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

Our understanding of the role of vitamin D in calcium-phosphorus metabolism has changed considerably in the last decade. Studies performed in tissue culture, animal, and man have firmly established that the natural compound requires hydroxylation in the liver at the C-25 position and in the kidney at the C-1 position to form the biologically active derivative 1,25-(OH)2D3. These hydroxylation reactions are finely regulated to maintain normal calcium-phosphorus homeostasis: We now regard 1,25-(OH)2D3 as a hormone which is released by the kidney during periods of hypocalcemia. This hormone acts on the intestinal mucosa to facilitate calcium absorption and on bone to increase calcium mobilization. Its function in other tissues is still being evaluated. The active metabolites of vitamin D and several closely related analogs have been synthesized. It has been clearly demonstrated that 1,25-(OH)2D3 and 1alpha-OH-D3 promote healing in uremic bone disease. Administration of small amounts of these compounds has corrected the biochemical disturbances in vitamin D-dependency and hypoparathyroidism. Limited clinical experience with 25-OH-D3 and 1,25-(OH)2D3 in children with familial hypophosphatemia has failed to show convincing evidence of a therapeutic effect. Further clinical studies are needed to fully evaluate the therapeutic potential of this new family of compounds.
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PMID:Vitamin D: the discovery of its metabolites and their therapeutic applications. 18 25

Ninety-nine patients with end-stage renal failure treated by maintenance home dialysis whose calcium and phosphorus balance was carefully controlled were studied for radiographic evidence of hyperparathyroidism. A total of 43 showed evidence of hyperparathyroidism despite excellent medical management. In 23 the abnormality was stable and the patients were asymptomatic with regard to the skeleton. The other 20 showed progressive bone disease. Sixteen of these patients were operated upon, and 14 were relieved of their symptoms by parathyroidectomy. Following operation, the radiographic evidence of bone disease halted dramatically, and a decided return toward normal was documented on subsequent films. Thus parathyroidectomy can control the skeletal deterioration and bone pain of hyperparathyroidism in patients who develop this complication. Serial radiographic studies are a reliable indicator of this circumstance.
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PMID:Autonomous hyperparathyroidism in patients on maintenance home dialysis. 18 19

Current status of our understanding of the metabolism of vitamin D and its implications in metabolic bone disease is reviewed. The details of metabolism of vitamin D3 to 25-hydroxyvitamin D3 in the liver and its further conversion in the kidneys to either 1,25-dihydroxyvitamin D3 or 24,25-dihydroxyvitamin D3 are presented. The latter conversions are regulated by the vitamin D status, serum calcium through the parathyroid gland system, and serum inorganic phosphorus concentration. The 1,25-dihydroxyvitamin D3 can now be regarded as a calcium- and a phosphate-mobilizing hormone and must be considered as one of the most important serum calcium-regulating hormones. Disruption of the vitamin D metabolic sequence or the signal system for 1,25-dihydroxyvitamin D3 results in several bone and calcium metabolism disorders such as renal osteodystrophy, hypoparathyroidism, pseudohypoparathyroidism, and vitamin D-dependency rickets. The use of the synthetic analogs of 1,25-dihydroxyvitamin D3 as well as 1,25-dihydroxyvitamin D3 itself in the management of these disease states is discussed.
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PMID:Vitamin D endocrinology. 18 79

States of hypersecretion of PTH may occur primarily, or in response to other physiologic abnormalities. Primary hyperparathyroidism must be considered in the differential diagnosis of hypercalcemia, nephrolithiasis, metabolic bone disease, and pancreatitis and peptic-ulcer disease. The clinical manifestations of this disease have become more subtle with improved detection. The serum calcium level is almost always elevated, and when it it accompanied by relatively high serum PTH levels or increased urinary cAMP excretion, the diagnosis is usually secure. Findings of hypophosphatemia, decreased renal tubular reabsorption of phosphorus, hypercalciuria, and characteristic roentgenographic changes support the diagnosis of hyperparathyroidism, but are not prerequisites for that diagnosis. Most cases will come to operation, and experienced intraoperative assessment is necessary for the correct distinction between multiglandular disease and that involving only a single gland. We expect that a clearer understanding of the histopathologic features of these diseases, and improvement in the methods for measurement of PTH will be the main areas of advancement in the diagnosis of hyperparathyroidism in the next few years.
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PMID:Diagnosis of hyperparathyroidism. 19 30

During the past decade, an explosion of information has become available on the metabolism and function of vitamin D which is of great importance to clinicians in the treatment of metabolic bone disease. We have learned that vitamin D is the precursor of at least one hormone and that this hormone carries out functions in calcium and phosphorus metabolism bringing about mineralization of bone on one hand, and the prevention of hypocalcaemic tetany on the other. It may also function in the prevention of such degenerative bone diseases as osteoporosis. An important analogue of this hormone, 1alpha-hydroxyvitamin D3 has been prepared and is used successfully in the treatment of a variety of clinical conditions. This presentation will summarize these findings and their possible implications in these metabolic bone diseases.
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PMID:Vitamin D metabolism. 20 16

