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Query: UMLS:C0151825 (bone pain)
 3,118 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty patients with Paget's disease of bone were reviewed with regard to the basis of their symptoms and the long-term results of treatment. Twenty-four patients (48%) presented with pain localised within bone, while 17 (34%) presented with symptoms of degenerative joint disease. Three patients presented with bone pain and arthritis and the remaining six with fractures, ataxia, or painless deformity. Symptomatic osteoarthritis of the hip (OA) developed in 25 patients (50%) with approximately half developing radiological changes identical to those of idiopathic OA. Among the other patients those with coxa vara tended to show medial (rather than superior) joint space narrowing and severe Paget's disease on both sides of the joint. Arthritic pain, stiffness, and reduced mobility in other joints (knee, ankle, and wrist) were associated clinically with bone deformity adjacent to the affected joint and radiologically with distorted articular surfaces and narrowed joint spaces; sclerosis, subarticular cyst formation, and osteophytosis were usually absent. Fifteen patients were treated with calcitonin for bone pain alone; all claimed long-term 'good to complete' relief. By contrast, none of the 14 with arthritic symptoms responded to calcitonin when assessed retrospectively. Results of surgical and other medical treatment were analysed. Careful clinical evaluation is a prerequisite for optimal treatment in Paget's disease.
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PMID:Bone and joint symptoms in Paget's disease. 624 Sep 66

Paget's disease of bone in 51 patients was treated with ethane-1, hydroxy-1,1 diphosphonate (EHDP) for six months at a dosage of 5 mg/kg/day. Clinically, the analgesic effect on bone pain is clear, with parallel reduction in radioisotope uptake observed by quantitative bone scintigraphy. There is also a reduction of about 70% of the excess level of serum alkaline phosphatase and total 24-hour urinary hydroxyproline. Histologically, there is a significant reduction in both the osteoclastic resorption surfaces and the number of osteoclasts. In contrast to that obtained by calcitonin, these clinical, biologic, and histologic changes continue for at least one year beyond the end of the treatment. That is the main characteristic of this treatment, of which the clinical and biologic tolerance is admittedly very satisfactory. Accumulation of osteoid tissue, which is indicative of a mineralization defect, does not appear at low dosages under the prescribed conditions. EHDP (5 mg/kg/day) can be regarded as effective treatment for some patients with Paget's disease of bone.
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PMID:Treatment of Paget's disease of bone with ethane-1, hydroxy-1,1 diphosphonate (EHDP) at a low dosage (5 mg/kg/day). 640 70

Glucagon, porcine calcitonin, and mithramycin were given to patients with Paget's disease of bone. There was rapid complete relief of bone pain accompanied by biochemical improvement or normalization in all cases. Calcitonin and glucagon appear to have additive properties in Paget's disease and the use of the 3 drugs in combination may reduce the incidence of side effects and the development of "drug resistance". The cost of treatment might also be reduced if periodic treatment as demonstrated in Case 1 is used.
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PMID:Control of osteitis deformans using glucagon, calcitonin, and mithramycin. 645 56

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

Eleven patients with Paget's disease of bone, treated intermittently for 2-4 years with porcine calcitonin (pCT) and clinically resistant to pCT [no modifications of serum alkaline phosphatase (ALP) and urinary hydroxyproline ( uHOP ) during pCT administration] were treated with 0.5-0.25 mg/day of human calcitonin (hCT) for 3-6 months. Nine of our patients showed biochemical improvement during the first 2 months of treatment, with reduction in ALP and uHOP . In one patient with slightly increased ALP and uHOP , and in another one during the second treatment course, hCT treatment did not modify the biochemical indices of bone disease. However all patients, including those with biochemical resistance, experienced a remarkable diminution of bone pain, which had not been observed during previous pCT treatment courses. Therefore, hCT appears to be indicated for therapeutic use in patients who are resistant to foreign calcitonins.
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PMID:Response of Paget's disease to human calcitonin in patients resistant to porcine calcitonin. 672 70

Two cases of women with adult hypophosphatasia illustrate the clinical spectrum and potential difficulties in the diagnosis of this condition. Both patients had subnormal serum alkaline phosphatase activity, absence of leukocyte alkaline phosphatase, increased amounts of urinary phosphoethanolamine, and normal levels of immunoreactive calcitonin and parathyroid hormone. In undecalcified bone biopsy specimens, the number of osteoblasts and the tetracycline-labeled calcification front were similar in the two patients, although the percentage of unmineralized bone matrix and the extent of osteoid-covered bone surface were different. Twenty years of bone pain, severe skeletal deformities, and a generalized increase of osteoid in one patient contrasted with an 18-month history of bone pain and patchy osteoid in the other. These cases suggest that adult hypophosphatasia is a heterogeneous disorder and may be more common than previously realized.
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PMID:Heterogeneity of adult hypophosphatasia. Report of severe and mild cases. 723 80

