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)

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

A case of osteomalacia associated with hypophosphatemia, decreased tubular reabsorption of phosphorus, hyperphosphaturia and renal glycosuria with associated bone pain and myopathy is presented. The patient was found to have multiple osteolytic lesions of bone which, on biopsy, proved to be sclerosing hemangiomas of bone. Treatment with oral phosphate and vitamin D effected a diminution in his symptoms of bone pain and muscular weakness. The literature on hypophosphatemic phosphaturic osteomalacia associated with mesenchymal tumors is reviewed. It has been suggested that certain mesenchymal tumors elaborate a yet to be identified humoral substance which decreased synthesis of 1 alpha, 25-dihydroxycholecalciferol causing decreased tubular reabsorption of phosphorus, hyperphosphaturia, hypophosphatemic osteomalacia and hypophosphatemic myopathy.
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PMID:Tumorous phosphaturic osteomalacia. Report of a case associated with multiple hemangiomas of bone. 22 41

In an initial safety study, phosphorus-32 (as diphosphonate) was administered intravenously to five patients with painful bone metastases from prostatic carcinoma; two patients received 9 mCi and three were given 3 mCi. Hematological, biochemical, ECG, x-ray, bone-scan data, and clinical observation, were followed for 2 mo. At both dose levels, bone-marrow depression was noted. One of the patients, who received 9 mCi, had only a slight dip in the levels of circulating white blood cells and platelets. The other 9-mCi patient was the only one with discrete metastases by bone scan; he had bone-marrow depression, from which he recovered, and was the only one of the five who had relief of bone pain.
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PMID:[32P] diphosphonate dose determination in patients with bone metastases from prostatic carcinoma. 41 89

The osteoblastic effect of inorganic phosphorus and the inhibitory action of calcium on parathyroid hormone secretion formed the basis for a therapeutic trial in which both elements were given intravenously in an alternating sequence for one year to five patients with severe osteoporosis. During treatment, calcium and phosphorus balances were positive, and serum phosphorus concentrations decreased. Iliac crest bone biopsy specimens obtained one year after beginning treatment demonstrated an increase in the thickness of cortical bone. All patients experienced lasting relief of bone pain, and the rate of spontaneous fractures decreased from at least one fracture per year to none following the beginning of treatment. These findings suggest that long-term treatment with alternating phosphorus and calcium infusions may result in lasting relief of symptomatic osteoporosis. It is proposed that the observed improvement reflects an increase in bone mass resulting from enhanced bone formation.
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PMID:Effects of alternating phosphorus and calcium infusions on osteoporosis. 97 42

Between 1969 and April 1975 24 patients with severe secondary hyperparathyroidism (sHPT) clinically presenting with uremic osteopathy required either total (n=5) or subtotal (n=18) parathyroidectomies, 17 patients were already supported by maintenance hemodialysis, 6 patients suffered from terminal renal insufficiency. The leading clinical symptoms consisted of general osteoporosis, spontaneous fractures, extraosseous calcifications and histologically proven dissecting fibroosteoclasia. After operation 18 patients experienced complete relief from their complaints and repair of their skeletal lesions, 2 patients required reexploration for an undetected hyperfunctioning 4th parathyroid gland, regretfully with no success. In 4 patients with subtotal parathyoidectomy a recurrence of varying intensity with increased PTH-secretion from the remnant had to be registered after months and years.-The indication for surgical treatment of sHPT due to chronic renal failure has to be based on two sets of findings: 1) inadequate longterm suppression of increased PTH secretion by conservative measures like high dialysate calcium concentration or oral calcium intake, serum phosphorus depletion by oral intake of aluminium hydroxyde and possibly also by Vit. D; 2) persistent hypercalcemia, progressive osteodystrophy and severe complaints like bone pain and pruritus.
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PMID:[Surgical aspects of secondary hyperparathyroidism (author's transl)]. 101 8

A 23-year-old man with medullary cystic disease had been undergoing hemodialysis for 5 years and had become confined to a wheelchair because of renal osteodystrophy. He was treated with 125-dihydroxycholecalciferol, 2.0 mug (later 1.0 mug) three times a week, administered by way of the venous end of the dialysis machine. Within 1 month bone pain lessened and his ability to stand and walk improved. By 3 months he was walking short distances and by 5 months, long distances. Calcium balance was near zero before treatment and was strongly positive during treatment. Bone mineral content in the lower femur, measured by photon absorptiometry, increased at a rate of 32.2% per year. In contrast, 26 other patients on long-term hemodialysis had a mean loss of bone mineral content of 14.0% per year. Radiographs taken during treatment showed a decrease in subperiosteal bone resorption and healing of a pseudofracture. A significant decrease in the mean serum alkaline phosphatase value was noted during treatment, but no significant changes in mean serum calcium or phosphorus values were seen.
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PMID:Effect of I,25-dihydroxycholecalciferol in renal osteodystrophy. 111 76

