scholarly journals Bone disease in hypoparathyroidism

2014 ◽  
Vol 58 (5) ◽  
pp. 545-552 ◽  
Author(s):  
Bart L. Clarke

Hypoparathyroidism is a rare disorder that may be acquired or inherited. Postsurgical hypoparathyroidism is responsible for the majority of acquired hypoparathyroidism. Bone disease occurs in hypoparathyroidism due to markedly reduced bone remodeling due to the absence or low levels of parathyroid hormone. Chronically reduced bone turnover in patients with hypoparathyroidism typically leads to higher bone mass than in age- and sex-matched controls. Whether this increased bone density reduces fracture risk is less certain, because while increased bone mineralization may be associated with increased brittleness of bone, this does not appear to be the case in hypoparathyroidism. Treatment of hypoparathyroidism with recombinant parathyroid hormone may reduce bone mineral density but simultaneously strengthen the mechanical properties of bone.

2012 ◽  
Vol 6 (1) ◽  
pp. 458-463 ◽  
Author(s):  
Yvonne Haba ◽  
Tobias Lindner ◽  
Andreas Fritsche ◽  
Ann-Kristin Schiebenhöfer ◽  
Robert Souffrant ◽  
...  

The objective of this study was to analyse retrieved human femoral bone samples using three different test methods, to elucidate the relationship between bone mineral density and mechanical properties. Human femoral heads were retrieved from 22 donors undergoing primary total hip replacement due to hip osteoarthritis and stored for a maximum of 24 hours postoperatively at + 6 °C to 8 °C. Analysis revealed an average structural modulus of 232±130 N/mm2 and ultimate compression strength of 6.1±3.3 N/mm2 with high standard deviations. Bone mineral densities of 385±133 mg/cm2 and 353±172 mg/cm3 were measured using thedual energy X-ray absorptiometry (DXA) and quantitative computed tomography (QCT), respectively. Ashing resulted in a bone mineral density of 323±97 mg/cm3. In particular, significant linear correlations were found between DXA and ashing with r = 0.89 (p < 0.01, n = 22) and between structural modulus and ashing with r = 0.76 (p < 0.01, n = 22). Thus, we demonstrated a significant relationship between mechanical properties and bone density. The correlations found can help to determine the mechanical load capacity of individual patients undergoing surgical treatments by means of noninvasive bone density measurements.


2021 ◽  
Vol 12 (1) ◽  
pp. 676-682
Author(s):  
Ahmed I Ansaf ◽  
Safa A Faraj ◽  
Rahan A Mohammed

Thalassemia is an inherited disorder causing an imbalance in the development of the globin chain with ineffective erythropoiesis and increased peripheral consumption. Expansion of bone marrow decreases bone mineral density. Bone disease in thalassemia is manifested as diffuse bone pain, scoliosis, spinal deformities, nerve compression, spontaneous fracture. Bone Mineral Density (BMD) is a useful indicator for bone monitoring and assessment and significant predictor of bone disease in thalassemia. The purpose of this study is to evaluate Bone Mineral Density in thalassemia patients and its correlation with other factors. The study was conducted in Hematology Center at Al-Karama Teaching Hospital, Wasit, Iraq, from the first of January to the thirty of April 2019. Fifty-eight thalassemia patients were enrolled in this study. Bone mineral density was assessed using Dual-Energy X-ray Absorptiometry technique (DEXA scan) for the lumber spine (L1-L4) at the Dexa unit in the rehabilitation Center in KUT. The patients were divided according to BMD by Z-Score ≤ 15 years old patients, T score for adults (>15 years old) into three groups: a score ≥ -1 defined as Normal BMD, Osteopenia (between −1 and −2.5 SD), and Osteoporosis (below −2.5 SD). The effect of Gender, Age, frequency of blood transfusion, Hb level, Serum Calcium, and Serum Ferritin on BMD was evaluated. Young patients (with age equal to or younger than 15 years) showed lower bone density than older patients. Also, Patients with Suboptimal blood transfusion had lower bone density than patients than good compliance blood transfusion program, P-value 0.001, 0.012, respectively. The results indicated a direct relationship between the age of the thalassemia patients and bone mass density, P-value = 0.0001, Pearson Correlation = 0.7. Low bone density was reported in young age and suboptimal blood transfusion.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4989-4989
Author(s):  
Tamara Berno ◽  
Kenneth Boucher ◽  
Fenghuang Zhan ◽  
Guido J. Tricot ◽  
Benjamin Mughal ◽  
...  

Abstract Abstract 4989 Background: Bone disease is present at diagnosis in almost all patients with multiple myeloma (MM) and can impact substantially on patient morbidity and quality of life. Decreased bone mineral density is also observed not only in MM but also in patients with monoclonal gammopathy of undetermined significance (MGUS). The pathogenesis of bone disease in MM is complex. The activity of proteasome inhibitor bortezomib has been linked to increased bone formation and osteoblastic activation. Evidence from the available clinical data indicates that bortezomib has a positive impact on bone health in MM and demonstrates a bone anabolic effect. Methods: We analyzed retrospectively 53 patients with MM and 16 with MGUS who have completed bone density at least at diagnosis. 21 patients have completed two bone density (3 MGUS and 18 MM). The bone density was obtained in all patients at baseline and in 16 patients repeated after bortezomib treatement with a median time of bortezomib exposure of 6 months. We analyzed T-score values at lumbar spine and at femoral neck. Results: With a median age of 66 years, 41 male and 28 female were analyzed. At baseline the mean lumbar spine T-score of all subjects and of 16 MM treated with bortezomib was -0.50 and -0.76 respectively. At baseline the mean femoral neck T-score for all subjects and for 16 MM treated with Bortezomib was -1.56 and -1.31 respectively. The baseline mean lumbar spine T-score for MGUS and MM was -0.71 and -0.43 respectively. The baseline mean femoral neck T-score of MGUS and MM was -1.61 and -1.54 respectively. In the group of 16 patients treated with Bortezomib we observed from baseline a change in lumbar bone mineral density T-score of 0.36 and at femoral neck bone density T-score of 0.25. Conclusion: These data show that patients treated with proteasome inhibitor showed moderate increment in bone mineral density at lumbar spine and at femoral neck. Disclosures: No relevant conflicts of interest to declare.


