scholarly journals Accuracy of Opportunistic Bone Mineral Density Assessment on Staging Computed Tomography for Gynaecological Cancers

Medicina ◽  
2021 ◽  
Vol 57 (12) ◽  
pp. 1386
Author(s):  
Catherine Anne O’Gorman ◽  
Sarah Milne ◽  
Gerard Lambe ◽  
Aleksandra Sobota ◽  
Peter Beddy ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Bone Mineral Density ◽  
High Risk ◽  
Bone Density ◽  
Bone Loss ◽  
Bone Mineral ◽  
Gynaecological Cancer ◽  
Mineral Density ◽  
Predictive Values ◽  
Density Assessment

Background and Objectives: Women with gynecological cancers constitute a high-risk cohort for loss of bone density. International guidance stipulates women undergoing cancer treatments associated with bone loss should have a quantitative assessment of bone density. Access to Dual-energy X-ray Absorptiometry (DXA) is limited. This study aimed to assess the accuracy of opportunistic bone density measurement on staging computed tomography (CT) scans for gynaecological malignancies, in comparison to the gold standard DXA. Materials and Methods: Women with a staging CT scan of the abdomen and pelvis for a new diagnosis of gynecological cancer were recruited. DXA was performed within 6 weeks of treatment for gynaecological cancer. Lumbar bone density was measured by CT attenuation values, in Hounsfield units (HU), of the anterior trabecular region. Correlations between CT and DXA parameters were analysed. Receiver Operating Characteristic(ROC) curves for diagnosis of low bone density and osteoporosis were analysed. Results: Final cohort included 48 of 50 women recruited. There was good diagnostic accuracy for abnormal bone density and osteoporosis, with areas under the ROC curve at L1 of 0.77 (p = 0.002) and 0.80 (p = 0.020) respectively. CT-HU of 170–190 yielded sensitivities of 87–90%, positive predictive values of 75–84% and negative predictive values of 71–75% for the diagnosis of low bone mineral density. CT-HU of 90–110 yielded specificities of 85–93% for the diagnosis of osteoporosis. Moderate correlations were found between CT-HU and both DXA T-scores and diagnostic categories. Conclusions: This is the first study to assess the opportunistic application of CT in the assessment of bone health in women with gynaecological cancer, a cohort at high-risk of osteoporosis. The correlation between bone density assessment in CT-HU and DXA, and strong AUC values for the diagnosis of low bone density (0.77) and osteoporosis (0.80) support this pragmatic solution in resolving the care-gap in cancer treatment-induced bone loss, often associated with poor access to DXA.

ANABOLIC THERAPY AND OPTIMAL TREATMENT SEQUENCES FOR PATIENTS WITH OSTEOPOROSIS AT HIGH RISK FOR FRACTURE

2020 ◽  
Vol 26 (7) ◽  
pp. 777-786 ◽  
Author(s):  
Felicia Cosman
Keyword(s):  
Bone Mineral Density ◽  
High Risk ◽  
Bone Density ◽  
Fracture Risk ◽  
Postmenopausal Women ◽  
Bone Mineral ◽  
Mineral Density ◽  
Anabolic Agents ◽  
Anabolic Therapy ◽  
Fracture Study

Objective: Provide an update regarding anabolic medications for osteoporosis, which are often considered to be the last resort for patients with osteoporosis, after multiple fractures have already occurred and other medications have already been administered. Methods: Literature review and discussion. Results: Recent pivotal trial data for anabolic agents and randomized trials comparing anabolic and antiresorptive medications suggest that three anabolic agents (teriparatide, abaloparatide, and romosozumab) reduce nonvertebral and vertebral fractures faster and to a greater extent than potent antiresorptive treatments. Furthermore, bone density accrual is maximized when patients are given anabolic agents first, followed by potent antiresorptive therapy. Since total hip bone density during or after osteoporosis treatment has emerged as an excellent surrogate for future fracture risk, attaining a greater hip bone mineral density is a treatment goal for high-risk osteoporosis patients. Conclusion: This review defines the highest-risk patients and summarizes the rationale for the evolving role of anabolic therapy in the management of postmenopausal women at high risk for fracture. Abbreviations: ACTIVE = Abaloparatide Comparator Trial in Vertebral Endpoints; ARCH = Active Controlled Fracture Study in Postmenopausal Women with Osteoporosis at High Risk; BMD = bone mineral density; FRAME = Fracture Study in Postmenopausal Women with Osteoporosis; FRAX = Fracture Risk Assessment Tool; PTH = parathyroid hormone; TBS = trabecular bone score

