Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151825 (bone pain)
 3,118 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

An 86-year-old woman with a history of treated hyperthyroidism and a 20-year history of untreated primary hyperparathyroidism developed generalized bone pain and a pseudofracture of the midshaft of the left femur. Laboratory examinations revealed elevated serum calcium, alkaline phosphatase, and C-terminal parathyroid hormone levels. Serum inorganic phosphate was below normal and 25-hydroxyvitamin D levels were low-normal. An undecalcified transiliac bone biopsy specimen following tetracycline double labeling revealed osteomalacia and osteitis fibrosa. Following treatment with vitamin D and phosphate, the serum inorganic phosphate level rose to normal. There was a decrease in bone pain, and the pseudofracture healed. However, the serum calcium, alkaline phosphatase, and C-terminal parathyroid hormone levels remained elevated. Longstanding primary hyperparathyroidism causes chronic hypophosphatemia and may lead to osteomalacia. Osteomalacia and its consequences may be part of the spectrum of bone disease seen in patients with longstanding primary hyperparathyroidism.
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PMID:Osteomalacia as a very late manifestation of primary hyperparathyroidism. 334 77

We performed bone biopsies on 13 patients who had been on dialysis from 11.1 to 17.6 years (mean 14.5 +/- 2.1 years) to evaluate renal osteodystrophy in long-term dialysis patients. Seven patients had osteitis fibrosa and 6 had a mineralization defect. Stainable bone aluminum was present in 9 of the patients. Serum phosphorus and parathyroid hormone levels were higher and bone aluminum lower in patients with osteitis fibrosa compared to those with a mineralization defect. Those seriously disabled with decreased mobility due to bone pain (7 of 13) had more bone aluminum than those patients with minimal or no disability (1.55 +/- 1.0 mm/mm2 vs. 0.11 +/- 0.18, respectively, p less than 0.01). A history of fractures during the years on dialysis was also associated with elevated stainable bone aluminum (p = 0.04). We conclude that in long-term dialysis patients aluminum-related osteodystrophy results in greater morbidity than osteitis fibrosa. We recommend that aluminum-containing phosphate binders be used sparingly in patients who are to remain indefinitely on dialysis.
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PMID:Renal osteodystrophy in patients on hemodialysis for more than 10 years. 380 34

We encountered 11 patients with aluminum-associated bone disease (AABD), and treated them with deferoxamine (DFO). In 3 patients, a second bone biopsy was done during DFO treatment. Clinical features of AABD were compared with surgically proven secondary hyperparathyroidism (2 degrees HPT) with osteitis fibrosa on X-ray. Patients with AABD had disabling bone pain. This disease showed radiological signs ranging from normal, localized bone atrophy, to multiple fractures. It was characterized by increased soft tissue activity and localized abnormal uptake of 99mTc-MDP, detected by skeletal scintigrams. Patients with AABD had low levels of parathyroid hormone and alkaline phosphatase, but high aluminum (Al) levels compared to those with 2 degrees HPT. Serum Al increased after DFO administration, and the patients improved both clinically and histologically. 1-alpha-Hydroxyvitamin D3 (1-alpha-OH D3) was not effective for AABD. We concluded that the administration of antacids containing Al should be minimized in dialysis patients.
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PMID:Clinical features of aluminum-associated bone disease in long-term hemodialysis patients. 394 60

We report data from three patients with severe Paget's disease of bone who were treated with mithramycin.Mithramycin infusion resulted in a fall in plasma calcium, phosphate, alkaline phosphatase, and urinary hydroxyproline excretion. There was an improvement in calcium and phosphorus balance in two of the three subjects studied. A pronounced or complete relief of bone pain occurred in all three.We suggest that mithramycin exerts its beneficial effect in Paget's disease of bone by stimulating parathyroid hormone release. The parathyroid hormone released has a predominantly anabolic action on bone since its catabolic action is blocked by mithramycin, which inhibits bone resorption.
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PMID:Treatment of Paget's disease of bone with mithramycin. 554 93

