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)

Twenty five hormone manipulated patients with prostate cancer and metastatic bone disease, treated at least 6/12 previously by hormone manipulation, were given intravenous infusions of Disodium Pamidronate (APD) over a 6 month period. Patients received 30 mg weekly for 4 weeks then twice monthly for 5 months. No other treatment was administered during study. Eleven of 17 patients with pain at the start of the study were pain free at the end. Fasting morning calcium excretion and serum osteocalcin fell significantly with Pamidronate (P less than 0.0001) and urine hydroxyproline was lowered in 13/20 evaluable patients at 6 months. Alkaline phosphatase fell in a proportion of patients and five of 17 patients with previously progressive bone scans stabilised (4) or regressed (1) on treatment. Rising acid phosphatase levels were also lowered in five patients. It is concluded that Pamidronate may be effective in palliating bone pain in some patients and has a stabilising influence on abnormally high bone turnover in metastatic prostate cancer. Further controlled studies of the compound are now warranted.
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PMID:Osteoclast inhibition by pamidronate in metastatic prostate cancer: a preliminary study. 200 84

A patient who developed severe metabolic bone disease is presented. He had received long-term home parenteral nutrition (HPN) following extensive small bowel resection after mesenteric vein thrombosis. Bone disease caused by aluminum intoxication had components of osteomalacia and low-turnover osteoporosis. Aluminum was detected at the surface of mineralized bone and was elevated in the serum, resulting in a positive deferoxamine infusion test. One year of treatment with high doses of calcium (up to 24 mEq per day) significantly diminished the patient's bone pain, increased the serum levels of calcium, abolished aluminum deposits in the mineralized trabecula, improved bone formation, and increased trabecular bone volume as assessed by repeated histomorphometric analysis.
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PMID:Successful high-dose calcium treatment of aluminum-induced metabolic bone disease in long-term home parenteral nutrition. 164 Jun 45

Congenital erythropoietic porphyria (CEP) is a rare disorder of heme biosynthesis that results in the production of large quantities of photoactive porphyrins. The clinical syndrome is dominated by extreme photosensitivity with mutilation of light exposed extremities and hemolytic anemia. Bone disease has been occasionally noted, but is not well characterised. We describe a man with CEP who developed bone pain and spinal crush fractures at the age of 22. Skeletal radiographs revealed features typical of other severe hemolytic anemias, but in addition there was loss of the terminal phalanges of the hand as a result of photomutilation. Spinal bone density (assessed by DPA) was reduced and at the hip bone density was at the lower limit of normal. The metacarpal cortical bone density was 2.9 standard deviations below normal. Biochemical and histological studies accelerated bone turnover. Although the serum 250H vitamin D concentration was very low (because of light avoidance) there was no evidence that the bone disease was a consequence of this. Treatment for one year with clodronate and a high transfusion regime was associated with small reductions in serum alkaline phosphatase and urine hydroxyproline excretion, but there was no improvement in bone mineral density. We conclude that CEP has a distinctive osteodystrophy comprising osteolysis of light-exposed extremities and a high turnover type of osteoporosis. Privational vitamin D deficiency may also occur. The effect upon bone of the new therapies for CEP should be considered.
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PMID:The osteodystrophy of congenital erythropoietic porphyria. 206 45

Data on the long-term treatment of myeloma bone disease with bisphosphonates are scanty. In a prospective pilot trial we evaluated the effect of long-term parenteral administration of dichloromethylene bisphosphonate (Clodronate), in addition to standard chemotherapy, in 30 patients with active myeloma bone disease. Patients were treated with a mean of 4 courses (range 2-8) of Clodronate: 300 mg/day i.v. for seven days followed by 100 mg/day i.m. for 10 days, administered at a mean interval of 4 months (range 3-6). The median follow-up was 24 months (range 8-36). Clodronate reduced bone pain rapidly and significantly, and reduced the mean values of the biochemical indices of bone resorption to within normal limits; these effects were maintained throughout the follow-up. In three hypercalcemic episodes serum calcium became normal after 2-5 days of treatment with Clodronate. No toxic or side effects were noticed. The occurrence of skeletal morbidity in patients treated with Clodronate was compared with that observed in the control group of myeloma patients (p less than 0.001) in severe bone pain as well as in the incidence of new osteolytic lesions and pathological fractures (p less than 0.001). Supportive Clodronate therapy contributes significantly in controlling the progression of myeloma bone disease.
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PMID:Long-term effects of parenteral dichloromethylene bisphosphonate (CL2MBP) on bone disease of myeloma patients treated with chemotherapy. 213 6

A 59-year-old male presented with systemic mastocytosis with extensive skeletal involvement resulting in vertebral compression fractures and bone pain. Histomorphometric analysis of bone revealed increased mast cells, elevated static parameters of bone resorption, and low bone formation. Serum calcium, phosphorus, and alkaline phosphatase were normal; however, serum 1,25-dihydroxyvitamin D3 and osteocalcin levels were low. Histamine levels in plasma and urine were elevated. Following therapy with ketotifen, the patient had resolution of bone pain along with decreased flushing and pruritus. Elevated plasma and urine histamine levels normalized, as did 1,25-dihydroxyvitamin D3 and osteocalcin levels. Indices of low bone formation improved on therapy. Eroded surfaces improved but remained elevated. This case is the first demonstration that bone symptoms and histomorphometric change in systemic mastocytosis are reversed with inhibition of mast cell degranulation. The role of mast cells and their products in bone metabolism is poorly understood, but the therapy of bone disease in systemic mastocytosis should include inhibition of the release of mast cell products along with the use of histamine antagonist.
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PMID:Inhibition of mediator release in systemic mastocytosis is associated with reversal of bone changes. 227 Jul 75

