scholarly journals Impact of Tenofovir-Based Pre-exposure Prophylaxis on Biomarkers of Bone Formation, Bone Resorption, and Bone Mineral Metabolism in HIV-Negative Adults

2019 ◽  
Vol 6 (10) ◽  
Author(s):  
Thomas L Nickolas ◽  
Michael T Yin ◽  
Ting Hong ◽  
Kenneth K Mugwanya ◽  
Andrea D Branch ◽  
...  
Keyword(s):  
Bone Remodeling ◽  
Bone Mineral ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Separate Analysis ◽  
Mineral Density ◽  
Bone Mineral Metabolism ◽  
Exposure Prophylaxis ◽  
The Impact ◽  
Hiv Negative

Abstract Background Pre-exposure prophylaxis (PrEP) with emtricitabine (FTC)/tenofovir disoproxil fumarate (TDF) reduces the risk of HIV seroconversion but may promote bone mineral density (BMD) decline. The mechanisms of BMD decline with FTC/TDF remain unclear, and studies in HIV-positive individuals have been confounded by the effects of HIV and concomitant antiretroviral medications. We evaluated the impact of FTC/TDF on biomarkers of bone remodeling and bone mineral metabolism in HIV-negative men and women enrolled in the Partners PrEP Study. Methods In a random sample of HIV-negative participants randomized to FTC/TDF PrEP (n = 50) or placebo (n = 50), serum parathyroid hormone (PTH), bone biomarkers (C-telopeptide, procollagen 1 intact N-terminal propeptide, and sclerostin), and plasma fibroblast growth factor 23 were measured at baseline and month 24, and the percentage change was compared between groups. In a complementary analysis, we compared the change in biomarkers between participants with and without a 25% decline in glomerular filtration rate (GFR) on FTC/TDF. Results Baseline characteristics were similar between the groups (median age, 38 years; 40% women). Vitamin D insufficiency was common, but baseline GFR and PTH were in the normal range. We observed a significantly greater percent increase in serum C-telopeptide in participants randomized to FTC/TDF vs placebo (P = .03), suggesting an increase in bone remodeling. We observed no differences in the other biomarkers, or in a separate analysis comparing participants with and without a decline in GFR. Conclusions Increased bone remodeling may mediate the BMD decline observed with tenofovir-containing PrEP and antiretroviral therapy, independent of a TDF-mediated decrease in kidney function.

scholarly journals Low Magnesium Exacerbates Osteoporosis in Chronic Kidney Disease Patients with Diabetes

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Jui-Hua Huang ◽  
Fu-Chou Cheng ◽  
Hsu-Chen Wu
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Mineral ◽  
Mineral Metabolism ◽  
Inverse Correlation ◽  
Mineral Density ◽  
Lower Serum ◽  
Patients With Diabetes ◽  
The Impact ◽  
Low Serum

The aim of this study is to investigate the impact of serum Mg on bone mineral metabolism in chronic kidney disease (CKD) patients with or without diabetes. A total of 56 CKD patients not receiving dialysis were recruited and divided into two groups, one group of 27 CKD patients with diabetes and another group of 29 CKD patients without diabetes. Biochemical determinations were made, and the estimated glomerular filtration rate (eGFR) was measured. Bone mineral density was measured by dual-energy X-ray absorptiometry. Serum Mg was inversely correlated with serum CaP=0.023and positively correlated with serum parathyroid hormone (PTH)P=0.020, alkaline phosphataseP=0.044, and phosphateP=0.040in the CKD patients with diabetes. The CKD patients with diabetes had lower serum albumin and a higher proportion of hypomagnesemia and osteoporosis than the nondiabetic patients didP<0.05. Serum Mg was inversely correlated with eGFR in the CKD patients with or without diabetesP<0.05. Serum Mg showed an inverse correlation with 25-hydroxyvitamin D in CKD patients without diabetesP=0.006. Furthermore, the diabetic CKD patients with low serum Mg had a lower iPTHP=0.007and a higher serum Ca/Mg ratioP<0.001than the other CKD patients. The lower serum Mg subgroup showed a higher incidence of osteoporosis than the moderate and higher serum Mg subgroups did (66.7%, 39.4%, and 29.4%, resp.). In conclusion, low serum Mg may impact iPTH and exacerbates osteoporosis in CKD patients, particularly with diabetes.

scholarly journals Alteration in Bone Mineral Metabolism in Children with Acute Lymphoblastic Leukemia (ALL): A Review

2009 ◽  
Vol 1 (1) ◽  
pp. 29
Author(s):  
Chowdhury Yakub Jamal
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Bone Mineral ◽  
Late Effects ◽  
Mineral Metabolism ◽  
Lymphoblastic Leukemia ◽  
Prostaglandin E ◽  
Mineral Density ◽  
Metabolic Alterations ◽  
Bone Mineral Metabolism ◽  
Pediatric Cancer Patients

