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At least 91 records · Page 5Linked to original sources
PubMed1999

Relative hypoparathyroidism and adynamic bone disease.

Renal bone disease results in significant morbidity in patients with end-stage renal failure. Renal osteodystrophy is a mixture of different conditions with different pathogenetic factors involved. Most recently a new form of renal bone disease, adynamic bone disease, has emerged as the most frequent finding on bone biopsy of patients on dialysis therapy. The etiology of this new entity is not fully understood, but relatively low levels of intact serum parathyroid hormone are frequently associated with this disorder and may play an important role in its pathogenesis.

Bone Diseases, Metabolic↗
PubMed1974

Effects of age, sex, and polycystic disease on progressive bone disease of renal failure.

A study of 150 patients undergoing haemodialysis has shown that age had a striking effect on the radiological presentation of renal bone disease, erosions being common in the young and uncommon in older patients and vascular calcification showing opposite trends to this. Men aged 20 to 59 years had a greater tendency to develop erosions than did women in this age range. Examination of a group of 53 patients over a period of five years showed that the half time for the development of vascular calcification was 4.6 years, erosions 26.7 years, and fractures 6.9 years. Nine out of 16 polycystic patients matched for age and sex with 50 controls did not develop erosions and had consistently less vascular calcification than the controls when examined over a six-year period.

Adolescent↗
PubMed2002

[Pathophysiology and clinical features of adynamic bone disease].

Adynamic bone disease is characterized by an extremely low bone turnover bone due to the lack of osteoid formation. An abnormal calcium metabolism refractory to hypocalcemia lies behind the development of adynamic bone. Extraskeletal calcification is often seen in patients with adynamic bone disease. Hypoparathyroidism appeared to be an life prognosis limiting factor in dialysis patients. Most of them are considered to be with adynamic bone disease.

English Abstract↗
PubMed1996

Development of an in vivo model of human multiple myeloma bone disease.

Osteolytic bone destruction and its complications, bone pain, pathologic fractures, and hypercalcemia, are a major source of morbidity and mortality in patients with multiple myeloma. The bone destruction in multiple myeloma is due to increased osteoclast (OCL) activity and decreased bone formation in areas of bone adjacent to myeloma cells. The mechanisms underlying osteolysis in multiple myeloma in vivo are unclear. We used a human plasma cell leukemia cell line, ARH-77, that has disseminated growth in mice with severe combined immunodeficiency (SCID) and expresses IgG kappa, as a model for human multiple myeloma, SCID mice were irradiated with 400 rads and mice were injected either with 10(6) ARH-77 cells intravenously (ARH-77 mice) or vehicle 24 hours after irradiation. Development of bone disease was assessed by blood ionized calcium levels, x-rays, and histology. All ARH-77, but none of control mice that survived irradiation, developed hind limb paralysis 28 to 35 days after injection and developed hypercalcemia (1.35 to 1.46 mmol/L) a mean of 5 days after becoming paraplegic. Lytic bone lesions were detected using x-rays in all the hypercalcemic mice examined. No lytic lesions or hypercalcemia developed in the controls. Controls or ARH-77 mice, after developing hypercalcemia, were then killed and bone marrow plasma from the long bones were obtained, concentrated, and assayed for bone-resorbing activity. Bone marrow plasma from ARH-77 mice induced significant bone resorption in the fetal rat long bone resorption assay when compared with controls (percentage of total 45Ca released = 35% +/- 4% v 11% +/- 1%). Histologic examination of tissues from the ARH-77 mice showed infiltration of myeloma cells in the liver and spleen and marked infiltration in vertebrae and long bones, with loss of bony trabeculae and increased OCL numbers. Interestingly, cultures of ARH-77 mouse bone marrow for early OCL precursors (colony-forming unit-granulocyte-macrophage [CFU-GM]) showed a threefold increase in CFU-GM from ARH-77 marrow versus controls (185 +/- 32 v 40 +/- 3 per 2 x 10(5) cell plated). Bone-resorbing human and murine cytokines such as interleukin-6 (IL-6), IL-1 alpha or beta, TGF-alpha, lymphotoxin, and TNF alpha were not significantly increased in ARH-77 mouse sera or marrow plasma, compared with control mice, although ARH-77 cells produce IL-6 and lymphotoxin in vitro. Conditioned media from ARH-77 cells induced significant bone resorption in the fetal rat long bone resorption assay when compared with untreated media (percentage of total 45Ca released = 22% +/- 2% v 11% +/- 1%). This effect was not blocked by anti-IL-6 or antilymphotoxin (percentage of total 45Ca released = 19% +/- 1% and 22% +/- 1%, respectively). Thus, we have developed a model of human multiple myeloma bone disease that should be very useful to dissect the pathogenesis of the bone destruction in multiple myeloma.

