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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal osteodystrophy is a metabolic bone disease resulted from chronic renal failure. The long-standing alterations in a mineral metabolism generated by renal failure have a profound effect on the skeleton and induce severe systemic metabolic bone disease. Iliac crest biopsies of 194 patients of chronic renal failure were taken and among them 10 cases were examined for Calcium(Ca), phosphorus (p), parathyroid hormone (PTH), 1,25(OH)2D3 and aluminium (Al). The histological bone changes are characterized by development of osteitis fibrosa, increase of bone resorption and the number of osteoclast, increase of osteoid volume (osteoblastic osteoid and acellular osteoid), active remodelling of bone and aluminum deposition in the bone. According to histological appearance, advanced renal bone disease could be subdivided into three groups namely: Secondary hyperparathyroid bone disease (high turnover uremic osteodystrophy), osteomalacia (low turnover uremic osteodystrophy) and mixed uremic osteodystrophy consisting of mild to moderate hyperparathyroid bone disease and defective mineralization. Aluminum-related bone changes might be obtained in various extent in all these groups. Although this classification does not fully represent all the separated entities, and there is also transformation from one form to another, it seems no less significant as a reference for clinical considerations.
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PMID:[Pathological analysis of renal osteodystrophy in 194 cases]. 181 63

Prevention of bone disease associated with impairment of the renal function is desirable. Attempts at such prevention inevitably also embrace prevention of the extraosseous consequences of autonomous hyperparathyroidism, such as the effects of hypercalcaemia, need for parathyroid surgery, and, perhaps, toxic effects of the parathyroid hormone. Strategies for prevention in early, moderate, and end-stage renal failure are reviewed and discussed with particular reference to dietary phosphorus restriction, use of gut phosphorus binders, control of acidosis, calcium supplementation, use of oral and intravenous calcitriol, and use of synthetic analogues of 1,25-dihydroxyvitamin D3. The onset of severe renal osteodystrophy can be delayed. Early attempts at prevention are logical, but we do not know whether these will reduce the need for parathyroid surgery or will make patients feel better or live longer. The costs of prophylaxis--both financial and in terms of incidence and severity of complications--remain to be defined. An individual approach to each patient with renal impairment seems at present appropriate.
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PMID:Prevention of renal osteodystrophy. 181 86

Phosphonoformate (PFA), a monophosphonate pyrophosphate analog, caused plasma biochemical and bone histomorphologic abnormalities in cats given 1,000 mg/kg/day as a continuous intravenous infusion for 14 days. Plasma biochemical alterations observed in young cats (10 weeks old) treated with PFA included increased calcium and decreased phosphorus, alkaline phosphatase, and calcitriol. Young cats treated with PFA developed rickets-like lesions characterized by widened growth plates, increased osteoid, and failure of mineralization. In addition, area of mineralized trabecular bone was decreased. Osteoclast size was increased whereas osteoclast perimeter and number were unaffected in young PFA-treated cats. Plasma alkaline phosphatase was decreased in adult cats (greater than or equal to 1 year old) treated with PFA but changes in calcium, calcitriol, and immunoreactive parathyroid hormone were highly variable and not significantly different. Adult cats treated with PFA exhibited osteomalacia characterized by increased osteoid area, perimeter, and width with failure of mineralization. In addition, static resorption indices were increased in PFA-treated adult cats but area of mineralized trabecular bone was not decreased. The monophosphonate PFA inhibited bone mineralization in young and adult cats similar to bisphosphonate treatment in other species. Because PFA is currently in phase I trials for use in AIDS, results of this study suggest a need to evaluate patients treated with PFA for metabolic bone disease.
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PMID:Age-related differences in phosphonoformate-induced bone toxicity in cats. 182 19

Bone mineral content, estimated by single-photon absorptiometry of the forearm, serum values of intact parathyroid hormone (PTH(1-84], osteocalcin, alkaline phosphatase, 1,25-dihydroxycholecalciferol (1,25(OH)2D3), and aluminium were determined during treatment with calcium carbonate (CaCO3) or aluminium hydroxide (Al(OH)3) in 11 dialysis patients participating in a randomised cross-over study. Each treatment period lasted 6 months. Serum phosphorus was maintained in the range 1.5-2.0 mmol/l. During Al(OH)3 treatment bone mineral content (BMC) decreased by 11% per half-year (mean), but only by 3% per half-year during CaCO3 treatment (P less than 0.05). Comparing the CaCO3 and Al(OH)3 periods the following differences were found: serum calcium increased during CaCO3 treatment, PTH(1-84) decreased (79% of initial values during CaCO3 versus 196% during Al(OH)3, mean area under curve, P less than 0.05), osteocalcin decreased (89% versus 117%, P less than 0.01), alkaline phosphatase decreased (92% versus 116%, P less than 0.05), and aluminium decreased (56% versus 189%, P less than 0.05). 1,25(OH)2D3 remained unchanged in both periods. No increase in soft-tissue calcification was demonstrated on X-ray of the shoulders in any of the periods. Thus, CaCO3 treatment seems to slow down loss of bone mineral content, and using CaCO3 as phosphate binder may have a more beneficial effect on the progression of uraemic bone disease than Al(OH)3 due to the reduction of hyperparathyroidism and bone turnover.
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PMID:Comparison of calcium carbonate and aluminium hydroxide as phosphate binders on biochemical bone markers, PTH(1-84), and bone mineral content in dialysis patients. 185 34

