Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a survey of 125 patients with hip fracture vitamin D deficiency was frequently observed, but overt osteomalacia was not found in the bone biopsies (Lips et al., 1982). In order to detect a possible hypomineralization in these vitamin D-deficient patients, we measured the bone mineral content in 64 transilial biopsies, embedded in methylmethacrylate for histomorphometric evaluation. The results were compared with those of 18 bone samples obtained at autopsy from subjects who did not suffer from metabolic bone disease. The calcium:hydroxyproline ratio, the phosphorus:hydroxyproline ratio, and the calcium:phosphorus ratio were similar in the two groups. The magnesium:hydroxyproline ratio was higher in the hip fracture group than in the controls. The ratios did not correlate with serum concentrations of the vitamin D metabolites. The results are not consistent with a decreased bone mineralization in patients with hip fracture.
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PMID:Bone mineral content of transilial biopsies in patients with hip fracture. 409 62

Eight Pakistani children with late rickets and two Pakistani women with osteomalacia were given a chupatty-free diet for seven weeks, substituting leavened bread of lower extraction. On this diet serum calcium levels rose to normal or near normal, levels of serum inorganic phosphorus rose slightly but significantly, and serum alkaline phosphatase levels showed a definite rise indicative of healing bone disease. It is concluded that the high phytate content of unleavened bread is the major cause of late rickets and osteomalacia in Pakistani and Indian communities in the United Kingdom. The simplest prophylactic measure seems to be the additional fortification with calcium carbonate of the high extraction flour used in preparing unleavened bread.
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PMID:Biochemical response of late rickets and osteomalacia to a chupatty-free diet. 506 21

An unusual metabolic bone disease which developed in 11 adults receiving total parenteral nutrition (TPN) for more than 3 months was characterised by the insidious onset of bone pain which became very severe and caused considerable disability. Serum levels of calcium, phosphorus, 25-hydroxy-vitamin D, and serum immunoreactive parathyroid hormone were normal. Patchy osteomalacia with impaired mineralisation and decreased bone turnover were seen on histomorphometric analysis of bone biopsy specimens. All patients receiving long-term TPN had hypercalciuria, but no biochemical features that distinguished patients with symptoms from those without. Skeletal symptoms generally resolved 1-2 months after stoppage of the TPN infusions, despite nutritional deterioration. The pathogenesis of this syndrome remains unknown.
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PMID:Bone disease associated with total parenteral nutrition. 610 76

Scintigraphic findings in ten cases of systemic mastocytosis are described. Four radionuclide bone patterns were noted: normal, unifocal, multifocal, and diffuse. Compared with radiographic surveys, bone images were better able to show the widespread skeletal involvement in patients with diffuse disease, and to detect a greater number of focal lesions. Serum calcium, phosphorus, and bone-derived alkaline phosphatase, as well as urinary calcium, phosphorus, and hydroxyproline levels, were usually within normal limits even when the bone scintigrams were clearly abnormal. Plasma and urinary histamine levels were highest in patients whose bone images detected widespread skeletal involvement. In systemic mastocytosis, not only does scintigraphy document active bone disease more effectively than laboratory studies of bone metabolism and radiographs of bone, but it also appears to reflect the general severity of the disease process.
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PMID:Patterns of skeletal scintigraphy and their relationship to plasma and urinary histamine levels in systemic mastocytosis. 623 29