Outcome Of Patients With Acute Myeloid Leukemia/High Risk Myelodysplastic Syndrome Based On Bone Mineral Density: Data From a Single center 2000-2012

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5008-5008
Author(s):  
Ankit Anand ◽  
Hussam Al-sharif ◽  
Mohamed Abdelfatah ◽  
Nairmeen Haller ◽  
Ali Al-Ameri
Keyword(s):  
Bone Mineral Density ◽  
Acute Myeloid Leukemia ◽  
Survival Analysis ◽  
High Risk ◽  
Bone Density ◽  
Bone Mineral ◽  
Myeloid Leukemia ◽  
X Rays ◽  
Mineral Density ◽  
Acute Myeloid

Abstract Background Acute myeloid leukemia results from clonal proliferation of myeloid precursors, resulting in accumulation of leukemic blasts in the bone marrow. The effect of leukemic blasts in the bone have not been well studied. It is hypothesized that leukemic blasts may affect the osteoblast and osteoclast balance. Aim The aim of this study is to describe the effect of osteoporosis/osteopenia on the survival of patients with AML/ high risk MDS Methods A retrospective study of all AML and high-risk MDS patients treated at Akron General Medical Center, Ohio during 2001-2012. Following IRB approval, patients' charts were reviewed for information on demographics, cytogenetics, and treatment. Patients were classified into low risk, intermediate risk and high risk MDS based on WHO criteria. Charts were reviewed for a diagnosis of osteoporosis/osteopenia. Overall survival rates were determined by Kaplan-Meier survival analysis. Patients were classified into osteopenia/osteoporosis based on bone density scans. An additional three patients were identified with osteopenia on the basis of lumbar X rays and one patient was diagnosed with osteoporosis on the basis of typical compression fracture for osteoporosis. Results During the study period, 187 patients were identified with AML/high risk MDS. A total of 31 patients were found to have osteopenia/osteoporosis based on radiological findings. Eight patients had osteoporosis and 24 patients had osteopenia. A survival analysis was performed on the study population based on bone mineral density. Group one (osteoporosis) included eight patients; group two (osteopenia) included 23 patients and group three (no radiological evidence of osteoporosis/osteopenia) included 156 patients. Results are depicted in the survival curve below. Conclusions Bone mineral density remains an unidentified factor in patient's survival, suffering from AML/ High risk MDS. It appears that patients with normal bone density may live longer than patients with osteopenia/osteoporosis, but this is not confirmed here statistically. Future studies with a larger patient sample may be helpful in further exploring this aspect and the role of bisphosphonates in patients with AML/high risk MDS. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Effect of Endocrine Therapies on Bone in Breast Cancer Patients

2011 ◽  
Vol 96 (2) ◽  
pp. 308-319 ◽  
Author(s):  
R. J. Santen
Keyword(s):  
Breast Cancer ◽  
Bone Mineral Density ◽  
Estrogen Receptor ◽  
Bone Density ◽  
Bone Loss ◽  
Bone Formation ◽  
Postmenopausal Women ◽  
Bone Mineral ◽  
Mineral Density ◽  
Markers Of Bone Formation

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.

scholarly journals Effect of Endocrine Therapies on Bone in Breast Cancer Patients

Endocrinology ◽  
2011 ◽  
Vol 152 (1) ◽  
pp. 332-332
Author(s):  
R. J. Santen
Keyword(s):  
Breast Cancer ◽  
Bone Mineral Density ◽  
Bone Density ◽  
Bone Loss ◽  
Bone Formation ◽  
Postmenopausal Women ◽  
Bone Mineral ◽  
Breast Cancer Patients ◽  
Mineral Density ◽  
Markers Of Bone Formation