Primary hyperparathyroidism is a common condition infrequently complicated by renal stones and overt bone disease. Most cases are asymptomatic or have vague, nonspecific symptoms. There is considerable debate as to whether mild or asymptomatic cases should be managed surgically or conservatively. Important chromosomal abnormalities have now been demonstrated in some parathyroid adenomas. Renal osteodystrophy remains a difficult condition to treat once it is fully established. The use of vitamin D metabolites in the early stages of renal failure and the maintenance of a normal serum calcium and phosphate appear to prevent the development of secondary hyperparathyroidism. Further studies are required to ascertain the optimum way of using vitamin D metabolites and how best to reduce serum phosphorus.
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PMID:Primary hyperparathyroidism and renal osteodystrophy. 188 4

Clinical and research laboratories routinely measure various hormonal and nonhormonal parameters of calcium and phosphorus metabolism, and markers of bone turnover. Such measurements may help clinical decision-making relating to metabolic bone disease and osteoporosis. Molecular biological and cell-culture techniques are being used in basic biochemical research on bone-cell metabolism. Results may aid understanding of normal and abnormal regulation of the bone-cell metabolism, and thus provide further insights relating to the diagnosis and prevention of osteoporosis.
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PMID:Use of non-collagen markers in osteoporosis studies. 193 93

Osteomalacia is a multifactorial bone disorder. Main causes are vitamin D deficiency and phosphorus depletion. Among patients with renal insufficiency the incidence of osteomalacia is variable and probable related to impairment of the synthesis of 1,25 dihydroxy-vitamin D3 (calcitriol). We report a patients with severe osteomalacia, hyperkalemic tubular acidosis, low serum calcitriol levels and insufficiency associated to a prolonged overuse of analgesic drugs. Differential diagnosis and pathophysiology are discussed.
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PMID:[Osteomalacia and renal tubular acidosis associated with analgesic abuse. A clinical case]. 198 8

We characterized the bone disease of transilial biopsy specimens from children with hereditary hypophosphatemic rickets with hypercalciuria (HHRH) and genetically related asymptomatic hypercalciuric subjects. All HHRH patients showed irregular mineralization fronts, markedly elevated osteoid surface and seam width, increased number of osteoid lamellae, and prolonged mineralization lag time. These findings are consistent with a mineralization defect and indicate unambiguously that the bone disease in HHRH is osteomalacia. The only abnormality seen in the asymptomatic hypercalciuric subjects was slightly extended osteoid surface. Parametric and nonparametric statistical analyses performed on a pooled sample of HHRH patients and asymptomatic hypercalciuric subjects revealed a very high inverse correlation and a tight linear relationship between serum phosphorus and osteoid parameters. Serum 1,25-dihydroxyvitamin D, which is low in other forms of hereditary hypophosphatemia and osteomalacia, is elevated in HHRH and correlated positively with osteoid parameters and the mineralization lag time. Serum alkaline phosphatase showed similar relationships. These results as well as the clinical, biochemical, and radiological remission of bone disease consequent to phosphate therapy strongly suggest that in HHRH 1) hypophosphatemia alone is sufficient to cause osteomalacia; and 2) the elevation of 1,25-dihydroxyvitamin D reflects the degree of the primary renal phosphate leak, but is not involved in the pathogenesis of the bone disease.
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PMID:Osteomalacia in hereditary hypophosphatemic rickets with hypercalciuria: a correlative clinical-histomorphometric study. 198 23

The mechanism of aluminum-induced bone disease was studied by experiments in vitro and in rats. After decalcification femur sections were treated with 0.1 M AlCl3 and implanted with control bone matrices into weanling male rats. After 4 or 8 weeks of implantation the tissue values of calcium(Ca), phosphorus(P) and aluminum(Al) were measured. The results showed that both Ca and P values in Al-treated bones were obviously lower than those of the controls (P less than 0.01), Al level in these bones remained considerably high. Histological examination indicated that aluminum deposited diffusely in Al-treated bones, the bone formation rate and mineralization rate markedly decreased, osteoclastic and osteoblastic activities were also inhibited. In collagenase incubation test the bone matrices pretreated with different concentrations of AlCl3 showed different degrees of resistance to digestion of collagenase. It is considered that aluminum forms tight complexes with bone collagen causing cross linkage and destroying the inductive effect in bone matrix, thus leading to aluminum-induced bone disease. Our study also suggests that the usage of chelating agents can remove aluminum from matrix and recover its abilities of bone formation and mineralization.
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PMID:[Experimental study of the mechanism of aluminum-induced bone disease]. 208 19

This study was designed to study the effects of small bowel resection on daily urinary excretion patterns, plasma and bone levels of magnesium, phosphorus and calcium in rats on long-term total parenteral nutrition (TPN). Male Sprague-Dawley rats weighing 300 to 350 g were randomly divided into two groups with six rats in each group. Control consists of rats whose small intestines were transected but anastomosed. Resected rats had 70% of their small intestine removed. After intestinal resection and transection, rats were infused with a balanced TPN solution for 17 days. Resected rats excreted significantly more calcium than transected rats during the first 10 days of TPN infusion. Peak excretion occurred between day 3 and 4 followed by a trend toward a slightly higher than normal level of calcium excretion between days 10 and 17. Urinary losses of phosphorus and magnesium were not influenced by bowel resection. Plasma and tibia calcium, phosphorus and magnesium levels were not altered. The effects of small bowel resection on urinary calcium loss is specific and our data demonstrate the involvement of gut in regulating urinary calcium excretion and suggest that gut may play a significant role in TPN induced metabolic bone disease.
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PMID:Small bowel resection-associated urinary calcium loss in rats on long-term total parenteral nutrition. 210 18


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