<p>In recent years there has been a significant increase in event free survival (EFS) and overall survival in children with cancer. As survival rates for childhood cancer have radically improved, late effects associated with the successful but highly intensive chemotherapy and/or radiotherapy have dramatically increased. Many possible late effects of cancer treatment are recognized in pediatric cancer patients as infertility, endocrine deficiency, renal failure, pulmonary and cardiac toxicity, obesity and osteopenia/osteoporosis. Decreased bone mineral density (BMD) and bone metabolism disturbances have been recognized and reported in literature. Osteopenia/osteoporosis skeletal abnormalities, osteonecrosis and pathological fractures are known to occur frequently in childhood acute lymphoblastic leukemia (ALL) at diagnosis, during and after treatment with chemotherapy. Various studies have revealed different metabolic alterations related to ALL. Some suggestions have been made about their relationship with the disease process. Various metabolic abnormalities may be encountered in the newly diagnosed ALL patients. It includes decreased and increased serum levels of calcium and phosphate. Hypercalcemia may result from leukemic infiltrations of bone and release of parathormone like substance from lymphoblast. Elevated serum phosphate can occur as a result of leukemic cell lysis and may induce hypocalcemia. It has been postulated by other authors that leukemic cells may directly infiltrate bone and produce parathroid hormone related peptides, prostaglandin E and osteoblast inhibiting factors. Hypomagnesemia, hypocalcaemia and hypothyroidisum have been demonstrated in patients with ALL. Some patients may have poor nutrition and decreased physical activities during treatment. However postulations have also been made that chemotherapy may play a role in creating metabolic alterations in children with ALL. Corticosteroid, methotraxate and cranial irradiations have all been assumed as a cause of loss of bone mass. Continuing chemotherapy in children with ALL was assumed with normal growth and normal or high collagen turnover and reduced alkaline phosphatase or impaired osteoblastic activity on mineralization of bone. Considering the derangements in bone mineral metabolism in ALL at diagnosis or with chemotherapy, it is imperative that specific attention and therapeutic measures should be considered.</p><p>DOI: 10.3329/bsmmuj.v1i1.3695</p> <p><em>BSMMU J </em>2008; 1(1): 29-32</p>

MO199DENOSUMAB: NOVEL APPROACH TO TREATMENT OF OSTEOPOROSIS IN RENAL DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Rosita Greco ◽  
Agata Mollica ◽  
Francesco Zincone ◽  
Teresa Papalia
Keyword(s):  
Bone Mineral Density ◽  
Renal Disease ◽  
Bone Mineral ◽  
Renal Allograft ◽  
Mineral Metabolism ◽  
Transplant Recipients ◽  
Mineral Density ◽  
Anca Vasculitis ◽  
T Score ◽  
Bone Mineral Metabolism

Abstract Background and Aims Denosumab is a fully human monoclonal antibody to the receptor activator of nuclear factor kappa-B ligand (RANKL), an osteoclast differentiating factor. It inhibits osteoclast formation, decrease bone resorption, increase bone mineral density (BMD), and reduce the risk of fracture. There is no restriction of its use in patients with renal disease, for whom biphosphonates are considered controindicated. The aim of our study was to evaluate the effectiveness in reducing facture risk and safety of Denosumab in patients with Osteoporosis and renal disease. Method This is a prospective analysis of 17 patients with Osteoporosis (average T-score below -2.5) admitted to our Nephrology Department for CKD in the last four years. in Vasculitis, Renal Allograft Recipients. Patients with severe Hyperparatiroidism were excluded. We estimated creatinine clearance (eGFR) using Cockcroft-Gault and classified levels of kidney function using the modified National Kidney Foundation classification of CKD. All patients were adequately supplemented with calcium and vitamin D before and while taking Denosumab 60 mg every 6 months. The primary endpoint is the change in bone mineral density (BMD) at one and two years. Secondary endpoints include changes in bone mineral metabolism parameters (Ca, P, PTHi, 25-OH VitD), incidence of fractures, and renal/allograft fuction at one and two years. Results The mean age was 52.5±4 years and 8/17 (47%) were females. N.13 patients (76.5%) were renal transplant recipients (RTR) on standard triple immunosoppression including steroids (prednisone 5 mg/day), CNI and MMF, with average eGFR 65.7±12.5 ml/min. N.2 patients (11.75%) were in hemodialysis. N.2 patients (11.75%) with Anca Vasculitis on steroid therapy and average eGFR 35.6±7.2 ml/min. All patients enrolled were with a BMD T-score of greater than -4.0 and less than -2.5. Only 2 patients had a history of fractures confirmed by a radiology report. Baseline parameters: calcium 9.8±0.32 mg/dl, phosphate 3.9±0.8 mg/dl, PTHi 137±91.0 ng/L, 25-OH VitD 18.3±8.9 ng/mL. From baseline at 1 month there were an increase in PTH and a decrease in calcemia in only 2 transplant recipients (CKD II and IV), that improved with an increased dose of Vit D. There were no significant difference in baseline bone mineral metabolism parameters to year 1 and 2 in all other patients. We found no difference in eGFR and proteinuria from baseline to 1 and 2 years in RTR and ANCA vasculitis. Significant improvement in T-score was observed at 1 year and 2 years (&lt; -1) in all patients. No one discontinued therapy for adverse events. Conclusion Denosumab may have advantages in patients with kidney dysfunction, because not excreted by the kidney and there is no need for dose adjustment. This prospective study showed a significant improvement in osteoporosis (at Dexa mean T-score ≤ -1), but particular attention should be paid to ensuring that patients are calcium and Vitamin D replete.