The discovery of the vitamin D endocrine system has opened up many possibilities in our understanding of metabolic bone disease. Of particular importance is the fact that we can now manage certain genetic disorders resulting in vitamin D-resistant rickets or vitamin D-resistant hypocalcemia with the new active hormonal forms of vitamin D and with intelligent dietary management to provide for correction of the mineral difficulty. Thus, in the case of vitamin D dependency, replacement need only be with the missing hormone, 1,25-(OH)2D3. On the other hand, familial hypophosphatemia requires adjustment of the plasma phosphorus by frequent administration of oral phosphate and the adjustment of intestinal calcium absorption by 1,25-(OH)2D3. Renal failure patients require the adjustment of plasma phosphorus concentration and parathyroid hormone status, and the administration of the missing hormone 1,25-(OH)2D3. Hypoparathyroid patients require oral calcium plus 1,25-(OH)2D3, and premature infants require administration of the 1,25-(OH)2D3 because the immature kidneys and immature parathyroid glands fail to produce the required amount of this hormone. Other vitamin D-resistant rachitic conditions cannot be discussed here for lack of space and for lack of information. Undoubtedly, such patients as those having rickets secondary to renal tubular acidosis and rickets secondary to hepatic disorders will eventually come under effecti dietary and hormonal management. In this sense, the vitamin D endocrine system and vitamin D-resistant rickets can serve as a prototype of management of a genetic disorder by dietary means.
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PMID:Vitamin D-resistant rickets. A prototype of nutritional management of a genetic disorder. 23 Sep 41

Long-term anticonvulsant drug therapy may lead to abnormalities of calcium metabolism resulting in osteomalacia. The prevalence and severity of altered calcium metabolism was studied in an adult outpatient population of persons with epilepsy receiving anticonvulsant therapy for a minimum of 2 years. Assessment of calcium metabolism was based on serum concentrations of calcium, phosphorus, alkaline phosphatase and 25-hydroxycholecalciferol and of plasma parathyroid hormone, intestinal absorption of isotopic calcium and skeletal bone mineral mass as determined by in vivo neutron activation or x-ray photodensitometry.Thirty-nine patients who had been receiving anticonvulsant therapy for an average of 20 years were studied; none had clinical evidence of metabolic bone disease. Decreased serum calcium concentration was noted in 10%, decreased serum phosphorus concentration in 10% and elevated serum alkaline phosphatase concentration in 44%. The mean serum 25-hydroxycholecalciferol concentration was significantly lower (P < 0.001) than in a control group (11.6 v. 19.6 mg/mL). None of 18 patients studied had an increased plasma concentration of parathyroid hormone, and only 1 of 17 patients had decreased intestinal absorption of isotopic calcium. Bone mineral mass was decreased in 44% of 32 patients studied.It was concluded that long-term treatment with anticonvulsant drugs leads to mild abnormalities of calcium metabolism and decreased bone mineral mass in a substantial percentage of adult outpatients with epilepsy. These abnormalities probably predispose the patients to the development of clinically significant metabolic bone disease.
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PMID:Calcium metabolism in adult outpatients with epilepsy receiving long-term anticonvulsant therapy. 41 65

The density of bone in the distal third of the radius is measured by I-125 photon absorptiometry in 38 RDT (Regular Dialysis Treatment) patients (19 mean and 19 women, age range from 17 to 65 years). In the majority of patients the bone density (BMC/W) is reduced. The clinical follow-up of dialysis patients demonstrates that the incidence and severity of clinical symtpoms do not always correlate closely with the bone density values, nor with the biochemistry and histopathological findings of bone disease associated with dialysis. Despite control of calcium and phosphorus metabolism, decreased mineralization of the appendicular skeleton persists. The advantages as well as disadvantages of bone density measurements in RDT patients are discussed.
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PMID:I-125 photon absorptiometric analysis of bone density in patients with regular dialysis treatment. 49 24

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

Despite regular long-term parenteral vitamin D2 treatment, four patients with biliary cirrhosis had multiple symptoms of bone disease and bone biopsy specimens showed osteomalacia without osteoporosis. Three patients also had a proximal myopathy. Plasma calcium values (after correction for albumin), phosphorus, magnesium, and serum 25-hydroxy-vitamin D were within normal limits. Treatment with 1,25-dihydroxy-cholecalciferol (1,25-(OH)2D3) relieved symptoms in three of the four patients and improved those in the fourth. Histological examination of bone showed improvement in all four patients, but serum and urinary biochemical changes were not pronounced. We conclude that 1,25-(0H)2D3 treatment has a beneficial effect on bone and muscle in hepatic osteomalacia, either because vitamin D 1-hydroxylation fails in biliary cirrhosis or because hepatic osteomalacia is resistant to vitamin D2 metabolites.
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PMID:Parenteral 1,25-dihydroxycholecalciferol in hepatic osteomalacia. 62 Feb 4


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