Animals↗
PubMed2003

[Renal bone disease].

Renal bone disease is a serious complication associated with chronic renal failure. The pathogenetic mechanisms are very complicated. The disorder develops as a result of hypophosphataemia, hypocalcaemia and calcitrol deficiency already during the period when renal functions decline below 50%. Formerly the form with an excessive bone turnover predominated, nowadays we encounter ever more frequently so-called a dynamic bone disease. A serious manifestation are extraosseous calcifications. In treatment phosphate binding substances in the gastrointestinal tract are involved (along with other provisions, correcting hypophosphataemia), supplementation of calcium in case of hypocalcaemia correction of metabolic acidosis and administration of the active vitamin D metabolite (continuously as supplementation in deficient endogenous production, in a pulsatile pattern with the aim to suppress the activity of parathyroid bodies). In case of "resistant" hyperparathyroidism surgery is indicated (parathyroidectomy). Treatment of the dynamic form is not known, prevention of suppression of excessive parathyroid activity is important. New trends in the treatment of renal bone disease are non-calcium phosphate binding substances in the gastrointestinal tract, vitamin D analogues (with a lower hypercalcaemic potential) and calcium mimetics.

Bone Remodeling↗
PubMed2004

Histopathologic changes in metabolic bone disease.

Metabolic bone disease encompasses a heterogeneous group of disorders that influence skeletal metabolism and structure. They are generally diagnosed at an advanced stage and manifest clinically with stunted skeletal growth in children and pathologic fractures in adults. Biochemical markers for bone metabolism are equivocal and microscopic examination of labeled bone remains the gold standard for the diagnosis and accurate monitoring of the response to therapy. This article reviews the role of microscopic bone changes in the diagnosis and management of metabolic bone disease.

Bone Diseases, Metabolic↗
PubMed2001

Treatment strategies for renal bone disease.

Renal bone disease encompasses a wide range of bone abnormalities that are intricately linked with metabolic systems that are driven by calcium, phosphorus, PTH, and D hormone levels. An integrated approach to treatment must involve both dietary measures, use of phosphate binders as appropriate, and D hormone replacement. Not incidentally, implementation of this integrated approach involves not only our patients but everyone associated in their care, especially the nephrologist, nephrology nurse, and renal dietitians. Improving patient outcomes--preventing or minimizing renal bone disease and the complications of secondary hyperparathyroidism--will require communication and cooperation between all of us on behalf of our patients.

Chronic Kidney Disease-Mineral and Bone Disorder↗
PubMed2006

[Metabolic bone diseases in patients with diabetes mellitus].

Both of genetic backgrounds and life-style are involved in pathogenesis of diabetes mellitus and osteoporosis. Nowadays they are common diseases in the elderly people in the developed countries. Quality of life in people who have diabetes and osteoporosis are frequently impaired. Thus, adequate care and treatment are needed for both diseases. Bone metabolism is regulated by complicated mechanisms that involve mineral metabolism and endocrine systems. Recent studies have shown that sympathetic nerve system, glucose and lipid metabolism are also involved in bone remodeling. Clinical studies have demonstrated that diabetes is an independent risk factor for fracture in the elderly women. Therefore, one should understand and care for disorders in bone metabolism in patients with diabetes individually, since pathophysiology of diabetes is complicated and diverse in each patient.

Bone Diseases↗
PubMed1982

Diphosphonates in the evaluation of metabolic bone disease.

