholarly journals Reduced Bone Mineral Density and Increased Bone Metabolism Rate in Young Adult Patients with 21-Hydroxylase Deficiency

2006 ◽  
Vol 91 (11) ◽  
pp. 4453-4458 ◽  
Author(s):  
Mariateresa Sciannamblo ◽  
Gianni Russo ◽  
Debora Cuccato ◽  
Giuseppe Chiumello ◽  
Stefano Mora
Keyword(s):  
Bone Mineral Density ◽  
Alkaline Phosphatase ◽  
Bone Metabolism ◽  
Type I Collagen ◽  
Whole Body ◽  
Type I ◽  
Healthy Controls ◽  
Mineral Density ◽  
Specific Alkaline Phosphatase ◽  
Bone Specific Alkaline Phosphatase

Abstract Context: Patients with congenital adrenal hyperplasia (CAH) receive glucocorticoids as replacement therapy. Glucocorticoid therapy is the most frequent cause of drug-induced osteoporosis. Objective: The objective of the study was to evaluate bone mineral density (BMD) and bone metabolism in CAH patients. Design: This was a cross-sectional observational study. Setting: The study was conducted at a referral center for pediatric endocrinology. Patients and Other Participants: Thirty young patients with the classical form of CAH (aged 16.4–29.7 yr) treated with glucocorticoid from diagnosis (duration of treatment 16.4–29.5 yr) and 138 healthy controls (aged 16.0–30.0 yr) were enrolled. Main Outcome Measures: BMD was measured in the lumbar spine and whole body by dual-energy x-ray absorptiometry. Bone formation and resorption rates were estimated by serum measurements of bone-specific alkaline phosphatase and C-terminal telopeptide of type I collagen, respectively. Results: CAH patients were shorter than controls (women −6.8 and men −13.3 cm). Therefore, several methods were used to account for the effect of this difference on bone measurements. Whole-body BMD measurements were significantly lower, compared with controls (P &lt; 0.03), after controlling for height (on average −2.5% in females and −9.3% in male patients). No differences were found in lumbar spine measurements. Bone-specific alkaline phosphatase and C-terminal telopeptide of type I collagen serum concentrations were higher in CAH patients than control subjects (P &lt; 0.04). BMD measurements and bone metabolism markers did not correlate with the actual glucocorticoid dose or mean dose over the previous 7 yr. Conclusions: Young adult patients with the classical form of CAH have decreased bone density values, compared with healthy controls. This may put them at risk of developing osteoporosis early in life.

Bone mineral density and biochemical markers of bone metabolism in predialysis patients with chronic kidney disease

2016 ◽  
Vol 64 (4) ◽  
pp. 861-866 ◽  
Author(s):  
Nuri Fidan ◽  
Ayca Inci ◽  
Melahat Coban ◽  
Cevval Ulman ◽  
Seyhun Kursat
Keyword(s):  
Bone Mineral Density ◽  
Chronic Kidney Disease ◽  
Alkaline Phosphatase ◽  
Kidney Disease ◽  
Bone Loss ◽  
Bone Mineral ◽  
Serum Alkaline Phosphatase ◽  
Mineral Density ◽  
T Score ◽  
Z Scores

The aim of the study was to evaluate the usefulness of serum bone turnover markers (BTM) and bone mineral density (BMD) determined by dual-energy X-ray absorptiometry (DEXA) in predialysis patients with chronic kidney disease (CKD). We enrolled 83 patients with CKD, 41 (49.4%) males, 42 (50.6%) females, with mean estimated glomerular filtration rate (eGFR) 23.90±12 (range=6.0–56.0). BMD of the lumbar spine (LS) (anteroposterior, L2 through L4), femoral neck (FN) and femoral trochanter (FT) were measured by DEXA. Biochemical BTM, including calcium (Ca), phosphorus (P), intact parathyroid hormone (PTH), serum specific alkaline phosphatase (serum AP), bone-specific AP (BSAP), plasma bicarbonate and 25-hydroxy-vitamin D (25hD) were used for the prediction of BMD loss. T score results of LS and FN were worse than FT. BMD levels were lower in females than in males (all p<0.05). According to different BMD T score levels, patients with age ≥65 years and patients in menopause were significantly more osteopenic (p=0.026) and there was no relation between different BMD T scores and presence of diabetes (p=0.654). A positive correlation was identified between the BMD of FN T-Z scores (r=0.270, p=0.029, r=0.306, p=0.012), FT T-Z scores (r=0.220, p=0.076, r:0.250, p=0.043) and serum HCO3, while the correlation with serum alkaline phosphatase (AP) and BSAP was considered to be negative. No statistically significant association was found between BMD of all the measured skeletal sites and eGFR. Loss of BMD was identified mostly in females over ≥65 years of age and after menopause. Higher serum levels of BSAP and AP can be determined in the advanced stages of renal failure and they reflect fracture risk of the femur, but not spine. Measurements of BMD by DEXA are useful to demonstrate bone loss, but not technical enough to distinguish the quantity of bone loss between different stages of CKD.

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