The objectives of this study were to evaluate the effects of vitamin D(3) (D(3)) and 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) on uremic bone disease independent of their action on the intestine. The histomorphology of tibial metaphyses in uremic (5/6 nephrectomized [5/6 Nx]) rats fed a low-calcium-low-phosphorus (LCLP) diet was compared with sham-operated (SO) rats fed an LCLP diet and 5/6 Nx rats fed an LCLP diet and given 15,000 IU D(3) or 5 units (135 ng) 1,25-(OH)(2)D(3) daily for 7 days. A marked osteomalacia characterized by an increased percentage of active and inactive trabecular osteoid surface and thickened growth plates developed in proximal tibial metaphyses in 5/6 Nx rats given the placebo, compared with SO rats. These bone changes were associated with relative hypophosphatemia, hypophosphaturia, and hypercalciuria in 5/6 Nx rats. In 5/6 Nx rats treated with D(3) or 1,25-(OH)(2)D(3) the growth plates had undergone mineralization and vascular invasion and were markedly reduced in thickness. Other parameters of osteomalacia in trabecular bone were not different from 5/6 Nx rats given the placebo. There was a significant decrease in osteoclasts per millimeter of trabecular surface perimeter in D(3)- and 1,25-(OH)(2)D(3)-treated rats. These bone changes were associated with hypercalcemia, hyperphosphatemia, and hyperphosphaturia, compared with 5/6 Nx rats given the placebo. It was concluded that in uremic rats fed the LCLP diet, shortterm treatment with either pharmacologic levels of D(3) or 1,25-(OH)(2)D(3) corrected only lesions in the growth plate. Osteoid seams were not reduced in treated rats, although the serum calcium-phosphorus product was elevated. The 5/6 Nx rat fed the LCLP diet appears to be a useful model for the rapid induction of uremic osteomalacia in adult animals.
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PMID:Short-term effects of vitamin D3 and 1,25-dihydroxyvitamin D3 on osteomalacia in uremic rats fed a low calcium-low-phosphorus diet. 626 57

One of the most important complication of patients with chronic renal failure is osteodystrophy. This causes skeletal deformities, growth failure, bone pain and decreased physical activity. Osteodystrophy is more frequent among children than uraemic adults. In fact, 50-80% of children with chronic renal failure may occur in metabolic bone disease and the incidence tends to be higher in those children who have been in uraemic state for a long time before starting chronic haemodialysis. Osteodystrophy is a result of: 1) lesions of rickets; 2) lesions of osteitis fibrosa: 3) osteosclerosis. In contrast to adult, metastatic calcifications are virtually never observed in uraemic children. Hyperphosphoraemia, that is secondary to the reduction of G.F.R., may be the principal responsible of hyperparathyroidism that is the main cause of osteodystrophy. Hyperparathyroidism is also maintained and increased by deficit of 1,25(OH)2D3 which is responsible for lesions of rickets. Haemodialysis may markedly improve osteitis fibrosa and it is efficacious in reversing the mineral defect. Dialysate calcium concentration should be maintained at approximately 3,5 mEq/l. In this case we can raise serum calcium. On the contrary dialysate has to be lacking in phosphorus to correct hyperphosphoraemia. It must be noted that we have to prepare a dialysate with deionized water lacking in aluminum to avoid encephalopathy compliance.
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PMID:[Osteodystrophy in children with chronic renal insufficiency in dialysis therapy]. 628 42

Vitamin D-resistant rickets (VDRR) in adults is characterized by low serum phosphorus and osteomalacia. Despite the disappearance of rickets after the closure of epiphyses, some adults with VDRR present with symptomatic bone disease while other are asymptomatic. In order to test the presumption that asymptomatic adults no longer have active bone disease, we have compared bone histology in 10 symptom-free adults to 6 age-comparable symptomatic adults presenting with bone pain and persistent deformities. Both groups had similar low serum phosphorus and increased serum alkaline phosphatase values. Serum calcium, parathyroid hormone, and vitamin D metabolite concentrations were not different in the two groups. Histomorphometric study of bone formation and resorption was made on undecalcified sections of iliac crest bone biopsies obtained after in vivo single or dual tetracycline labeling. Bone histology revealed that both groups of patients had comparable osteomalacia, as evidenced by increased amount of osteoid tissue, prolonged mineralization lag time, and reduced bone formation rate. Despite the presence of osteomalacia, the trabecular calcified bone volume was within or above normal values in the two groups, implying a remodeling imbalance between the rates of bone resorption and formation. The data show that despite the absence of symptoms and the disappearance of rickets, adults with VDRR still have active bone disease characterized by moderate to severe osteomalacia. The normal to increased trabecular bone mass implies that the occurrence of painful symptoms results from factors other than trabecular osteopenia. These observations thus lead one to question the utility of active medical treatment with vitamin D and/or phosphate in asymptomatic adults with VDRR.
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PMID:Bone histomorphometry in asymptomatic adults with hereditary hypophosphatemic vitamin D-resistant osteomalacia. 630 50

