Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 20-year-old woman with a severely crippling myositis ossificans progressiva was treated with a diphosphonate (EHDP), 10-20 mg/kg/day. While being treated with this drug, surgical removal of ectopic bone was performed. Although ectopic calcification recurred postoperatively, considerable functional improvement was achieved. At the highest dosage of EHDP, hypercalcaemia gradually appeared, but was reversible upon cessation of drug treatment. It is probably related to a direct effect of EHDP on the bone.
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PMID:Myositis ossificans progressiva. Clinical and metabolical observations in a case treated with a diphosphonate (EHDP) and surgical removal of ectopic bone. 42 28

Etidronate disodium (EHDP) therapy is often instituted emergently for treatment of hypercalcemia associated with malignancy, and a staging bone scan is part of the evaluation of the patient with extensive metastatic disease. In these patients in whom high dose EHDP therapy has been instituted, uptake of the bone scan agent is markedly diminished. The case presented illustrates this finding: a breast cancer patient who had received two 500-mg intravenous doses of EHDP prior to bone scan staging. No skeletal visualization was present at 3 hr after 99mTc-MDP injection. Blood-pool activity and uptake in large metastatic sites were observed.
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PMID:Skeletal nonvisualization in a bone scan secondary to intravenous etidronate therapy. 156 85

Progressive bone disease in multiple myeloma frequently leads to osteolysis, bone resorption, pathologic fractures, vertebral compression, and hypercalcemia. We conducted a double-blind study in 173 newly diagnosed multiple myeloma patients of etidronate disodium (EHDP), a diphosphonate compound that reduces bone resorption by inhibiting osteoclastic activity. The patients were randomly assigned to receive oral EHDP 5 mg/kg/d or placebo until death or discontinuation due to intolerance or refusal. The extent of vertebral deformity was measured by a vertebral index as well as height. The frequency of pathologic fractures, hypercalcemia, and bone pain was regularly assessed, as well as size and number of osteolytic lesions. All patients received melphalan and prednisone daily for 4 days every 4 weeks as the primary chemotherapy for their disease. Although the repeated measures analysis showed a significant height loss, there was no difference between treatment arms (P = .98). There was no significant difference in bone pain, episodes of hypercalcemia, or development of pathologic fractures. Patients on EHDP showed less deterioration in their vertebral index, but this difference only approached statistical significance (P = .07). We conclude that EHDP therapy used in this dosage schedule does not have a clinically significant impact in multiple myeloma.
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PMID:Effect of daily etidronate on the osteolysis of multiple myeloma. 171 35

Hypercalcemia is a major source of morbidity and mortality in patients with cancer. Gallium nitrate and the bisphosphonate, etidronate, are new agents that have recently become available for treatment of this disorder. To directly compare therapeutic effectiveness, we conducted a randomized, double-blind, multicenter study of gallium nitrate compared with etidronate for acute control of cancer-related hypercalcemia. Gallium nitrate was administered by continuous intravenous (IV) infusion at a dose of 200 mg/m2/d. Etidronate was administered as a 4-hour IV infusion at a dose of 7.5 mg/kg. Both drugs were given daily for 5 consecutive days. Eligible patients had persistent moderate-to-severe hypercalcemia (total serum calcium [corrected for serum albumin] greater than or equal to 12.0 mg/dL) after 2 days of hospitalization and IV hydration. Seventy-one patients were randomized and treated. Twenty-eight of 34 patients (82%) who received gallium nitrate achieved normocalcemia compared with 16 of 37 patients (43%) who received etidronate (P less than .001). Patients who received etidronate required significantly greater amounts of IV fluids (P = .04) and more hypocalcemic drug treatment (P less than .05) during the poststudy period than patients who received gallium nitrate. Kaplan-Meier analysis showed a significantly longer median duration of normocalcemia for patients treated with gallium nitrate (8 days v 0 days, P = .0005). A significantly higher proportion of patients treated with gallium nitrate developed asymptomatic hypophosphatemia compared with patients treated with etidronate (97% v 43%, P less than .001). We conclude that gallium nitrate is highly effective and superior to etidronate for acute control of moderate-to-severe cancer-related hypercalcemia.
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PMID:A randomized double-blind study of gallium nitrate compared with etidronate for acute control of cancer-related hypercalcemia. 190 32