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.

scholarly journals Profiles of Endogenous Circulating Cortisol and Bone Mineral Density in Healthy Elderly Men1

1999 ◽  
Vol 84 (9) ◽  
pp. 3058-3063 ◽  
Author(s):  
E. Dennison ◽  
P. Hindmarsh ◽  
C. Fall ◽  
S. Kellingray ◽  
D. Barker ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Lumbar Spine ◽  
Bone Density ◽  
Bone Loss ◽  
Bone Mineral ◽  
Loss Rate ◽  
Cortisol Concentration ◽  
Mineral Density ◽  
Healthy Elderly ◽  
Bone Loss Rate

Exogenous glucocorticoids are known to increase the risk of osteoporosis. However, the contribution made by endogenous circulating cortisol concentrations to adult skeletal status remains unknown. We examined this issue in a sample of 34 healthy men, aged 61–72 yr. Venous blood samples were obtained under standard conditions every 20 min over a 24-h period. Measurements were made of serum cortisol and cortisol-binding globulin. Bone mineral density was measured at the lumbar spine and proximal femur using dual energy x-ray absorptiometry. Measurements were made at baseline and 4 yr later. There was a weak negative association between integrated cortisol concentration and lumbar spine bone density (r = −0.37; P < 0.05); similar relationships (P < 0.05) existed at three of five proximal femoral sites. There were also statistically significant positive associations between the trough cortisol concentration and bone loss rate at the lumbar spine (r = 0.38; P < 0.05), femoral neck (r = 0.47; P < 0.001), and the trochanteric region (r = 0.41; P = 0.02) over the 4-yr follow-up period. The cross-sectional relationships between cortisol concentration and bone density were removed by adjustment for body mass index, but the influence on bone loss rate remained significant after adjusting for adiposity, cigarette smoking, alcohol consumption, dietary calcium intake, physical activity, and serum testosterone and estradiol levels. These observations suggest that the endogenous cortisol profile of healthy elderly men is a determinant of their bone mineral density and their rate of involutional bone loss.

Treatment of Osteopenia/Osteoporosis in Pediatric Hematopoietic Cell Transplantation.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 57-57
Author(s):  
Jean E. Sanders ◽  
Paul A. Hoffmeister ◽  
Barry E. Storer
Keyword(s):  
Bone Mineral Density ◽  
Bone Density ◽  
Bone Loss ◽  
Cell Transplantation ◽  
Bone Mineral ◽  
Hematopoietic Cell Transplantation ◽  
Chronic Gvhd ◽  
Time Interval ◽  
Z Score ◽  
Mineral Density

