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

A clinical, biochemical and radiological study was carried out in 28 patients on maintenance haemodialysis in order to assess the prevalence of bone disease, particularly with regard to osteomalacia and/or osteopenia. The patients were selected from dialysis units using softened or deionized water, and the aluminium levels measured in the different water supplies. The results showed that symptomatic osteomalacia/osteopenia occurs more frequently in the units using softened water, which has a higher aluminium content, than in the de-ionized water unit. The patients dialysed on softened water also have significantly higher serum calcium and phosphorus levels. It is suggested that in Johannesburg, water softening alone is inadequate, and that the high aluminium levels in our water may be responsible for accelerated osteomalacia/osteopenia.
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PMID:Bone disease in patients on maintenance haemodialysis using softened or de-ionized water. 55 Mar 66

The dialysis encephalopathy syndrome has a geographical distribution related to the aluminium content of the dialysis water supply. There is a close relationship between concentrations of water aluminium and serum aluminium, and patients with dialysis encephalopathy have serum aluminium concentrations greater than 400 microgram/litre. High serum aluminium is also associated with osteomalacic bone disease, and worsening anaemia. In dialysis encephalopathy, elevated concentrations of aluminium are found in CSF and in grey matter, and an aluminium burden of 2-8 g is calculated from whole body in vivo analysis. There is sufficient evidence for an aluminium toxicity syndrome to warrant specific removal of aluminium by water purification systems.
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PMID:Aluminium studies in dialysis encephalopathy. 74 Jun 62

The management of patients with chronic renal failure is complicated and demanding for both physician and patient, but is frequently rewarding. When specific treatment of the underlying cause is not possible, therapy is aimed at making the maximum use of existing nephrons and preventing further loss of nephrons through hypertension and infection. Careful attention to salt and water balance is necessary, and all patients and all drugs prescribed must be considered with care. Special problems exist with regard to anaemia, bone disease, pericarditis and hyperkalaemia. An important aspect of care at this time is the education of patients about the next major phase of management, dialysis and transplantation.
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PMID:The conservative management of chronic renal failure. 93 26

Aluminum (Al) accumulation in renal failure is an etiological factor in the pathogenesis of low turnover bone disease. Aluminum-induced impairment of mineralization has been related to a reduced extent of active bone-forming surface. The present study investigated the effect of fluoride, a potent stimulator of osteoblast number, on the toxicity of aluminum in rats with renal failure (Nx). Following a large parenteral aluminum load (3.2 mg/kg x day) over a period of nine weeks, bone histomorphometry of vertebral cancellous bone revealed a severe low-turnover osteodystrophy as evidenced by a fall in osteoblastic osteoid surfaces and mineral apposition rates. Concurrent administration of fluoride [20 mg/liter (F20) or 40 mg/liter (F40) supplied with the drinking water] resulted in a significant increase in the number of osteoblasts (Nx+Al+F40 vs. Nx+Al, 33.75 +/- 2.83 vs. 1.81 +/- 0.43 mm-1, P less than 0.001) together with an overall reduced deposition of aluminum in bone (469.3 +/- 24.6 vs. 592.2 +/- 28.3 micrograms/g, P less than 0.01). However, there was an increase in the fraction of osteoid surface exhibiting stainable aluminum at the bone-osteoid interface (70.7 +/- 7.1 vs. 44.3 +/- 6.0%, P less than 0.005). Fluoride-exposed rats accumulated a significantly larger osteoid volume, suggesting an exacerbation of the osteomalacic lesion, and furthermore, dynamic histomorphometric parameters remained depressed. These results indicate that fluoride has a distinct effect on the pattern of aluminum deposition in bone. In addition, fluoride antagonizes the aluminum-induced reduction in osteoblast number but provides no amelioration of the impaired mineralization in aluminum-intoxicated rats. Thus, in this model a decrease in the extent of osteoblast surface does not account for the development of aluminum-related bone disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of fluoride on aluminum-induced bone disease in rats with renal failure. 161 48

Mycobacterium szulgai is a newly recognised species of mycobacteria whose pathogenicity in man can only be confirmed following certain criteria. We report a new observation comprising three points of interest. M. szulgai appears to be directly responsible for pulmonary infection and the clinical and radiological progress is very rapid. The human disease probably comes from infected water in aquaria. We have reviewed other cases of M. szulgai in the literature and for two out of three amongst these there is pulmonary involvement resembling tuberculosis; in the other cases cutaneous disease, synovial disease and bone disease have been described.
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PMID:[Pulmonary infection with Mycobacterium szulgai]. 185 28

Aluminum contaminates several chemical compounds that are administered intravenously to patients. The most highly contaminated are calcium and phosphate salts, followed by albumin and heparin. Parenteral administration of aluminum bypasses the gastrointestinal tract, which serves as a protective barrier to aluminum entry into the blood. In the past, parenteral administration of aluminum as a contaminant of water used in hemodialysis and of casein hydrolysate, the former source of protein in parenteral nutrition solutions, was associated with a low-turnover osteomalacic bone disease and, in the case of uremic patients, encephalopathy. Groups currently at risk for aluminum accumulation in tissue resulting from parenteral administration include premature infants receiving long-term parenteral nutrition and patients receiving plasmapheresis therapy with albumin. Both groups may develop metabolic bone disease; the pathogenesis may involve aluminum. The Food and Drug Administration is currently considering regulation of aluminum in fluids used for parenteral nutrition. No changes are presently proposed with regard to albumin.
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PMID:The aluminum content of parenteral solutions: current status. 190 89