40 patients with bone disease due to chronic renal failure have been treated with 1 alpha-hydroxyvitamin D3 or 1,25-dihydroxyvitamin D3 for a total of 750 patient-months. Both compounds were very effective in relieving bone pain and muscle weakness, and in reversing the radiographic and biochemical indices of disturbed skeletal metabolism. Their effects as judged from bone biopsies were, however, less complete, and histological improvement occurred only in a few patients. Patients with the combination of osteitis fibrosa and osteomalacia responded better than patients with either abnormality alone. Factors of importance in adversely influencing the outcome of treatment included a high pre-treatment level of calcium or immunoreactive parathyroid hormone, and a failure to augment secretion of calcitonin during treatment. It is concluded that a major therapeutic advantage of 1 alpha-OHD3 and 1,25(OH)2D3 over previously available forms of vitamin D is their rapid onset and reversal of action. These drugs do not invariably reverse bone disease and may give rise to unwanted effects. They should therefore only be used with adequate clinical, biochemical and radiographic supervision. They should not be used indiscriminately in all renal patients.
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PMID:An evaluation of 1 alpha-hydroxy-and 1,25-dihydroxyvitamin D3 in the treatment of renal bone disease. 735 70

Clodronate (clodronic acid, dichloromethylene bisphosphonate) is a bisphosphonate which has demonstrated efficacy in patients with a variety of diseases of enhanced bone resorption including Paget's disease, hypercalcaemia of malignancy and osteolytic bone metastases. In addition, early reports demonstrating potential efficacy of clodronate in the treatment of osteoporosis suggest a possible role in this debilitating disease. Short term intravenous administration (usually 300 mg/day for 5 days) or longer courses of oral clodronate (usually 1600 mg/day for 6 months) effectively reduced bone pain and/or improved mobility in most patients with Paget's disease, and these effects persisted for up to 12 months after discontinuing clodronate. When administered intravenously (300 mg/day for up to 12 days) to patients with malignant hypercalcaemia, serum calcium levels declined significantly within 2 days of starting treatment and approximately 70 to 95% of patients became normocalcaemic. While there is less experience with oral administration, clodronate (800 to 3200 mg/day) achieved normocalcaemia in the majority of patients, usually within 1 week, and serum calcium levels remained significantly reduced from baseline for up to 6 months with continued treatment. Clodronate is clearly superior to placebo and, based on a retrospective analysis, appears to produce greater and more sustained reductions in serum calcium levels than calcitonin in patients with malignant hypercalcaemia. The few available prospective comparative trials showed that clodronate is at least as effective as etidronate, but comparisons with alendronate and pamidronate produced results of questionable clinical relevance because of low bisphosphonate dosages used in these trials. Nevertheless, single intravenous doses of clodronate 600 mg or alendronate 7.5 mg (both agents repeated on day 3 if necessary) were comparable in efficacy, whereas a single intravenous dose of pamidronate 30 mg was more effective than a single intravenous dose of clodronate 600 mg. Normocalcaemic patients with osteolytic bone metastases due to advanced breast cancer experienced significant reductions in the number of episodes of hypercalcaemia and terminal hypercalcaemia, incidence of vertebral fractures and overall rate of morbid events, including the need for radiotherapy to treat bone-related pain, following treatment with clodronate 1600 mg/day for 3 years in a large placebo-controlled study. A similar large placebo-controlled trial in patients with multiple myeloma demonstrated that clodronate 2400 mg/day orally for 2 years significantly reduced progression of osteolytic bone lesions. Follow-up data from clinical trials revealed that the effects on development of fractures and hypercalcaemia persisted for at least 12 months after the drug was discontinued.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clodronate. A review of its pharmacological properties and therapeutic efficacy in resorptive bone disease. 752 33

Hypercalcemia of malignancy is most commonly due to the effects of parathyroid hormone-related peptide, which acts as a humoral factor to cause generalized osteoclast-mediated bone resorption and reabsorption of calcium by the kidney tubule, and may also act as a local resorptive factor adjacent to bone metastases. Local resorptive mechanisms are less common causes of malignant hypercalcemia than previously believed. Treatment begins with intravenous fluid rehydration, followed by a furosemide diuresis and the bisphosphonate pamidronate, 60-90 mg, intravenously. Gallium nitrate is an efficacious but inconvenient alternative to pamidronate. Calcitonin combined with pamidronate is a reasonable initial therapy for severe hypercalcemia to hasten normalization of the serum calcium. Steroids should be reserved for hypercalcemia due to tumor production of 1,25 dihydroxyvitamin D, or for steroid-responsive malignancies. Oral or parenteral bisphosphonates can be used to maintain normocalcemia. In addition to improving the morbidity of acute hypercalcemia, bisphosphonate therapy has been shown to reduce bone pain and pathological fractures in patients with bone metastases, and calcitonin also has a potent analgesic effect in these patients. Treatment for hypercalcemia should therefore be considered in the majority of patients in the palliative care setting.
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PMID:Hypercalcemia of malignancy in the palliative care patient: a treatment strategy. 754 27

Hypercalcemia is the most common paraneoplastic syndrome associated with cancer. This paper addresses the etiology and pathogenesis of hypercalcemia of malignancy and discusses the relative contributions of local and humoral effects on bone and renal calcium homeostasis. The roles of parathyroid hormone-related protein and other osteolytic cytokines are outlined. New biochemical markers that enable more specific monitoring of the response of bone metastases to treatment are introduced, including urinary excretion of the collagen crosslinks pyridinoline and deoxypyridinoline. The clinical management and prevention of hypercalcemia is systemically outlined, including indications for bisphosphonate, glucocorticoid, and calcitonin therapy. The results of recent trials of bisphosphonate therapy for the prevention of tumor progression and its subsequent problems such as bone pain, fracture, and hypercalcemia also are discussed.
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PMID:Hypercalcemia and bone resorption in malignancy. 763 18


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