1996 ◽  
Vol 89 (8) ◽  
pp. 457-461 ◽  
Author(s):  
D J Torgerson ◽  
C Donaldson ◽  
D M Reid

Bone mineral density measurements have been criticized on the grounds that they are not a worth-while screening tool. In this paper we argue that bone mineral measurements can be an efficient diagnostic tool even if they are not of proven value for screening. There is complex relationship between the costs of a measurement, the intervention and the predictive value of the test all of which must be accounted for when assessing the value of a bone density measurement. For bone density measurements to be used for screening, a wider evaluation needs to be undertaken compared with that for their use as a diagnostic tool. We address some common objections, for example, that low compliance with screening would undermine efficiency, and show that these are not relevant. Evaluations of screening need to address issues that are likely to affect efficiency.


Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
Mahrukh Khalid ◽  
Vismay Deshani ◽  
Khalid Jadoon

Abstract Background/Aims  Vitamin D deficiency is associated with more severe presentation of primary hyperparathyroidism (PTHP) with high parathyroid hormone (PTH) levels and reduced bone mineral density (BMD). We analyzed data to determine if vitamin D levels had any impact on PTH, serum calcium and BMD at diagnosis and 3 years, in patients being managed conservatively. Methods  Retrospective analysis of patients presenting with PHPT. Based on vitamin D level at diagnosis, patients were divided into two groups; vitamin D sufficient (≥ 50 nmol/L) and vitamin D insufficient (≤ 50 nmol/L). The two groups were compared for age, serum calcium and PTH levels at diagnosis and after mean follow up of 3 years. BMD at forearm and neck of femur (NOF) was only analyzed in the two groups at diagnosis, due to lack of 3 year’s data. Results  There were a total of 93 patients, 17 males, mean age 70; range 38-90. Mean vitamin D level was 73.39 nmol/L in sufficient group (n = 42) and 34.48 nmol/L in insufficient group (n = 40), (difference between means -38.91, 95% confidence interval -45.49 to -32.33, p &lt; 0.0001). There was no significant difference in age, serum calcium and PTH at the time of diagnosis. After three years, there was no significant difference in vitamin D levels between the two groups (mean vitamin D 72.17 nmol/L in sufficient group and 61.48 nmol/L in insufficient group). Despite rise in vitamin D level in insufficient group, no significant change was observed in this group in PTH and serum calcium levels. BMD was lower at both sites in vitamin D sufficient group and difference was statistically significant at NOF. Data were analyzed using unpaired t test and presented as mean ± SEM. Conclusion  50% of patients presenting with PHPT were vitamin D insufficient at diagnosis. Vitamin D was adequately replaced so that at 3 years there was no significant difference in vitamin D status in the two groups. Serum calcium and PTH were no different in the two groups at diagnosis and at three years, despite rise in vitamin D levels in the insufficient group. Interestingly, BMD was lower at forearm and neck of femur in those with sufficient vitamin D levels and the difference was statistically significant at neck of femur. Our data show that vitamin D insufficiency does not have any significant impact on PTH and calcium levels and that vitamin D replacement is safe in PHPT and does not impact serum calcium and PTH levels in the short term. Lower BMD in those with adequate vitamin D levels is difficult to explain and needs further research. Disclosure  M. Khalid: None. V. Deshani: None. K. Jadoon: None.


2012 ◽  
Vol 25 (3) ◽  
pp. 331-340 ◽  
Author(s):  
Susan Ziglar ◽  
Tracy S. Hunter

Maximizing bone mass in youth is touted as the best strategy to offset the natural losses of aging and the menopausal transition. Not achieving maximum peak bone mineral density (BMD) is an independent risk factor for osteoporosis and thus a public health concern. Adolescence is a critical time of bone mineralization mediated by endogenous estradiol. Research has shown that the highest velocity of bone mass accrual occurs 1 year before menarche and after the first 3 years. Low-peak attainment of BMD in young women is associated with contributing factors such as diets low in calcium, eating disorders, lack of exercise, smoking, and low estrogen states. Oral contraceptives (OCs) suppress endogenous estradiol production by suppressing the hypothalamic–pituitary–ovarian axis. Thus, OCs, by replacing endogenous estradiol with ethinyl estradiol (EE), establish and maintain new hormone levels. The early initiation and the use of very low dose of EE raises the possibility that bone mass accrual at a critical time of bone mineralization in young women or adolescents may be jeopardized. This review examines the studies of BMD in adolescents and young women that use combination hormonal contraception. Some studies had inherent limitations, such as small trial, poor control of confounders, failure to exclude women with prior use of hormonal contraceptives, or prior pregnancy from control groups. The vast majority of reviewed studies showed OCs containing 20 to 30 µg of EE interfere with acquisition of peak BMD. Limited numbers of studies examine the effects of OCs containing 35 µg on adolescents and young adults. Additionally, studies are needed evaluating the progestin component of OCs as their differing androgenic properties may affect bone mineralization as well.


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