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)

1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental sodium and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need sodium restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for malabsorption and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term sodium restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.
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PMID:Nutritional management of the child with mild to moderate chronic renal failure. 876 44

We have previously established a rat model of chronic uremia, which is suitable to investigate the effect of various treatment modalities on renal osteodystrophy [1]. After four months subsequent to 5/6 nephrectomy, some animals were treated by gavage for 9 weeks with tap water (controls), or with aluminium (Al-citrate) 3 x 25 mg/week/kg b.wt +/- subsequent deferoxamine (DFO) 3 x 50 mg/week/kg b.wt. for 4 weeks. At termination of the study, serum clinical chemistry, femoral chemical composition and mechanical properties, calvarial parathyroid hormone (PTH)-elicited adenylate cyclase (AC) and phospholipase C (PLC) activities, cross-sectional femoral area, as well as bone histomorphometry, were analyzed. Animals given Al displayed moderately enhanced serum Al and bone Al accumulation, however, DFO-treatment did not fully alleviate bone Al retainment. A small increase in serum PTH was seen in all animals rendered uremic. Furthermore, a marked fall in serum alkaline phosphatase (ALP) below normal controls was observed in Al +/- DFO-treated animals compared with uremic controls. The uremic condition led to reduced femoral ratios of hydroxyproline (HYP) over Ca(2+) and phosphate (P(i)), while Al-intoxication alone enhanced femoral Hyp contents above values seen for normal controls. The protracted ureamia caused a deterioration of long bone resilience and brittleness, however, Al +/- DFO-treatment seemed to normalize the latter. Contrastingly, Al +/- DFO-gavage enhanced time to fracture. Uremic rats intoxicated with Al showed a complete loss of calvarial PTH-sensitive AC and PLC activities. DFO-treatment normalized PTH-elicited PLC, while PTH-susceptible AC remained super-normal. Al apparently exerts a long term down-regulation of both PTH-sensitive signaling systems as evidenced by studies of rat UMR 106 osteosarcoma cells in culture. The uremic condition enhanced endosteal bone resorption as shown by femoral shaft dimension analysis, while Al +/- DFO-treatment insignificantly reversed the condition. Finally, histomorphometrical analyses showed that DFO-administration tended to normalize aberrant trabecular bone volume, while rectifying both bone resorption and degree of mineralization. In conclusion, we assert that Al-intoxication hampers both processes (i.e. formation and resorption) of bone turnover, and that DFO-treatment to a certain extent prevents the uremia- and Al-induced bone disease in rats.
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PMID:Aluminium-induced bone disease in uremic rats: effect of deferoxamine. 886 40

The bisphosphonates have been investigated over the past two decades for the treatment of various diseases of bone and calcium metabolism that are characterized by increased bone resorption, including osteoporosis, Paget's disease, primary hyperparathyroidism, hypercalcemia of malignancy and metastatic bone disease. The bisphosphonate alendronate was recently approved by the U.S. Food and Drug Administration as a therapy for postmenopausal osteoporosis. This agent is currently the bisphosphonate of choice for clinical use. In postmenopausal osteoporosis, alendronate has been shown to increase bone mineral density and to decrease the rate of new fractures. Adverse effects are not usually a problem when 10 mg per day of alendronate is given with at least 6 oz of water 30 minutes before ingestion of the first food or beverage of the day.
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PMID:Alendronate: a bisphosphonate for treatment of osteoporosis. 890 Mar 45

Patients with urinary diversions present unique challenges to internists who have an important role in their long-term management. Advances in surgical techniques over the past 30 years have given rise to a number of urinary diversion procedures that use various intestinal segments. In its normal function, the intestine absorbs water and solutes. When placed in contact with the urinary stream, the intestine can create numerous metabolic abnormalities. These include bone disease, hepatobiliary disease, infection, malignancy, neurologic complications, nutritional deficiencies, and a number of electrolyte and acid-base disorders. An overview of these metabolic abnormalities and their causes is provided, as well as recommendations for screening and management of patients.
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PMID:Metabolic complications of urinary diversions: an overview. 921 45