In a multicentre open trial 530 patients suffering from primary osteoporosis, secondary osteoporosis and Sudeck's disease were enrolled to assess synthetic human calcitonin efficacy on bone pain relief. Spontaneous pain, pain on movement, provoked pain, functional impairment and patient's assessment were recorded. During the first 30 days of treatment, all the parameters significantly improved (p less than 0.01) and the tolerability was satisfactory. Four hundred and ten patients entered a follow-up study, this number gradually decreasing over a 6-month period due to a satisfactory outcome. Efficacy on bone pain remained very high in most of the patients, many of whom continued to improve. These results suggest that synthetic human calcitonin is highly effective on pain and functional impairment in bone disease and is well tolerated.
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PMID:Human calcitonin in the management of osteoporosis: a multicentre study. 241 7

We report a patient on maintenance dialysis with oxalosis and radiographical signs typical of hyperparathyroid bone disease in patients with end-stage renal insufficiency. The patient underwent a subtotal parathyroidectomy. Because his bone pain worsened during long-term dialytic therapy, a bone biopsy was performed and revealed crystalline deposits in trabecules and the bone marrow characteristic of oxalate. Trabecular destruction and signs of defective mineralization of bone were also found. When the diagnosis was made, the patient had become addicted to narcotic analgesics; he died from an overdose. The case underscores the limits of skeletal radiographs for the diagnosis of oxalosis in bone. Furthermore, the radiographic findings may lead to erroneous conclusions in patients with renal osteodystrophy because the radiographic signs of oxalosis can mimic those of hyperparathyroid bone disease.
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PMID:Oxalosis in bone causing a radiographical mimicry of renal osteodystrophy. 243 94

Bone-seeking radionuclides have been used to treat bone pain due to metastatic bone disease for over 40 years. More than 10 clinical studies using radiostrontium (Sr-89) have shown benefit in about 70-80% of patients having refractory bone pain from prostate, breast and other metastatic bone cancers, with minimal hematological toxicity. Other radionuclides, such as, radiophosphate (P-32), Yttrium-90, lodine-131, Rhenium-186, have also been used. Tumor necrosis has been found within the range of beta irradiation from the surrounding shell of bone incorporating the radionuclide. New strategies using radionuclides may be able to provide more effective methods of treatment, perhaps, beyond palliation. For example, the effect of low dose continuous radiation can be potentiated by hypoxic cell sensitizers. In addition, the kinetics of radionuclide uptake and retention can be modulated to increase the dose of radiation delivered to osteoblastic metastatic lesions, such as osteosarcoma.
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PMID:A new look at radionuclides therapy in metastatic disease of bone (review and prospects). 246 20

D-lactate accumulates in some patients with malabsorption who continue oral intake of carbohydrate leading to a clinical syndrome of acidosis and encephalopathy. To assess the possibility that D-lactate contributes to acidosis and/or metabolic bone disease in patients with malabsorption receiving long-term parenteral nutrition yet maintaining oral intake, D-lactate levels in serum and urine were measured in 14 long-term parenteral nutrition subjects (average duration of support 74 months) and 27 control subjects. Significant elevations in both serum and urine D-lactate were found in only two parenteral nutrition subjects. Both subjects with elevated D-lactate levels had bone pain, x-ray evidence of fractures, and biopsy evidence of osteomalacia. These studies suggest that D-lactate accumulation may be a heretofore unappreciated metabolic abnormality associated with metabolic bone disease and acidosis in patients with malabsorption who are supported by long-term parenteral nutrition.
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PMID:D-lactate and metabolic bone disease in patients receiving long-term parenteral nutrition. 249 43

Metastatic bone disease represents the most disabling complication in patients with prostatic carcinoma. In an open multicenter trial 80 out of 92 patients with bone metastasis due to prostatic carcinoma experienced a dramatic improvement of bone pain after treatment with 300 mg clodronate infused intravenously daily for 10 days. Further to this, 56 patients were randomly allocated to four single-blind controlled therapeutic trials, assessing bone pain by daily consumption of analgesic drugs and by visual analogue scale. In the first protocol the effects of 2 weeks' treatment with intravenous infusion of either 300 mg clodronate dissolved in 500 ml saline (7 patients) or 500 ml saline (6 patients) were compared. The differences in both pain score and analgesic consumption were so striking that the trial was not extended for ethical reasons and all patients on placebo were given clodronate intravenously. Oral administration of 1200 mg clodronate for 2 weeks was completely ineffective in 11 patients. Intramuscular administration of 100 mg clodronate for 2 weeks induced in 12 patients a significant fall in analgesic consumption but not in the pain score. In most of the 13 patients given clodronate intravenously for 2 weeks bone pain relapsed fairly soon. However, in 18 patients a maintenance therapy with 1200 mg clodronate/day for at least 6 weeks after a 2-week intravenous treatment course did prevent the relapse of bone pain. In all patients given clodronate routine biochemical examination was carried out during and after treatment. For an overall follow-up of 42 patient-years hematologic toxicity was never observed. These results confirm that clodronate represents the most effective and convenient conservative treatment of patients with painful bone metastasis from prostatic carcinoma.
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PMID:Clodronate therapy of metastatic bone disease in patients with prostatic carcinoma. 252 1


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