Abstract The bone mineral density during childhood and the teen years is an important determinate of adult bone health. Decreased bone mineral density has been found to be a relatively common complication following adult hematopoietic cell transplantation (HCT), but has not been well studied after HCT among pediatric patients. Not surprisingly, an effective therapeutic approach to decreased bone mineral density has also not been developed for children. Patients and Methods: The records of 196 children <18 years of age who received HCT between 1/97-6/03 who survived for 1 year or more after HCT were reviewed. Patients selected for analysis had decreased bone mineral density (Z-score of <-1 standard deviation (SD) corrected for patient sex and age) and 2 or more bone mineral density (DEXA) scans performed after HCT. Change in bone density was calculated as the difference in L2-4 lumbar spine SD score. Variables associated with change in bone density were analyzed. Results: Among the 143 patients who had a DEXA scan performed, 82 (57%) demonstrated bone loss defined as <-1 SD Z-score. Fifty-six (68%) of these 82 patients had two or more DEXA scans and were analyzed. These 56 patients received an HCT when they were a median 10.8 (1.1–17.9) years of age, 33 were male, and 40 had chronic GVHD treated with corticosteroids and calcinurin inhibitor therapy. Patients were grouped according to treatment received for the bone loss. Nine patients changed therapy and were analyzed twice in separate treatment categories, hence there were 65 patients in 3 groups: 16 received a bisphosphonate or calcitonin (B/C), 37 calcium supplement only, and 12 no therapy. The B/C group included patients receiving pamidronate, zometa, fosamax, or calcitonin. Baseline median Z-scores were −2.6 SD for the B/C group, −2.2 SD for calcium, and −1.4 SD for no therapy. The median length of therapy was 446 days for the B/C group and 365 days for the calcium group. For the no therapy group, the time interval between DEXA scans was 324 days. Treatment with B/C or calcium compared with no therapy was significantly associated with improved bone density (p=0.0004). Corticosteroids, length of corticosteroid therapy (months), presence of chronic GVHD, gender, TBI received in preparative regimen, and patient age at therapy were not associated with change in bone mineral density. The mean change in bone mineral density per year was +1.16 SD for the B/C group, +0.16 for calcium, and +0.52 for no therapy. Although not statistically significant (p=0.44), concomitant steroid use for more than half the time interval between DEXA scans decreased therapeutic gains in the B/C group by −0.59 SD/year and −0.38 SD/year for the calcium group. The only observed side effect was hypocalcemia in one patient receiving pamidronate. Conclusions: These data demonstrate that the greatest improvement in bone mineral density was observed in patients receiving a bisphosphonate or calcitonin. Minimal to no toxicity was observed.

scholarly journals Cancer Treatment–Induced Bone Loss and Role of Denosumab in Nonmetastatic Prostate Cancer: A Narrative Review

2021 ◽  
Vol 42 (03) ◽  
pp. 240-246
Author(s):  
Deepak Dabkara
Keyword(s):  
Prostate Cancer ◽  
Bone Mineral Density ◽  
High Risk ◽  
Bone Loss ◽  
Cancer Patients ◽  
Bone Mineral ◽  
Subcutaneous Administration ◽  
Narrative Review ◽  
Mineral Density ◽  
Dose Modifications

AbstractBone loss is an important complication of prostate cancer and its associated treatments, especially androgen-deprivation therapy (ADT). There is a 5 to 10 times increased loss of bone mineral density (BMD) in men receiving ADT with yearly 4 to 13% BMD loss. The risk of fracture increases yearly by 5 to 8% with ADT. ADT associated bone loss of 10 to 15% of BMD doubles the risk of fractures. Hence, BMD evaluation through dual-energy X-ray absorptiometry and evaluation of individual fracture risk assessed before initiating ADT. The use of vitamin D, calcium, bisphosphonates, and denosumab has shown improved bone health in men with prostate cancer receiving ADT. Denosumab 60 mg is approved to increase bone mass in men at high risk for fractures receiving ADT for nonmetastatic prostate cancer. Denosumab has shown improvement of 5.6% BMD at 2 years in nonmetastatic prostate cancer patients, with significant improvements seen at the total hip, femoral neck, and distal third of the radius. Denosumab has shown a 62% decreased incidence of new vertebral fractures at 36 months. Furthermore, denosumab delays the onset of bone metastases in high-risk nonmetastatic prostate cancer patients. Denosumab can be preferred over other bone modifying agents owing to several advantages, such as subcutaneous administration and no requirement of hospitalization, no dose modifications in renal impairment and less incidence of acute phase anaphylactic reactions. We review the available evidence of denosumab for managing bone loss in nonmetastatic prostate cancer patients. The relevant articles used in this narrative review were obtained through general search on google and PubMed using the key terms “non-metastatic prostate cancer,” “denosumab,” “bone loss,” “bone mineral density,” “fracture,” “CTIBL,” and “chemotherapy induced bone loss.”

Impaired Estrogen Sensitivity in Bone by Inhibiting Both Estrogen Receptor a and b Pathways*

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Bone Mineral Density ◽  
Estrogen Receptor ◽  
Bone Loss ◽  
Bone Turnover ◽  
Bone Mineral ◽  
Female Rats ◽  
Wild Type ◽  
Mineral Density ◽  
Transgenic Rats ◽  
Estrogen Sensitivity

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.

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