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)

The present study was an attempt to assess the cause of persistent pain in lower limbs among children from Kashmir. The study was conducted on one hundred children attending Paediatric out-patient department of Sher-i-Kashmir Institute of Medical Sciences, Srinagar. All the children were in the age group of 5 to 14 years. They showed markedly raised levels of serum alkaline phosphatase, whereas serum phosphorus, serum calcium levels and antistreptolycin O-titres were normal in 93% cases. None of them had any rheumatic or rheumatoid pathology. Among 15 suspected clinical rickets only three were established radiologically. Dietary and socio-economic history revealed deficient vitamin D intake and less exposure to sun. It was hypothesized that sub-clinical vitamin D deficiency could be a major cause of persistent pain in lower limbs and raised serum alkaline phosphatase could be the earliest marker of vitamin D deficiency. It was confirmed by injecting single dose of vitamin D (3 lac I. U.) which relieved bone pain and lowered the levels of serum alkaline phosphatase to normal within 14 weeks of initiation of therapy.
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PMID:Persistent limb pain and raised serum alkaline phosphatase the earliest markers of subclinical hypovitaminosis D in Kashmir. 262 Sep 72

In the courses of six years a severe hypophosphataemic osteomalacia, painful motor impairment and multiple rib fractures developed in a 51-year-old man. The symptoms gradually improved within one year under treatment with 3 micrograms daily of 1,25-dihydroxycholecalciferol, 3 g phosphorus and 3 g calcium, and biochemical parameters and the bone scintigram became normal. Ultimately, computed tomography, scintigraphy and digital subtraction angiography revealed a highly vascularized tumour in the condylar aspect of the right femur, and it was chiselled out. Histologically it was a mesenchymal phosphaturic tumour of haemangiopericytoma type of questionable benignity. After the operation the patient was symptom-free for some weeks without any drug treatment, but the latter was then resumed because of renewed bone pain. By now, two years later, he is essentially without pain and has full mobility. However, repeat scintigraphy and angiography revealed renewed tumour growth in the right femoral condyle.
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PMID:[Oncogenic hypophosphatemic osteomalacia]. 273 97

Two boys aged six and four with the syndrome of hereditary resistance to 1,25-dihydroxyvitamin D3 with rickets alopecia and growth retardation are presented. After unsuccessful therapeutic trials with pharmacologic doses of vitamin D or its active metabolites, the patients were treated by long-term intracaval infusions of calcium through an implantable catheter. A total of 0.5 to 0.9 g of elemental calcium was infused daily for 18 months and the serum calcium concentration was maintained at 9 to 10 mg/dl. Bone pain subsided within one week of treatment. Serum phosphorus, immunoreactive parathyroid hormone, and 1,25-dihydroxyvitamin D concentrations and alkaline phosphatase activity were normalized within four to nine months. Radiographs of the knees and hands revealed progressive healing of rickets with complete resolution after one year of treatment. The patients gained 12 cm and 8 cm per year in height as compared with 3 cm and 2 cm, respectively, in the previous year. A transilial bone biopsy obtained from one patient prior to treatment revealed severe osteomalacia associated with osteitis fibrosa. A follow-up biopsy examined after 12 months of therapy showed almost complete healing of osteomalacia and normal mineralization. These observations indicate the following: (1) Long-term intracaval calcium infusions are an effective mode of therapy for these patients, and (2) When adequate serum calcium and phosphorus concentrations are maintained, healing of rickets and normal growth rate could be achieved even in the absence of a normal 1,25-dihydroxyvitamin D3 receptor-effector system.
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PMID:Long-term intracaval calcium infusion therapy in end-organ resistance to 1,25-dihydroxyvitamin D. 282 6

