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

We evaluated bone disease in eight white men between the ages of 49 and 61 years who had been abusing alcohol for at least 10 years. The mean density of vertebral cancellous bone was 58% of normal, whereas the mean density of appendicular cortical bone was 90% of normal. Marked reduction in active bone resorption and bone formation was seen without evidence of osteomalacia. Serum levels of calcium and magnesium were in the lower range of normal; serum levels of phosphorus, calcifediol, and calcitriol were normal; and serum levels of parathyroid hormone and nephrogenous cyclic adenosine monophosphate were in the higher range of normal. These data suggest that bone disease in these subjects is not due to inhibition of parathyroid hormone secretion or function, or abnormal vitamin D metabolism, but to an inhibition of bone remodeling by a mechanism independent of the calciotropic hormones.
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PMID:Bone disease in alcohol abuse. 298 90

A case of renal hypophosphatemic osteomalacia (RHO) that was unmasked by hyperthyroidism is presented. The patient presented at age 64 with pathologic leg fractures. There was no family history of osteomalacia or rickets. Initial evaluation revealed hyperthyroidism, which was treated with radioactive iodine. Despite control of thyroid function, the patient had recurrent pathologic fractures. Further evaluation revealed histologically proven osteomalacia and the biochemical findings of RHO: elevated serum alkaline phosphatase, decreased serum phosphate and tubular resorption of phosphate, and normal serum calcium, parathyroid hormone, and vitamin D levels. Other causes of osteomalacia were excluded. Treatment with phosphate and calcitriol reversed the osteomalacia. This case demonstrates that hyperthyroidism, and possibly other illnesses that affect vitamin D or bone metabolism, may unmask metabolic bone disease and that physicians should be alert for the subtle clinical and biochemical indicators of unrecognized metabolic bone disease in adults.
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PMID:Renal hypophosphatemic osteomalacia unmasked by hyperthyroidism. 301 39

Osteoporosis is a significant cause of morbidity and mortality in the elderly. As the population in the United States becomes more aged, the magnitude of this problem will certainly become greater. Significant progress has been made in recent years with regard to the diagnosis and treatment of osteoporotic bone disease. Future treatment possibilities being investigated include cyclical coherence programs and cyclical parathyroid hormone administration. While showing some initial promise, these new modalities have been used only in a limited number of patients and must be considered highly experimental. Despite the progress being made in the treatment of osteoporosis, hope for the future clearly rests with prevention. Arresting bone loss has proven to be much more effective than rebuilding a depleted skeleton. Advances must be made in determining the pathogenesis of osteoporosis with the goal of identifying those individuals at highest risk at a young age, when skeletal mass is still increasing. Intervention could then be aimed at maximizing the peak bone density through a combination of proper nutrition, exercise, and lifestyle changes. Clearly, there is much more to learn about this very common and debilitating disease.
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PMID:Osteoporosis. 305 Jul 24

A 14-year-old boy presented with the clinical and radiological features of rickets. Serum inorganic phosphate levels were constantly low, whereas serum calcium and parathyroid hormone levels were within the normal range. Laboratory investigation did not show any evidence for vitamin-D deficiency, chronic renal insufficiency, Fanconi syndrome, tubular acidosis, hepatic disease or intestinal malabsorption. A family study comprising 34 members over four generations revealed 10 other individuals to be affected and the mode of inheritance to be autosomal dominant. In addition to hypophosphataemia and normocalcaemia, the disease is characterized by elevated serum 1,25 dihydroxyvitamin D levels and hypercalciuria. This hereditary syndrome of renal hypophosphataemia differs from the common familial X-linked hypophosphataemia and the recently described autosomal recessive hypophosphataemic rickets with hypercalciuria by its dominant mode of inheritance; it differs from hypophosphataemic non-rachitic bone disease by the elevated serum 1,25 dihydroxyvitamin D levels and hypercalciuria.
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PMID:Autosomal dominant hypophosphataemia with elevated serum 1,25 dihydroxyvitamin D and hypercalciuria. 315 20

