Long Term Dialysis with Low-Calcium Solution (1.0 Mmol/L) in Capd: Effects on Bone Mineral Metabolism

1996 ◽  
Vol 16 (3) ◽  
pp. 260-268 ◽  
Author(s):  
Thomas Weinreich ◽  
Eberhard Ritz ◽  
Jutta Passlick-Deetjen ◽  
A. Colombi ◽  
H.H. Echterhoff ◽  
...  
Keyword(s):  
Bone Mineral ◽  
Serum Calcium ◽  
Mineral Metabolism ◽  
Phosphate Binders ◽  
Mineral Density ◽  
Bone Mineral Metabolism ◽  
Upper Limit ◽  
Low Calcium ◽  
Dialysate Calcium

Objective Peritoneal dialysate solutions with conventionally high-calcium (Ca) concentrations (1.75 mmol/L) are now widely replaced by solutions with a lower, more physiological calcium content to prevent hypercalcemia in patients treated with oral calcium-containing phosphate binders and/or calcitriol. While there is still debate on how far the dialysate calcium should be lowered (1.25 mmol/L or less), little information is available concerning the effects of a long-term treatment with low-calcium solutions on secondary hyperparathyroidism and bone mineral metabolism in general. Design A prospective, randomized, controlled multicenter study to compare the effects of low-calcium (LCa, dialysate calcium 1.0 mmol/L) versus standard calcium dialysate solution (SCa, dialysate calcium 1.75 mmol/L)on bone mineral metabolism in continuous ambulatory peritoneal dialysis (CAPD) patients over 2 years of treatment. Setting Nephrology and dialysis units of primary and tertiary hospitals in Germany and Switzerland. Patients All CAPD patients in the participating centers between 18 and 80 years of age, stable on CAPD for at least 1 month, free of aluminum bone disease or prior parathyroidectomy were invited to enter the study. Sixty-four patients could be randomly allotted to LCa (n = 35) or SCa (n = 29) treatment in a 2-year protocol; 34 finished the study as planned. Interventions Calcium carbonate (CaCO3) was given as oral phosphate binder to maintain serum phosphate <2.0 mmol/L. If hypercalcemia supervened, CaCO3 was exchanged stepwise for aluminium hydroxide (AI(OH)3)’ until normocalcemia was obtained. Patients received calcitriol (0.25 μg/day per os) if parathyroid hormone (PTH) exceeded the upper limit of normal by a factor of 2 or more. Main Outcome Measures We assessed total and ionized serum calcium, phosphate, serum aluminum, alkaline phosphatase, osteocalcin, PTH (intact molecule), and phosphate binder intake at regular intervals. Measurements of bone mineral density and hand skeleton x-rays were obtained at the start and after 6 months and 2 years, respectively. Results With LCa, mean total and ionized serum calcium levels were within the normal range (total Ca: 2.0 2.6 mmol/L; ionized Ca: 1.19–1.32 mmol/L), but throughout the treatment period were significantly lower than with SCa. The incidence of hypercalcemia (>2.8 mmol/L) was three times higher in patients on SCa, despite the significantly higher amount of AI(OH)3 and less CaCO3 given in this group. In parallel, serum aluminum increased with SCa throughout the study, whereas it was slowly decreasing with LCa. Median PTH levels remained stable at about two times the upper limit of normal over the 2 years of study with LCa. However, 23% of the patients on LCa developed severe hyperparathyroidism, with PTH levels exceeding ten times the upper limit of normal compared to only 10.3% of the patients on SCa. With SCa, median PTH decreased towards near normal levels. Alkaline phosphatase and serum osteocalcin correlated positively with PTH levels. Bone mineral density was in the lower normal range in both groups a n d remained unchanged at the end of the study. Skeletal x-ray films showed only minor alterations in very few patients in both groups with no correlation to serum PTH or treatment modality. Conclusion In CAPD patients low-calcium dialysate solutions can be used successfully over prolonged periods of time with stable control of serum calcium. The risk of hypercalcemia resulting from calcium-containing phosphate binders and the need to use aluminum-containing phosphate binders is markedly diminished. However, there is a certain risk that severe secondary hyperparathyroidism with long-term LCa therapy will develop, even if normocalcemia is maintained. Thus, LCa dialysis requires closeand continuous monitoring of PTH and bone metabolism.

scholarly journals Role of reduced thyroid hormone status on bone mineral metabolism

2021 ◽  
Vol 19 (2) ◽  
pp. 26-29
Author(s):  
X Lourdes Sandy ◽  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Bone Mineral ◽  
Serum Calcium ◽  
Mineral Metabolism ◽  
Bone Mineral Metabolism ◽  
Hormone Status ◽  
Calcium And Phosphorus ◽  
Hypothyroid Patients