To study the causes, diagnosis and treatment of aluminum toxicity in patients with chronic renal failure, the serum aluminum concentration was determined in 27 normal subjects, 28 patients of various kinds of diseases with normal renal function and 81 patients of chronic renal failure with hemodialysis in 65 and without in 16, of whom 41 patients were determined the aluminum concentration in the bone tissue. Clinical symptoms were carefully observed in all patients and desferrioxamine (DFO) test was performed in 17 patients, of whom 10 were treated with DFO. The results showed that treatment with improperly processed water and administration of aluminum compound were the major causes of aluminum toxicity in uremic patients. Aluminum toxicity may induce anemia, encephalopathy and bone disease, but its clinical features were nonspecific and the diagnosis may require several serum aluminum determinations or DFO test. DFO can chelate aluminum in a variety of tissues so that the latter may be released into the blood circulation. The DFO test may be used to assess the actual aluminum load in the bone tissue. The changes in serum aluminum concentration after intravenous infusion of DFO correlated closely with bone aluminum level, suggesting that the DFO test may be useful for the diagnosis of aluminum toxicity. The DFO therapy may be indicated for, 1, patients with uremia having hyperaluminumnemia due to treatment with improperly processed water and intake of aluminum-containing agents. 2. those who had serum aluminum concentration of higher than 200 micrograms/L and positive DFO test and 3. patients whose aluminum concentration in the bone tissue was 10 times greater than normal values. In this study, DFO was given intravenously in a dose of 20-40 mg/kg, twice a week. Satisfactory results were obtained in 3 to 6 months and there were no severe side effects when the agent was administered slowly.
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PMID:[The causes, diagnosis and treatment of aluminum toxicity in patients with chronic renal failure undergoing dialysis]. 927 45

Bisphosphonates are a group of osteotropic substances able to modulate bone metabolism in different ways. They all display similar pharmacokinetic characteristics when administered in proportional dosages and assessed by similar methods. With the exception of olpadronate which is soluble in water, bisphosphonates have poor solubility, and may easily precipitate in the digestive media. In spite of their low digestive absorption (Bioavailability: 0.3-5%), they are effectively administered by oral route. Once in plasma they distribute rapidly, being uptaked by mineralized tissues, plasma proteins or eliminated by renal filtration in few minutes. The fraction retained in bones may be stored for long periods (from months up to 10 years depending on the compound) in an apparent inactive compartment. The risks of newly released molecules may be related to the potency of the drug. Within the clinical range of doses, bisphosphonates are not retained in soft tissues. This may explain the lack of extraskeletal collateral effects. Plasma blood levels are scarcely related to the clinical activity. Therefore, dosage may be guided better by biochemical markers of the bone disease than by the standard kinetic variables. On the other hand, dose is independent from age and/or body weight. Only renal impairment may induce additional dose adjustments.
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PMID:[Clinical application of bisphosphonate's pharmacokinetic principles]. 956 59

Aluminum (Al) may be a pathogenic factor in dialysis associated osteodistrophy. Aluminon and Acid Solochrome Azurine have been used for the detection of Al deposits in bone. We compared Aluminon and Acid Solochrome Azurine stains in normal (N) and uremic (U) rats. Both received intraperitoneal injections of aluminum chloride (AlCl3), until a cumulative dose of 5 mg/Al (NAL5; UAL5) or 30 mg/Al (NAL30; UAL30). The control groups received an equal volume of distilled water by means of intraperitoneal injections. Histomorphometric analysis showed that formation parameters (osteoid volume-OV/BV and osteoid surface-OS/BS), were significantly greater in the uremic groups than the control groups. In addition, the aluminum intoxication increased these values. When we compared the aluminum deposits in the undecalcified bone detected by both staining methods, we observed that Acid Solochrome Azurine was more sensitive than Aluminon in the normal renal function group and uremic treated with 5 mg of AlCl3. All our results were compared with atomic absorption spectrophotometry, showing that Al content presented a positive correlation with Aluminon stain in U and N rats, nevertheless it was not observed using Acid Solochrome Azurine stain. We conclude that histochemistry is important in diagnosing and monitoring aluminum bone disease.
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PMID:Histochemical staining of bone aluminum: comparison of aluminon and acid solochrome azurine and their correlation with bone aluminum content. 956 66

Contamination of parenteral nutrition solutions with aluminum may result in accumulation of this element in bones and, in premature infants, may inhibit bone calcium uptake and induce cholestasis. We measured the aluminum concentration of small-volume parenterals, amino acid solutions, lipid emulsions, and special solutions containing glucose, amino acids, electrolytes, and trace elements (standard I for children with a body weight of 3-5 kg, standard II for children with a body weight of 5-10 kg). The method used was graphite furnace atomic absorption spectrometry GTA-AAS (SpectrAA-400 Plus, Varian, PtY Ltd., Mulgrave, Australia). Quality control was run with the use of control serum (Seronorm, Nycomed, Oslo, Norway). The aluminum contents of parenterally administered solutions were: pediatric trace elements, 130 micrograms/L, and pediatric trace elements, 3000 micrograms/L; phosphorus salts: K-phosphates, 9800 micrograms/L, and Na/K phosphates, 13,000 micrograms/L; 10% calcium gluconate, 4400 micrograms/L; 6.5% amino acids, 30 micrograms/L; 10% amino acids, 120 micrograms/L; 12.5% amino acids, 121 micrograms/L; 20% lipid emulsion, 30 micrograms/L; 20% lipid emulsion, 180 micrograms/L; water-soluble vitamins, 12 micrograms/L; lipid soluble vitamins, 360 micrograms/L; standard I, 55 micrograms/L; standard II, 90 micrograms/L; The aluminum intake from parenteral nutrition was 6.6-10.8 micrograms.kg-1.d-1--a dose exceeding the safety limit of 2 micrograms.kg-1.d-1. The possible association of aluminum not only with metabolic bone disease, but also with encephalopathy, dictates caution when dealing with the pediatric population on long-term parenteral nutrition. In the absence of reliable label information, it seems proper to monitor the aluminum concentration in parenteral nutrition products and to report it in professional journals.
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PMID:Aluminum contamination of parenteral nutrition additives, amino acid solutions, and lipid emulsions. 1046 17