A simple method of quantifying skeletal uptake of 99Tcm-methylene diphosphonate, using a rectilinear scanner and a simultaneously image standard, is described. The pattern of quantified uptake in ten regions of the skeleton, the sacro-iliac joints and kidneys in 57 controls and 54 patients with various metabolic bone disease is presented. This method distinguishes patients with primary hyperparathyroidism and osteomalacia from controls with a sensitivity adequate for clinical purposes. In primary hyperparathyroidism the increased skull uptake of tracer correlated well with levels of serum alkaline phosphatase, plasma parathyroid hormone, urinary hydroxyproline excretion and the degree of intracortical resorption in the metacarpal bones. The skull uptake in oestoporosis was normal or moderately elevated and correlated well with bone mass density measurements of the radius. Patients with osteomalacia also showed the greatest increase in tracer uptake in the skull. Patients with thyrotoxicosis differed from most other patients by showing moderately increased uptake in shafts of long bones. We propose our method of quantitative bone uptake as a useful noninvasive test to detect metabolic bone disease and to monitor responses to therapy of bone disease.
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PMID:Quantitative radionuclide scanning in metabolic bone disease. 315 46

Primary hyperparathyroidism presenting with advanced bone disease is an important differential diagnosis of 'tumours' affecting the craniofacial skeleton. We describe a case of primary hyperparathyroidism presenting with a brown tumour of the maxilla causing local symptoms. Differentiation from other giant cell lesions of the maxilla is necessary. The histological and radiological features of brown tumour, non-ossifying fibroma and reparative granuloma are all similar. Differentiation relies on plasma calcium estimation and the diagnosis of hyperparathyroidism is confirmed by serum parathyroid hormone assay.
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PMID:Primary hyperparathyroidism presenting with a maxillary tumour and hydrocephalus. 322 32

The efficacy of 1 alpha-hydroxycholecalciferol in the prevention of renal osteodystrophy in children commencing continuous ambulatory peritoneal dialysis was studied in 12 patients, 0.8-17 years of age, who were randomly assigned to either group I receiving standard therapy or to group II receiving in addition 10-20 ng/kg body weight/day of 1 alpha-hydroxycholecalciferol. Calcium carbonate compounds were used to control hyperphosphataemia. Mean plasma calcium (total and ionised) and phosphate levels were not significantly different between the two groups. All group I patients continued to have elevated plasma immunoreactive parathyroid hormone levels at 6 months compared to only 1 patient in group II (p less than 0.05). Four patients in group I developed subperiosteal erosions on radiography compared to the healing of mild lesions in 2 patients in group II. Bone histomorphometry on iliac crest needle biopsy specimens revealed a significant reduction in osteoid index and seam width in group II. Serum aluminum levels decreased during the course of continuous ambulatory peritoneal dialysis, and the significant staining for bone aluminum in 6 patients at the beginning of the study was no longer present in 5 patients at 6 months. Our data demonstrate that 1 alpha-hydroxycholecalciferol is beneficial in the prevention and treatment of bone disease in children on continuous ambulatory peritoneal dialysis.
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PMID:Renal osteodystrophy in children on CAPD: a prospective trial of 1-alpha-hydroxycholecalciferol therapy. 325 85