There have been several reports of etidronate disodium (EHDP) interference upon the biodistribution of 99mTc-methylene diphosphonate (MDP). With the increasing use of etidronate for the treatment of Paget's disease, hypercalcemia, and osteoporosis, nuclear physicians can expect to encounter increasing numbers of cases in which EHDP-induced artifacts impair the diagnostic utility of bone scans. The temporal duration of this effect is unknown yet obviously important. We report serial bone scintigraphy in a patient who received a single dose of EHDP for hypercalcemia. Normal biodistribution of 99mTc-MDP was noted at 15 days, suggesting that 2 wk are sufficient before performing a bone scan after a single intravenous dose of etidronate.
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PMID:Duration of etidronate effect demonstrated by serial bone scintigraphy. 190 91

Severe hypercalcemia is a medical emergency requiring urgent treatment. It most commonly is caused by malignant tumors, as in the case study, but can also be caused by advanced hyperparathyroidism or high serum levels of vitamin D. The patient described in the case study shows clinical evidence of volume contraction due to hypercalcemia-related anorexia and vomiting. His elevated serum concentrations of urea nitrogen and creatinine reflect intravascular volume depletion and hypercalcemia-induced reduction of renal perfusion. He is also likely to have irreversible renal damage as a result of nephrocalcinosis. His central nervous system depression is most likely a result of hypercalcemia, but other central nervous system disorders such as cerebral metastases should be considered. Appropriate treatment would include intravenous fluids to correct volume depletion, dilute extracellular fluid calcium, and promote renal calcium excretion. Before waiting for the effects of volume expansion, the first dose of an inhibitor of bone resorption should be given. The agent of choice now (this may change when second-generation bisphosphonates become available) is plicamycin. Etidronate is a reasonable second choice. Because both drugs require at least 48 hours before their hypocalcemic action is manifest, calcitonin could be used to accelerate the rate of decline of the serum calcium. As the patient becomes more alert, weight-bearing and ambulation should be encouraged. With this combination of therapeutic modalities, this patient's serum calcium level should be corrected within 3 to 5 days. Intermittent injections of mithramycin or etidronate could be given on an outpatient basis approximately once a week in order to maintain the serum calcium within the normal range. One of the most important aspects of treatment in hypercalcemic patients is eradication of the underlying disease, which usually calls for specific antitumor therapy, including chemotherapy, radiation therapy, or surgery. Most of the agents currently available for the correction of hypercalcemia have cumulative toxicities or are only transiently effective and, therefore, their use should be considered a temporizing measure until specific treatment directed at the primary disease takes effect.
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PMID:Management of severe hypercalcemia. 200 13

Paget's disease of bone occurs in elderly people and resembles no other disease. The most frequent diagnostic errors are made when it is discovered in young adults, especially after an injury. Forms with osteolysis of the lower limbs are the most misleading, and it is better to avoid biopsies in such cases, as they may be followed by fractures. In geriatric pathology the failure to recognize that cerebral, spinal cord and cardiac manifestations are due to a specific vascular disorder of pagetic origin is a serious error as it deprives the patient of calcitonin which is the only effective therapy. Errors in the interpretation of laboratory results are easily avoided if a low hydroxyproline diet is prescribed during the week that precedes the tests. The biochemical activity should be correlated with the pagetic bone mass. Histology may wrongly suggest primary hyperparathyroidism, but patients with Paget's disease have no hypercalcaemia unless they are bedridden. Treatment relies on calcitonin and/or disodium etidronate (EHDP). Only 50% of the patients require this treatment the indications of which must carefully be weighed. EHDP may have adverse effects on bones, including fractures and pseudosarcomatous osteolysis, notably when it is given in high doses or for limited and/or osteolytic lesions. Pre and post-operative calcitonin therapy is recommended in patients undergoing surgery.
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PMID:[Paget's disease: errors to be avoided]. 249 20