Renal failure inevitably leads to metabolic bone disease. Low turnover disease or adynamic bone disease (ABD) is characterized by a low number of osteoblasts with normal or reduced numbers of osteoclasts. Mineralization proceeds at a normal rate, resulting in normal or decreased osteoid thickness. Recently, it became clear that the relative contribution of the various types of renal osteodystrophy (ROD) to the spectrum of the histologic picture in renal failure patients underwent profound changes during the last 25 years. At the moment, the exact physiopathological mechanisms behind ABD are not yet elucidated, and thus the reason(s) for its increasing prevalence remains poorly understood. A number of epidemiological and experimental data suggest a multifactorial pathophysiologic process, in which hypoparathyroidism and suppression of the osteoblast are the main actors. Compared to adynamic bone disease, osteomalacia has now become a much rarer disease (around 4%), at least in Western countries. On the other hand, recent studies indicate that this particular bone disease entity might still regularly occur in less developed countries. Osteomalacia originates from a direct effect on the mineralization process. With this type of renal bone disease, the effects of secondary hyperparathyroidism on bone are overridden by a number of metabolic abnormalities that finally result in a defective bone mineralization, as occurs, for instance, when the lag time between osteoid deposition and its mineralization is increased. The relationship between exogenous and endogenous vitamin D deficiency (mainly calcitriol) and the histologic finding of osteomalacia in uremic patients is well known. Recent data showed distinctly lowered 25-(OH) vitamin D3 levels in the presence of unaffected calcitriol concentrations in patients with osteomalacic lesions, as assessed radiologically by the presence of Looser's zones. Recently, we found that bone strontium levels were increased in patients with osteomalacia as compared to all other types of ROD. Strontium accumulation appeared to originate mainly from the use of strontium-contaminated dialysate, which resulted from the addition of strontium-containing acetate-based concentrates. Evidence for a causal role of the element in the development of a mineralization defect could be tested experimentally by adding strontium to drinking water in a chronic renal failure rat model.
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PMID:Low bone turnover in patients with renal failure. 1084 38

Epidemiological studies during 1963-1997 were conducted in 45,725 children exposed to high intake of endemic fluoride in the drinking water since their birth. Children with adequate (dietary calcium > 800 mg/d) and inadequate (dietary calcium < 300 mg/d) calcium nutrition and with comparable intakes of fluoride (mean 9.5 +/- 1.9 mg/d) were compared. The toxic-effects of fluoride were severe and more complex and the incidence of metabolic bone disease (rickets, osteoporosis. PTH bone disease) and bony leg deformities (genu valgum, genu varum, bowing, rotational and wind-swept) was greater (> 90%) in children with calcium deficiency as compared to < 25% in children with adequate calcium who largely had osteosclerotic form of skeletal fluorosis with minimal secondary hyperparathyroidism. The syndrome of skeletal fluorosis and associated metabolic bone disease and deformity is a unique clinical entity classified as a variant of osteosclerotic form of skeletal fluorosis. This syndrome chiefly results from the biological impact of excess fluoride, low calcium, high PTH and 1,25 (OH)2D3 separately and through their interactions on bone structure and metabolism as studied by radiology, bone scanning, bone histomorphometry and relevant metabolic and endocrine laboratory investigations. Metabolically active and vascular bones of children accumulate fluoride at faster and greater rate than adults (at the sites of active growth). In calcium deficient children the toxic effects of fluoride manifest even at marginally high (> 2.5 mg/d) exposures to fluoride. Fluoride toxicity also exaggerates the metabolic effects of calcium deficiency on bone. The findings strongly suggest that children with calcium deficiency rickets reported in the literature should be re-investigated for possible fluoride interactions. Deep bore drinking water supply with fluoride < 0.5 ppm and improvement of calcium nutrition provide 100% protection against the toxic effects of fluoride and are recommended as the cost effective and practical public health measures for the prevention and control of endemic fluorosis.
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PMID:Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India: year 2000. 1077 88


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