Although more than 50 patients with the tumor-induced osteomalacia syndrome, characterized by remission of unexplained osteomalacia after resection of a coexisting tumor, have been reported, the pathogenesis of this syndrome is still not clear. We investigated the cause of biopsy-confirmed osteomalacia which was resistant to treatment with 1 alpha-hydroxyvitamin D3 in a 54-yr-old man. He had severe hypophosphatemia, a high serum alkaline phosphatase level, a low plasma 1,25-dihydroxyvitamin D level, and remarkably increased urinary phosphorus excretion. A tumor, with histological characteristics of a hemangiopericytoma, was found on his left thigh. After surgical removal of this tumor, his plasma 1,25-dihydroxyvitamin D and serum phosphorus levels increased to normal levels, and his bone pain subsided. The tumor was transplanted to athymic nude mice. A nodule formed in each mouse, with histological features identical to those of the original tumor, and the tumor-bearing mice had hypophosphatemia, high serum alkaline phosphatase levels, and increased urinary phosphorus excretion. When extracts of the original tumor were added to primary cultures of renal tubular cells, renal cAMP levels did not change, but 25-hydroxyvitamin D-1 alpha-hydroxylase activity was significantly inhibited. These data indicate tumoral production of some humoral factor(s) inhibiting 25-hydroxyvitamin D-1 alpha-hydroxylase activity and phosphorus reabsorption unrelated to adenylate cyclase-cAMP production in proximal renal tubules.
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PMID:Hemangiopericytoma-induced osteomalacia: tumor transplantation in nude mice causes hypophosphatemia and tumor extracts inhibit renal 25-hydroxyvitamin D 1-hydroxylase activity. 283

Following a four-day control period during which an elevated serum calcium level either stabilized or continued to rise despite maximally tolerated saline diuresis, 12 patients with neoplastic hypercalcemia were treated with intravenous etidronate disodium (etidronate) 7.5 mg/kg/day for up to seven days. Serum calcium reverted to normal levels in all patients, with the mean pretreatment serum calcium level of 12.5 +/- 0.4 mg/dl dropping to 9.2 +/- 0.2 mg/dl (p less than 0.01) by Day 7. Elevated urinary calcium (1,107 +/- 134 mg/g creatinine) and hydroxyproline levels (154 +/- 16 mg/g creatinine) declined to 245 +/- 52 mg/g creatinine and 75 +/- 14 mg/g creatinine, respectively, suggesting a marked reduction in bone resorption following treatment. Serum phosphorus levels were unchanged, but urinary phosphorus levels dropped rapidly from 1,181 +/- 125 mg/g creatinine before treatment to 723 +/- 94 mg/g creatinine after two days. Serum parathyroid hormone levels (mid-molecule assay) were suppressed before treatment (64 +/- 16 pg/ml), but rose rapidly to 223 +/- 68 pg/ml by Day 7 of treatment. The value of serum 1,25-dihydroxyvitamin D was initially below normal (16 +/- 3 pg/ml), but rose rapidly with treatment to 42 +/- 12 pg/ml by Day 7. Symptoms of hypercalcemia and bone pain improved with treatment, and no serious adverse reactions to treatment were encountered. Intravenous etidronate is apparently an effective and safe treatment for neoplastic hypercalcemia.
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PMID:Neoplastic hypercalcemia: physiologic response to intravenous etidronate disodium. 303 98

Home total parenteral nutrition (HTPN) is in its infancy but has proved to be lifesaving for patients unable to manage on enteral nutrition alone. However, this mode of nutrition therapy is not without problems. Aside from mechanical and other metabolic complications, a peculiar metabolic bone disease has been reported to occur in some HTPN recipients. The disease, characterized by abnormalities in calcium and phosphorus homeostasis, often results in osteomalacia, bone pain, and fractures. Reports of approximately 50 cases of metabolic bone disease have been published by centers in the United States and Canada. Factors that have been implicated as possible causes include infusion of excess vitamin D, aluminum, calcium, protein, or glucose; cyclic vs. continuous TPN administration; and the patient's previous nutritional state. Although removal of vitamin D or aluminum from the TPN solution and discontinuation of TPN altogether have been associated with improvement in symptoms, histology, and laboratory values, no single factor has been identified as the cause of this troubling phenomenon.
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PMID:Metabolic bone disease in home total parenteral nutrition. 311 Feb 49