The bone scan may be of value in the assessment of patients with metabolic bone disease. However the superiority of the bone scan when compared to radiology in conditions such as renal osteodystrophy, osteomalacia, primary hyperparathyroidism, and osteoporosis requires substantiation with the newer radiopharmaceuticals which have a higher affinity for bone. Two methods of quantitating skeletal uptake of tracer have been assessed to try to remove the subjective aspect of bone scan evaluation. Measurements of bone to soft tissue ratios have proved clinically disappointing, but 24 hour whole body retention of diphosphonate appears to provide a sensitive index of increased bone turnover.

Bone Diseases, Metabolic↗
PubMed2001

[The pathophysiology of adynamic bone disease].

Adynamic bone disease was first noted in the early 1980s. It now represents the predominant bone lesion in peritoneal dialysis patients and is nearly as prevalent as osteitis fibrosis in hemodialysis patients. Bone turnover is markedly reduced in this disorder but, A in contrast to osteomalacia, there is no increase in osteoid formation. Although the pathophysiology of adynamic bone disease is still obscure, skeletal resistance to the calcemic action of PTH is important factor. Recently several study, whose reveal the down regulation of PTH receptor, osteoclast inhibitory factor and a assay of PTH, whole PTH play a role on the pathophysiology of skeletal resistance, were reported.

English Abstract↗
PubMed1997

Bone scintigraphy in metabolic bone disease.

The bone scan has well-recognized appearances in metabolic bone diseases, with its main clinical value found in focal conditions or the focal complications of disease. In clinical practice, the bone scan is most widely used to detect fractures in osteoporosis and pseudofractures in osteomalacia and to evaluate Paget's disease.

Bone Diseases, Metabolic↗
PubMed1998

Diagnostic and prognostic value of biochemical markers in malignant bone disease: a prospective study on the effect of bisphosphonate on pain intensity and progression of malignant bone disease.

Seventy cancer patients with malignant osteolytic bone disease received pamidronate every three weeks for a maximum of six cycles. Bone resorption parameters, urinary calcium excretion, and pain parameters were assessed at baseline and throughout the study. At baseline, 80-95% of patients showed elevated urinary pyridinoline, deoxypyridinoline, Osteomark NTx and serum ICTP levels, whereas only 35% of patients had elevated urinary CrossLaps excretion rates. During bisphosphonate therapy, significant decreases in Osteomark NTx, CrossLaps and calcium excretion were observed, which were not related to the clinical outcome. The baseline levels of bone resorption markers were used to predict the probability of non-progressive bone disease or reduction in pain intensity during bisphosphonate therapy. Significant predictors of non-progressive bone disease were urinary pyridinoline and serum ICTP levels; significant predictors of reduction in pain intensity were urinary free deoxypyridinoline and serum ICTP levels. Our data indicate that serum ICTP levels predict significantly the response to bisphosphonate therapy in patients with advanced malignant osteolytic bone disease. CrossLaps did not predict the clinical outcome, but decreased significantly during bisphosphonate therapy. Our data demonstrate that the different bone resorption markers are reflecting different aspects of bone metabolism, and therefore differ in their diagnostic and prognostic properties.

Aged↗
PubMed2000

[The relationship between bone mineral density and secondary hyperparathyroidism bone disease].

The bone mineral density (BMD) and Z score in distal 1/3 radius were measured with dual energy X-ray absorptiometry (DEXA) in 185 hemodialysis (HD) patients, meanwhile serum parathyroid hormone (PTH), alkaline phosphatase (ALP) and hand X-rays were detected. Results showed that BMD in HD patients was significantly lower than that in control group(P < 0.05), and decreased with dialysis duration increasing. BMD in HD patients was negatively related with PTH, ALP and rate of subperiosteal erosions. By using Z score to diagnose hyperparathyroidism bone disease, receiver operating characteristic (ROC) curve was worked out. If Z score < or = -2.02, the sensitivity was 79.41% and specificity was 78.15%. In conclusion the measurement of BMD is a useful tool for the detection of hyperparathyroid bone disease.

Absorptiometry, Photon↗