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

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

A 53-year-old man with a history of long-term aluminum hydroxide antacid ingestion reported diffuse bone pain and multiple stress fractures over a two-year period. An undecalcified transiliac bone biopsy specimen revealed osteomalacia with osteitis fibrosa; plasma parathyroid hormone and cyclic AMP levels were normal. Following withdrawal of antacids and treatment with calcium and phosphorus, an initially elevated plasma, 1,25-dihydroxyvitamin D level fell to within the normal range, accompanied by decreased bone pain, healed stress fractures, and increased axial bone mineral content as determined by computed tomography of lumbar trabecular bone. Phosphate deprivation and 1,25-dihydroxyvitamin D excess may contribute to the poor mineralization and exaggerated resorption of bone observed in this syndrome. The clinical, biochemical, radiologic, and histologic features of previously reported cases are reviewed. Early recognition of this syndrome is important, since appropriate therapy promotes skeletal remineralization and prevents morbidity.
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PMID:Osteomalacia and osteitis fibrosa in a man ingesting aluminum hydroxide antacid. 632 94

Because calcitonin administration has been shown to decrease the serum calcium level in certain hypercalcemic conditions, 10 patients on maintenance dialysis with renal osteodystrophy and persistent hypercalcemia were treated with salmon calcitonin for 3 months. While plasma calcium concentrations were reduced by calcitonin therapy in four patients, therapy was ceased in two patients due to a worsening of their hypercalcemia, although in another two patients the initial worsening of the hypercalcemia settled with continued therapy. No significant changes in calcium levels occurred in the remaining two patients. Analysis of the data suggests that a hypocalcemic effect of calcitonin was most likely in the presence of osteomalacia, while predominant osteitis fibrosa favored a hypercalcemic response. Calcitonin administration caused a mean increase in parathyroid hormone (PTH) secretion 3.6 +/- 1.5 to 6.5 +/- 1.7 ng/ml; p less than 0.05) after 6 weeks of therapy. Three patients reported improvement in their bone pain. These studies show that despite possible symptomatic and morphological effects of calcitonin, its hypocalcemic effect in patients with renal osteodystrophy and hypercalcemia is inconsistent.
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PMID:Effect of calcitonin on hemodialysis patients with hypercalcemia and renal osteodystrophy. 653 90

Deficiency of circulating 1 alpha-25-dihydroxyvitamin D3 (1 alpha,25(OH)2D) regularly occurs in hypoparathyroidism (HP) and pseudohypoparathyroidism (PHP). Osteomalacia is occasionally found in the two diseases. Two patients, one with HP and the other with PHP, both with symptomatic and biopsy-proven osteomalacia, were studied before and after treatment with 1 alpha,25(OH)2D3. Laboratory values before treatment were as follows: serum immunoreactive parathyroid hormone was undetectable in the patient with HP and was elevated in the patient with PHP. Serum 25-hydroxyvitamin D, measured by binding assay, was 131.5 and 61.9 nmol/l (normal: 69.1 +/- 15.9 nmol/l); serum 24,25-dihydroxyvitamin D, measured by binding assay, was 13.9 and 3.8 nmol/l (normal: 3.4 +/- 1.4 nmol/l); serum 1 alpha,25(OH)2D, measured by bioassay, was 28.6 and 29.0 pmol/l (normal: 77.3 +/- 22.8 pmol/l) and, measured by receptor assay, was 36.2 and 41.0 pmol/l (normal: 71.8 +/- 35.8 pmol/l) in the HP and PHP patients, respectively. Serum calcium was low and serum inorganic phosphate was high in both cases. Treatment with 1 alpha,25(OH)2D3 (3-5 micrograms per day for 10-12 months) restored serum calcium and inorganic phosphate to normal, alleviated bone pain and healed the osteomalacia as shown on repeat bone biopsy. Our results provide further evidence that isolated deficiency of 1 alpha,25(OH)2D may cause osteomalacia or rickets.
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PMID:1 alpha,25-dihydroxyvitamin D3 corrects osteomalacia in hypoparathyroidism and pseudohypoparathyroidism. 668 71


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