Background: The most common endocrine disorder is hypothyroidism which accounts to 11%. Thyroid hormones have a wide array of functions such as physiological growth and development of skeletal system, maintenance of basal metabolic rate and regulation of various metabolisms, including mineral metabolism. Nowadays due to its direct action on bone turn over, thyroid hormones are considered to have an important role on bone mineral metabolism. Thyroid disorders are important cause for secondary osteoporosis. So the present study was done to know the levels of bone minerals, calcium and phosphorus in hypothyroidism and its relation with thyroid hormone levels. Methods: A case-control study was conducted on 30 hypothyroid patients and 30 euthyroid healthy controls in the age group of 20-60 years. Blood samples were collected from all the study population. Serum total triiodothyronine, total thyroxine and TSH by Enzyme-Linked Immunosorbent Assay, Serum calcium by Arsenazo III method, phosphorous by ammonium molybdate method were estimated. Results: Serum calcium levels in cases was found to significantly reduced when compared to controls (p<0.001). Serum phosphorous levels also showed considerable elevation in cases when compared to controls (p<0.001). There was a significant negative correlation between TSH and serum calcium in cases. Conclusion: The present study indicated the important role of reduced thyroid hormone status on bone mineral metabolism. This study concludes that serum calcium was significantly reduced and phosphorus levels were significantly increased in hypothyroid patients when compared to euthyroid control subjects. So frequent monitoring of serum calcium and phosphorus in hypothyroid patients would reduce the burden of bone pathologies.

Abnormal Bone Mineral Metabolism after Long-Term Anticonvulsant Treatment

1994 ◽  
Vol 28 (1) ◽  
pp. 47-48 ◽  
Author(s):  
Christopher P. Alderman ◽  
Catherine L. Hill
Keyword(s):  
Alkaline Phosphatase ◽  
Serum Concentration ◽  
Bone Mineral ◽  
Serum Alkaline Phosphatase ◽  
Mineral Metabolism ◽  
Bone Mineral Metabolism ◽  
Hepatic Microsomal Enzyme ◽  
Grand Mal ◽  
Anticonvulsant Treatment

OBJECTIVE: To present a case of anticonvulsant-induced disturbances of bone mineral metabolism associated with long-term phenytoin treatment. CASE SUMMARY: An 87-year-old woman was hospitalized with generalized acroparesthesia. Her medical history was significant for grand mal epilepsy, which had been treated with phenytoin for more than ten years. On admission she was found to be hypocalcemic, and her alkaline phosphatase concentration was markedly elevated. DISCUSSION: Further investigations revealed that the patient's serum concentration of 25-hydroxycalciferol was well below the expected range. Phenytoin treatment was withdrawn, and calcitriol supplementation commenced. Ten weeks later she was normocalcemic, and the calcitriol dosage was reduced. Radiologic investigations at this time revealed an ununited hip fracture, as well as widespread evidence of bone demineralization. CONCLUSIONS: Minor elevations of liver enzymes observed in association with anticonvulsant treatment may reflect hepatic microsomal enzyme induction. Marked elevation of serum alkaline phosphatase, particularly when seen in concert with hypocalcemia, may be markers of anticonvulsant-induced bone disease. Under these circumstances, further radiologic investigations and measurement of the vitamin D serum concentration should be undertaken.

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 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.

Glucocorticosteroid-induced osteoporosis in adult primiparous Göttingen miniature pigs: effects on bone mineral and mineral metabolism

2007 ◽  
Vol 293 (1) ◽  
pp. E385-E395 ◽  
Author(s):  
K. E. Scholz-Ahrens ◽  
G. Delling ◽  
B. Stampa ◽  
A. Helfenstein ◽  
H.-J. Hahne ◽  
...  
Keyword(s):  
Bone Mineral ◽  
Calcium Absorption ◽  
Mechanical Stability ◽  
Mineral Metabolism ◽  
Systemic Disease ◽  
Control Group ◽  
Mineral Density ◽  
Short Term ◽  
Trabecular Thickness

Information on the pathophysiology of glucocorticoid-induced osteoporosis (GIO) is limited, since its clinical picture often reflects a combined effect of glucocorticoids (GC) and the treated systemic disease (i.e., inflammation and immobility). In 50 healthy adult (30-mo-old) primiparous Göttingen minipigs, we studied the short-term (8 mo, n = 30) and long-term (15 mo, n = 10) effect of GC on bone and mineral metabolism longitudinally and cross-sectionally compared with a control group ( n = 10). All animals on GC treatment received prednisolone orally at a dose of 1.0 mg·kg body wt−1·day−1for 8 wk and thereafter at 0.5 mg/kg body wt−1·day−1. In the short term, GC reduced bone mineral density (BMD) at the lumbar spine by −47.5 ± 5.1 mg/cm3from baseline ( P < 0.001), which was greater ( P < 0.05) than the loss [not significant (NS)] in the control group of −11.8 ± 12.6 mg/cm3. Calcium absorption decreased from baseline by −2,488 ± 688 mg/7 days ( P < 0.001) compared with −1,380 ± 1,297 mg/7 days (NS) in the control group. Plasma bone alkaline phosphatase (BAP) decreased from baseline by −17.8 ± 2.2 U/l ( P < 0.000), which was significantly different ( P < 0.05) from the value of the control group of −1.43 ± 4.8 U/l. In the long term, the loss of BMD became more pronounced and bone mineral content (BMC), trabecular thickness, mechanical stability, calcium absorption, 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, and parathyroid hormone tended to be lower compared with the control group. There was a negative association between the cumulative dose of GC and BMD, which was associated with impaired osteoblastogenesis. In conclusion, the main outcomes after GC treatment are comparable to symptoms of GC-induced osteoporosis in human subjects. Thus the adult Göttingen miniature pig appears to be a valuable animal model for GC-induced osteoporosis.

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.

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