The current recommendations for the nutritional management of children treated with CAPD/CCPD will be reviewed. The optimal caloric intake for pre-pubertal children undergoing dialysis should at least be determined by the recommended daily allowances (RDA) of the National Academy of Science for healthy children of the same height and age. For pubertal and post-pubertal patients, the prescribed energy intake is similar to the RDA for adolescents, 60 kcal/kg for males, and 48 kcal/kg/day for females. Dietary complex carbohydrates should provide about 35% of dietary energy intake. Dietary fat should provide 50% of the dietary intake, and the PS:S fatty ratio should be about 1.5:1.0. The recommended protein intake for children less than 3 years of age should range between 2.5-3.0 gm/kg/day; for children between 3 years of age and puberty 2.5 gm/kg/day; for pubertal patients 2.0 gm/kg/day, and post-pubertal patients 1.5 gm/kg/day. In general, sodium, potassium and water intake vary markedly among patients and should be managed individually. Vitamins, folic acid 1 mg/day; peridoxine, B6 5-10 mg/day; and ascorbic acid 75-100 mg/day. Vitamin D sterols (i.e., calcitriol) and phosphate binding agents mainly calcium carbonate are needed for the prevention and control of renal bone disease in such patients. Aluminum containing gels should be avoided in order to prevent aluminum accumulation secondary to the ingestion of aluminum containing gels.
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PMID:The nutritional approach for pediatric patients undergoing CAPD/CCPD. 198 17

Aluminum-induced bone disease in uremic patients receiving dialysis was first described a little more than 10 years ago. The epidemic form of the disease was seen in centers where there was a high aluminum content in the water dialysate. Although this problem has been corrected, sporadic forms of the disease continue to be noted in dialyzed and nondialyzed patients. Multiple fractures are a radiological feature of aluminum-related bone disease. Fractures of the ribs and hips and vertebral crush fractures are the usual manifestations. We present four patients whose nontraumatic fractures involved large bones, without evidence of multiple fractures. In two of the patients symptoms were vague and subacute; a third patient with a subcapital fracture was ambulatory. Only in one patient (fractured dens) were symptoms acute enough to warrant immediate radiography. One of the patients had no symptoms pertaining to a fracture of C5 with retrolisthesis. Rib fractures are common in this condition but were seen in only one patient, in whom they were detected 8 years previously. Healing was not seen in any of the fractures. In patients receiving dialysis the presence of spontaneous fractures of large bones or cervical vertebrae, which may be clinically silent or vaguely symptomatic, should raise the possibility of aluminum-induced osteomalacia even if these fractures are solitary.
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PMID:Solitary, spontaneous cervical and large bone fractures in aluminum osteodystrophy. 202 Aug 68

The clinical relevance of regular serum aluminium monitoring in dialysis patients was investigated in a multicentre study by 6-monthly determination of the serum aluminium during 4 consecutive years. In a group totalling 1193 patients, a striking decrease of mean serum aluminium was observed the last 2 years of the study. This phenomenon was accompanied by a substantial reduction of the prescribed dose of aluminium hydroxide (Al(OH)3) and its partial replacement by calcium carbonate (CaCO3) and/or magnesium hydroxide (Mg(OH)2). Under this policy serum phosphate control remained satisfactory. In all the centres, water treatment was found to be adequate, yielding dialysate aluminium around 2 micrograms/l. Dialysis patients with clinically overt liver disease showed a significantly greater median serum aluminium concentration than that observed in a control dialysis population. Compared to the latter group, the median serum aluminium concentration of dialysis patients with diabetes mellitus did not differ significantly. Results further indicated that patients with biopsy-proven osteomalacia presented a significantly greater median serum aluminium compared to that of patients without osteomalacia. We demonstrated that a serum aluminium of 60 micrograms/l provides a relatively sensitive (82%) and specific (86%) index for the detection of aluminium-related bone disease (ARBD). Provided the aluminium determinations are performed by a qualified laboratory, serum monitoring in dialysis patients (a) allows the safer use of aluminium-containing phosphate binders, and (b) is of value in the diagnosis of overload/toxicity.
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PMID:Value of serum aluminium monitoring in dialysis patients: a multicentre study. 131 84

Sixteen patients treated exclusively by haemodialysis using reverse osmosis water treatment for up to 7 years (mean 49.3 +/- 17 months) were assessed for evidence of bone aluminium accumulation and toxicity. All patients were treated with aluminium hydroxide phosphate binders for the duration of dialysis but the dosage was restricted to a maximum of 2.85 g daily (mean daily dose 2.6 +/- 0.8 g). The mean plasma phosphate over the 12 months prior to the study was 1.68 +/- 0.42 mmol/l and in only three patients was adequate control of the plasma phosphate not achieved. No patient had evidence of fracturing bone disease. Bone aluminium staining was present in only two patients but was seen at the calcification front in only one of these. Three patients had histological evidence of osteomalacia, but in none was aluminium staining present. Mean bone aluminium was moderately high at 36.67 +/- 31 micrograms/g and in only three patients exceeded 40 micrograms/g. This study indicates that adequate control of the plasma phosphate can be achieved with low dosage of aluminium hydroxide, and in the medium term is not associated with evidence of bone aluminium toxicity.
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PMID:Can low-dosage aluminium hydroxide control the plasma phosphate without bone toxicity? 249 99


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