Ten patients with calcitriol-resistant rickets caused by a defect in the ligand-binding domain of the vitamin D receptor are described. Eight patients, 1.7 to 13.8 years of age, received high doses of elemental calcium (range, 0.4 to 1.4 gm/m2) through indwelling intracaval catheters for periods of 1.8 to 3.8 years. Two other patients, aged 1.1 and 2.2 years, were given oral calcium therapy as the sole mode of treatment. In five of the intravenously treated patients, oral calcium therapy was initiated after radiologic evidence of healing of the rickets. To maintain normal serum calcium concentration, the patients required daily doses of elemental calcium of 3.5 to 9 gm/m2 body surface area. Clinical improvement was observed within a week of the start of intravenous therapy, with disappearance of bone pain; several of the younger patients started to walk for the first time. Growth velocity increased within 2 to 3 months, from a pretreatment rate of -0.8 to -6.3 standard deviation score (SDS), to a posttreatment rate of +0.1 to +5.1 (SDS). Serum calcium, parathyroid hormone, phosphorus, and alkaline phosphatase values returned to normal within a year. Radiologic signs of healing occurred more rapidly in the intravenous treatment groups and in younger patients. Episodes of septicemia occurred frequently in those receiving parenteral therapy and required replacement of the catheter. We recommend that in the treatment of calcitriol-resistant rickets, oral calcium therapy be started at the youngest possible age, in doses to the limit of intestinal tolerance. When rickets is present, calcium should be infused through a large vessel in doses high enough to produce normocalcemia, normophosphatemia, and suppression of parathyroid hormone. Only after radiologic healing has been observed can oral calcium therapy be introduced.
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PMID:Calcium therapy for calcitriol-resistant rickets. 133 89

Total parenteral nutrition (TPN) for a prolonged period of time can be associated with bone pain and osteomalacia. We performed a study on the phosphorus/calcium metabolism and serum levels of osteocalcin (BGP), a protein proposed as constituting the bone turnover index in 31 patients receiving TPN (age 57 +/- 14 years, 22 males and 9 females) diagnosed as suffering from pathology of the digestive tract or geno-urinary pathology. The duration of the TPN was from 9.1 +/- 6.6 days (range 2-31 days). We observed and increase of FA (178 +/- 101 U/l), with a significant decrease of BGP (2.2 +/- 2.0 ng/ml vs. 3.7 +/- 1.3 ng/ml in controls; p less than 0.001). Serum levels of phosphorus and calcium corrected according to proteins were within normal limits. Hypercalciuria was detected in the urine (328 +/- 278 mg/24 hours), and phosphaturia (607 +/- 522 mg/24 hours). Based on the BGP results, we can conclude that patients subjected to TPN for a short period of time undergo a decrease in bone turnover.
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PMID:[Effect of total parenteral nutrition on bone metabolism]. 139 Nov 9

Management of bone pain in patients with multiple osseous metastases is a significant clinical problem. Phosphorus-32 has been used as systemic radioisotope therapy for the management of bone pain for over 40 years. However, significant hematological depression usually results and its use is limited. More recently, the bone-seeking radiopharmaceuticals strontium-89, samarium-153-ethylenediaminetetramethylene phosphonic acid, and rhenium-186-hydroxyethylidene diphosphonate have all been used as palliative treatment for patients with clinically significant bone pain. Excellent clinical responses with acceptable hematological toxicity have been observed. The clinical results rival those of external beam radiation therapy, with fewer systemic and hematological side effects. Systemic radionuclide therapy is indicated in the management of patients with painful metastatic prostate cancer in bone as soon as they escape primary hormonal management. This therapy also should play a role in the management of many patients with advanced breast cancer metastatic to bone. The role of radionuclidic therapy in osseous metastases from other malignancies is still being investigated. These compounds also hold promise as primary therapy for tumors of osseous origin. Systemic radionuclide therapy of painful bony metastases will become common in nuclear medicine practice in the next decade.
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PMID:Radionuclide therapy of intractable bone pain: emphasis on strontium-89. 158 3

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


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