The pathogenesis, clinical features, indications for therapy, and current pharamacologic management of Paget's disease are reviewed. Paget's disease is a bone disorder of unknown etiology primarily affecting the elderly. Overactive bone resorption leads to the accelerated formation of disorganized, weak bone. Pain and fractures are common clinical features. Neurologic, cardiovascular, metabolic, and neoplastic complications are also reported. Because most patients are asymptomatic, the disease is often detected during routine roentgenography or laboratory tests. Primary indications for pharmacologic intervention include bone pain, neural compression, immobilization hypercalcemia or hypercalciuria, cardiac failure, and orthopedic surgery. Recurrent or non-healing fractures and rapidly progressing complications are additional indications. Drugs used in the management of Paget's disease include calcitonin, etidronate disodium, and plicamycin. Although these agents are efficacious, each has disadvantages. Clinical resistance to animal calcitonins may develop, and the cost of therapy may be prohibitive. Etidronate may induce ostemalacia. The use of plicamycin is limited by potentially severe toxicities. Dichloromethylene and aminohydroxypropylidene are promising diphosphonate compounds but are still investigational In those patients who are unresponsive to single-agent regimens, combination therapy may prove effective. Although many patients with Paget's disease do not require pharmacologic therapy, calcitonin and etidronate are the agents of choice when it is indicated.
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PMID:Pharmacologic management of Paget's disease. 266 12

This study was designed to assess the capacity of etidronate disodium (etidronate) to affect neoplastic involvement of bone by murine tumors. Using sublines of the Walker 256 carcinoma, differing in the pattern of bone involvement, etidronate was found to inhibit hypercalcemia caused by systemically acting humoral factors, to inhibit bone metastasis following inoculation of tumor cells into the abdominal aorta, and to reduce the invasion of bone adjacent to tumors. Etidronate was also found to prevent bone metastasis in syngeneic rat mammary carcinoma. Etidronate was found devoid of direct antineoplastic activity, whether administered intramuscularly, subcutaneously, or intravenously, in a series of murine tumors of different histologic varieties. At the same time, it was shown that etidronate did not modify the antineoplastic activity of any of the major chemotherapeutic agents used in these studies, nor did it demonstrate any degree of immunosuppression. The experimental models used for this study should prove useful in evaluating agents that may affect the various types of bone involvement seen in neoplastic disease. The drug's apparent lack of interference with the antineoplastic activity of standard cytotoxic agents and its lack of immunosuppressive activity suggest that it may be readily adaptable to combination chemotherapy regimens.
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PMID:Effect of etidronate disodium on the interactions between malignancy and bone. 310 35

Clinical effects of EHDP on relief of bone pain, changes in bone lesions on X-ray and 99mTc-MDP scintigram and performance status were investigated in 19 patients with bone metastasis from urogenital cancers (4 renal cell cancers, 1 renal pelvic cancer, 4 bladder cancers and 10 prostatic cancers). EHDP was effective in relieving bone pain in prostatic cancer patients with osteoblastic lesions. Bone lesions on X-ray and 99mTc-MDP scintigram were slightly improved in prostatic cancer patients with osteoblastic lesions. Administration of EHDP did not improve the performance status. Changes in laboratory data such as serum alkaline phosphatase, serum calcium and urinary total hydroxy-proline following EHDP administration indicated inhibition of osteolytic activity with no effect on bone formation in the early period of treatment (in 4 weeks) and development of both osteolytic activity and bone formation in the later period (from 8 to 12 weeks). No marked side effects were observed. EHDP seems to be effective in relieving bone pain in prostatic cancer patients with osteoblastic bone metastasis. Moreover, some diphosphonate groups including EHDP are expected to be useful to the patients with malignant hypercalcemia.
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PMID:[Effects of etidronate disodium (EHDP) on urogenital malignancies with bone metastasis: a multicentered collaborative evaluation]. 313 34


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