This is a report of six patients with cirrhosis of the liver in whom primary hyperparathyroidism occurred due to a solitary parathyroid adenoma 3 months to 9 years after undergoing emergency portacaval shunt for hemorrhage from esophageal varices. The presenting symptoms in all six patients were weakness and bone pain. Three patients had a bone fracture after insignificant trauma, one and probably two passed kidney stones, and a duodenal ulcer developed in two. Bone x-ray films showed generalized osteoporosis in all patients. Renal function and arterial blood pH were within normal limits in every patient. The diagnosis of primary hyperparathyroidism in each patient was based on repeated demonstrations of hypercalcemia, hypophosphatemia, and markedly elevated serum immunoreactive parathyroid hormone concentrations. In all six patients, removal of the parathyroid adenoma resulted in disappearance of symptoms; normalization of serum calcium, phosphorus, and immunoreactive parathyroid hormone levels; and in four of the six, improvement in radiographic evidence of osteoporosis during follow-up of from 1 to 6 years. The association of cirrhosis, portacaval shunt, and primary hyperparathyroidism has not been documented previously. Our six patients with primary hyperparathyroidism constitute 3.4 percent of 174 survivors of emergency portacaval shunt in a series of 264 unselected, consecutive patients with cirrhosis and bleeding esophageal varices. Hepatic osteodystrophy is known to have occurred in only 11 of these 174 survivors. Primary hyperparathyroidism may be a more common cause of hepatic osteodystrophy than has been previously recognized, and should be considered in patients with cirrhosis in whom weakness, bone pain, and bone demineralization develop, particularly if they have a portacaval anastomosis.
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PMID:Hyperparathyroidism, cirrhosis, and portacaval shunt. A new clinical syndrome. 325 57

The etiology, clinical presentation, and management of hypophosphatemia are reviewed. Phosphorus is a major intracellular anion and plays an important role in many biochemical pathways relating to normal physiologic functions. Approximately 60 to 90% of the 1 to 1.5 g of daily dietary phosphorus intake is absorbed, and of that amount, about two thirds is excreted in the urine. The overall incidence of hypophosphatemia is about 2 to 3% of all hospitalized patients. Factors associated with hypophosphatemia include phosphate-binding antacid therapy, nasogastric suction, liver disease, sepsis, alcoholism, and acidosis associated with diabetic ketoacidosis. Patients receiving parenteral nutrient solutions were also at higher risk for hypophosphatemia before the routine supplementation of these formulations with phosphate. Patients with hypophosphatemia may be asymptomatic or may experience weakness, malaise, anorexia, bone pain, and respiratory arrest. The major systems involved include the neuromuscular, hematologic, and skeletal systems. Phosphorus-containing products used to treat hypophosphatemia are a combination of monobasic and dibasic phosphate salts. Therefore, it is essential to calculate doses in millimoles rather than milligrams or milliequivalents to more accurately reflect the phosphorus concentration and to avoid potentially serious dosage errors. Normal daily requirements are readily maintained by dietary sources of phosphorus such as milk products or may be supplemented by phosphate-containing products administered orally or intravenously. Since phosphorus is a key factor in many organ systems, it is essential to monitor serum phosphorus concentrations in patients at risk for hypophosphatemia.
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PMID:Management of hypophosphatemia. 328 Feb 19

This is a report of a 6-year-old girl with the rare syndrome of hyperostosis with hyperphosphatemia. Only eight cases have been previously reported. The main features of this syndrome are repeated attacks of bone pain and swelling, the radiologic finding of periosteal reaction with cortical hyperostosis, and the laboratory finding of increased serum phosphorus level with normal serum calcium and parathyroid hormone levels. The purpose of this article is to review the clinical picture, laboratory and radiological findings, and the differential diagnosis.
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PMID:Hyperostosis with hyperphosphatemia: a case report and review of the literature. 328 8

Gallium nitrate, an agent known to inhibit bone resorption, was evaluated in patients with bidimensionally measurable hormone-refractory prostatic cancer. The starting dose was 200 mg/m2 iv by continuous infusion over 7 days. Two patients (10%; 95% confidence limits, 0%-22%) achieved short partial remissions of 1 and 6+ months, while seven of 23 (30%; 95% confidence limits, 14%-52%) showed a diminution of bone pain. Serial indices of bone turnover including serum calcium, phosphorus, and urinary hydroxyproline excretion showed a significant decrease at the completion of the infusion which returned to baseline prior to the next cycle. The data suggest the effect on bone was too short to produce consistent improvement. Reasons for the dissociation of pain relief and antitumor activity are discussed.
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PMID:Gallium nitrate in prostatic cancer: evaluation of antitumor activity and effects on bone turnover. 330 78


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