scholarly journals Bone mineral density in children with juvenile idiopathic arthritis after one year of treatment with etanercept

2018 ◽  
Vol 146 (5-6) ◽  
pp. 297-302
Author(s):  
Gordana Susic ◽  
Marija Atanaskovic ◽  
Roksanda Stojanovic ◽  
Goran Radunovic
Keyword(s):  
Bone Mineral Density ◽  
Juvenile Idiopathic Arthritis ◽  
Rheumatoid Factor ◽  
Bone Mineral ◽  
Mineral Metabolism ◽  
Z Score ◽  
Mineral Density ◽  
Bone Mineral Metabolism ◽  
Systemic Jia ◽  
One Year

Introduction/Objective. Juvenile idiopathic arthritis (JIA) is the most frequent chronic inflammatory, rheumatic disease of childhood, associated with disturbance of bone mineral metabolism, which develops gradually and progressively, and if untreated eventually leads to osteoporosis in adulthood. The aim of our study was to evaluate bone mineral density (BMD) in patients with JIA treated with etanercept over a period of one year. Methods. The prospective cohort study included 94 JIA patients (66 female, 28 male), their median age being 14.77 years. BMD was measured by dual-energy X-ray absorptiometry on the lumbar spine. Disease activity was assessed using the American College of Rheumatology Pedi 50 criteria. Results. After one year of treatment with etanercept, we found a statistically significant increment in all osteodensitometry variables (p < 0.001). Annual enhancement for the whole group was as follows: bone mineral content 15.8%, BMD 7.2%, BMDvol 4.2%. Z-score improved from -0.86 to -0.58 SD at the last visit, but decreased in rheumatoid factor-positive polyarthritis patients. Patients with systemic JIA had the lowest Z-score. Z-score correlated with functional disability level. BMD was lower in the group treated with glucocorticoids. Conclusion. Our results showed significant improvement of bone mineral density in children with JIA after one year of treatment with etanercept. Rheumatoid factor-positive and systemic JIA subtypes and treatment with glucocorticoids are the risk factors for impairing bone mineral metabolism.

Bone mineral metabolism, bone mineral density in patients with chronic pancreatitis

Pancreatology ◽  
2016 ◽  
Vol 16 (4) ◽  
pp. S107
Author(s):  
Ancuta Didita ◽  
Mihaela Dranga ◽  
Irina Ungureanu ◽  
Cristina Cijevschi Prelipcean ◽  
Catalina Mihai
Keyword(s):  
Bone Mineral Density ◽  
Chronic Pancreatitis ◽  
Bone Mineral ◽  
Mineral Metabolism ◽  
Mineral Density ◽  
Bone Mineral Metabolism

scholarly journals How Physical Activity across the Lifespan Can Reduce the Impact of Bone Ageing: A Literature Review

2020 ◽  
Vol 17 (6) ◽  
pp. 1862 ◽  
Author(s):  
Maria Felicia Faienza ◽  
Giuseppe Lassandro ◽  
Mariangela Chiarito ◽  
Federica Valente ◽  
Loredana Ciaccia ◽  
...  
Keyword(s):  
Physical Activity ◽  
Physical Exercise ◽  
Bone Remodeling ◽  
Bone Mineral ◽  
Oxygen Species ◽  
Mineral Density ◽  
Physiological Mechanisms ◽  
Control Bone ◽  
The Impact ◽  
Bone Ageing

Bone remodeling is a lifelong process, due to the balanced activity of the osteoblasts (OBs), the bone-forming cells, and osteoclasts (OCs), the bone-resorbing cells. This equilibrium is mainly regulated by the WNT-ß-cathenin pathway and the RANK-RANKL/OPG system, respectively. Bone ageing is a process which normally occurs during life due to the imbalance between bone formation and bone resorption, potentially leading to osteoporosis. Bone loss associated with bone ageing is determined by oxidative stress, the result of the increasing production of reactive oxygen species (ROS). The promotion of physical exercise during growth increases the chances of accruing bone and delaying the onset of osteoporosis. Several studies demonstrate that physical exercise is associated with higher bone mineral density and lower fracture incidence, and the resulting bone mineral gain is maintained with ageing, despite a reduction of physical activity in adulthood. The benefits of exercise are widely recognized, thus physical activity is considered the best non-pharmacologic treatment for pathologies such as osteoporosis, obesity, diabetes and cardiovascular disease. We reviewed the physiological mechanisms which control bone remodeling, the effects of physical activity on bone health, and studies on the impact of exercise in reducing bone ageing.

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