Bone disease related to aluminum toxicity (aluminum-related bone disease) presents with variable clinical and biochemical findings in patients with renal failure. Bone pain and muscle weakness are common, although afflicted patients can be asymptomatic. Bone pain can be generalized or localized to the hips, back, feet, or ankles; proximal muscle weakness is common. Most cases in the United States arise from the ingestion of aluminum-containing gels by patients on long-term dialysis treatment. Patients at increased risk for developing aluminum-related bone disease include those with earlier parathyroidectomy, failed renal transplant, previous bilateral nephrectomy, and diabetes mellitus. Biochemical features that are common with aluminum-related bone disease include plasma aluminum levels greater than 100 to 150 micrograms/L, serum parathyroid hormone (PTH) levels equal to or lower than those in dialysis patients without bone disease, and normal or slightly elevated serum calcium levels. Plasma alkaline phosphatase levels are often elevated. In our experience, microcytic anemia has been uncommon. An increase in plasma aluminum levels greater than 200 micrograms/L 24 to 48 hours after the infusion of the chelating agent deferoxamine (DFO) correlates with an increased bone aluminum content, and an increment greater than 400 micrograms/L suggests marked aluminum accumulation. Radiographs are usually nonspecific. When results from indirect diagnostic procedures are equivocal, a bone biopsy is necessary. After a diagnosis of aluminum-related bone disease is established, therapy with DFO may be useful. DFO increases both the total plasma aluminum level and its ultrafilterable fraction. After an infusion of DFO, the removal of aluminum increases from 50 to 300 micrograms to 4 to 8 mg per dialysis session. Aluminum removal is similar during continuous ambulatory peritoneal dialysis after either intravenous (IV) or intraperitoneal (IP) administration of DFO. Usually, 2 to 4 g of DFO is administered once weekly, but the optimal dose and duration of therapy have not been determined. Symptoms usually improve after 4 to 12 weeks, and bone biopsies show improvement after treatment for 6 to 12 months. Further experience with DFO is needed, both to identify the optimal dosage and to clarify the risks of long-term therapy in patients with renal failure.
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PMID:Diagnosis of aluminum-related bone disease and treatment of aluminum toxicity with deferoxamine. 329 88

Bone disease is recognized as a major problem in dialysis patients. initially, hyperparathyroidism was thought to be the major cause of bone disease in these patients. However, an aluminum-related bone disease has been identified in dialysis patients receiving exogenous aluminum. Patients with hyperparathyroidism and aluminum toxicity present with similar clinical and laboratory features; therefore, diagnosis of these two bone abnormalities is often difficult. Understanding normal bone development helps to elucidate the distinctions between aluminum and renal osteodystrophy. Patients with either bone syndrome may present with hypercalcemia, elevations in parathyroid hormone levels, bone pain, fractures, and radiographic evidence of subperiosteal resorption. The subtleties of these syndromes must be understood to avoid misdiagnosis. A diagnosis of hyperparathyroidism may lead to a parathyroidectomy, exacerbating the development of aluminum toxicity. Hyperparathyroidism is associated with increased surface osteoid, a high bone formation rate, increased numbers of bone cells, abnormal "twoven" osteoid, and low serum aluminum levels. Aluminum toxicity is associated with a low rate of bone turnover, paucity of bone cells, maintenance of a "laminar" osteoid, and significant aluminum bone deposition. Serum aluminum level measurements are key to the diagnosis of aluminum toxicity. For patients displaying intermediate aluminum values, the deferoxamine (DFO) challenge test is necessary for diagnosis. If noninvasive methods fail to determine a definitive diagnosis, a bone biopsy is required.
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PMID:Aluminum and renal osteodystrophy. 329 91

Hypercalcemia has been infrequently associated with Hodgkin's disease. When seen, most cases have been attributable to skeletal invasion by disease. Herein is described a 40-year-old man with a 15-year history of Hodgkin's disease. Each of four disease recurrences was heralded by hypercalcemia occurring in the absence of bone disease or elevation of parathyroid hormone levels. Marked elevations of 1,25-dihydroxyvitamin D levels were observed that paralleled his disease course and response to therapy. The repetitive association of hypercalcemia with an elevation of 1,25-dihydroxyvitamin D in this case provides further evidence of lymphoma-associated production of this vitamin.
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PMID:Recurrent hypercalcemia and elevated 1,25-dihydroxyvitamin D levels in Hodgkin's disease. 333 20


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