Weights and histopathological changes in parathyroid glands were evaluated in relation to clinical and biochemical parameters in 42 patients who underwent parathyroidectomy for hyperparathyroidism (HPT) secondary to chronic renal failure. There was a positive relation (r = 0.71, p less than 0.01) between duration of renal insufficiency and total parathyroid glandular weight. The glandular weight was also closely related to the serum levels of parathyroid hormone (r = 0.67, p less than 0.01). No correlation was found between total parathyroid glandular weight or histopathological findings and clinical symptoms, serum levels of calcium, phosphate, alkaline phosphatases, calcium X phosphorus product or radiological evidence of bone disease. The enlargement of the glands was mostly uniform in the individual patient and all patients showed multiple gland involvement. This indicates that when parathyroid surgery is performed in patients with uraemia and secondary HPT, a radical approach, i.e. total parathyroidectomy with autotransplantation or subtotal parathyroidectomy, should always be used. In smaller glands only diffuse hyperplasia of parenchymal cells was generally found; fat cells were present in near-normal amounts. With increasing glandular weight, fat cells were more sparse and nodularity was common. In general, the proportion of oxyphil cells increased parallel with the total glandular weight, suggesting that this cell type is sensitive to stimulation. As a group, patients undergoing conservative renal treatment had suffered longer with renal disease, had larger parathyroid glands with more nodularity, and had more oxyphil cells than those undergoing parathyroidectomy while on haemodialysis.
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PMID:Parathyroid pathology in hyperparathyroidism secondary to chronic renal failure. 637 60

Patients receiving long-term treatment with total parenteral nutrition often develop bony abnormalities characterized by patchy osteomalacia and low bone turnover. The patients present evidence of physiologic hypoparathyroidism, although low levels of iPTH cannot entirely explain the osteomalacia. Abnormally low serum levels of 1,25(OH)2-vitamin D have been demonstrated, but the significance of these reduced levels in the pathogenesis of the bone lesions is not defined. Aluminum has been detected in large quantities in the plasma, urine, and bone of some patients treated with TPN, and there is mounting evidence that aluminum may be associated with skeletal pathology, particularly osteomalacia. There is, however, no clear documentation that aluminum accumulation produces the skeletal lesions observed, although it could be a contributing factor. There has been the unusual empiric observation that the removal of vitamin D2 from the infusate is associated with a decrease in the quantity of unmineralized osteoid in TPN patients. A possible role of vitamin D2 in producing osteomalacia is not easy to understand since normal serum levels of 25(OH)-D2, the circulating form of vitamin D2, have been reported. The long-term consequences of intravenous nutritional support for many aspects of metabolism remain unknown. Administration into the systemic circulation of predetermined quantities of calcium and phosphorus via a route that bypasses their passage across the intestinal mucosa, the portal system and the liver may have adverse consequences. It is possible that bypassing homeostatic mechanisms may affect bone formation and metabolism or lead to alterations in vitamin D sterols. Alternatively, a deficiency of an essential trace metal or the accumulation of a toxic trace substance could be responsible for the bony abnormalities. Much remains to be clarified concerning calcium homeostasis and bone disease during total parenteral nutrition. Among various possible factors, it seems likely that the significance of the low levels of 1,25(OH)2-vitamin D and of the accumulation of aluminum in this condition will soon be clarified.
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PMID:Metabolic bone disease associated with total parenteral nutrition. 643 13

A 38-yr-old woman with Crohn's disease and short bowel on home total parenteral nutrition was studied. Metabolic bone assessments were done prospectively. Daily total parenteral nutrition included 500 IU vitamin D2, 6 to 8 mmol calcium, 10 to 15 mmol phosphorus, 12 to 16 mmol magnesium, and trace elements including zinc, cooper, and chromium. After 6 months, while asymptomatic, chemistries and x-rays were normal. Calcium bone index was 0.79. The bone biopsy showed mild hyperkinetic picture. At 26 months, she had a spontaneous rib fracture and bone pains in the hands and lower back. Chemistries were normal except that calcium bone index was 0.75. Bone biopsy showed mild osteomalacia. Vitamin D2 was withdrawn for 2 months and then restarted at 1000 IU/wk. She improved symptomatically for 4 months, but then developed rib fractures, and the bone pains recurred. After 48 months, chemistries were normal, except that the calcium bone index was 0.57 and bone biopsy showed regression of osteomalacia toward normal. Vitamin D2 was now withdrawn for 6 months, resulting in loss of bone pain. Vitamin D2 may produce a metabolic bone disease, requiring prolonged withdrawal for improvement.
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PMID:Metabolic bone disease in a patient on long-term total parenteral nutrition: a case report with review of literature. 644 Oct 20


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