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)

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

A 59-year-old woman with hypercalcemia due to hyperparathyroidism and 1-year-old boy with cryptogenic hypercalcemia were referred for bone scanning. There were increased accumulations of the technetium-phosphate complex in thyroid, stomach, lung, heart, and kidney. 99mTc-MDP bone scanning was useful for detecting metastatic calcification.
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PMID:[Metastatic calcifications detected by Tc-99m MDP bone scanning in patients with hypercalcemia: case report]. 234 17

A 53-year-old male with Bence Jones lambda myeloma developed hypercalcemia and acute renal failure (calcium 14.4 mg/dl, BUN 40 mg/dl, creatinine 3.0 mg/dl) after initial response to chemotherapy. A 99mTc-MDP bone scan revealed unusual isotope accumulation in the left hypochondrium. Extensive calcium deposition was confirmed in the gastric mucosa in the postmortem examination. Detection of gastric calcification by a bone scan is very rare. Only two cases of gastric calcification visualized on bone scans can be found in the literature, one with multiple myeloma) and one in Hodgkin's disease).
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PMID:Metastatic calcification in the stomach demonstrated by a bone scan in Bence Jones lambda myeloma. 310 83

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

A patient exhibited an unusual constellation of findings: His extraosseous lymphoma sequestered [99mTc]MDP, a bone-seeking agent, while at the same time it appeared to produce a factor that caused hypercalcemia. The dispersed lymphoma cells took up more [99mTc]MDP in vitro than did cultured lymphoblasts suggesting that the in vivo sequestration may have been, at least in part, an active intracellular process.
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PMID:What causes uptake of technetium-99m methylene diphosphonate by tumors? A case where the tumor appeared to secrete a hypercalcemia-causing substance. 315 21

Uptake of Tc-99m MDP by extraskeletal tissues is a rare, serendipitous finding during bone scanning studies. It can be clinically correlated with the presence of hypercalcemia in association with renal failure, as may occur in multiple myeloma. While the precise mechanism of non-osseous uptake of MDP is not certain, it may represent metastatic calcification based upon histological examination. A critical calcium-phosphate ion product appears to be requisite for deposition within soft tissues, and all cases in the literature for which data were available exceeded this ion product value. While MDP bone scanning is not generally useful in the diagnosis or staging of multiple myeloma, these findings may indicate secondary effects of the disease. The authors report the first case of liver, spleen, and lung uptake by MDP in a patient with hypercalcemia secondary to multiple myeloma, with a review of the literature.
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PMID:Non-osseous bone scan abnormalities in multiple myeloma associated with hypercalcemia. 324 15

Abnormal pulmonary uptake of Ga-67 citrate and Tc-99m MDP and reversible liver uptake of Tc-99m MDP was seen in a patient with hypercalcemia of lymphoma and biopsy-proven metastatic pulmonary calcification. Abnormal lung uptake of Tc-99m MDP may confirm the diagnosis of pulmonary calcification, lessening the need for invasive procedures to evaluate pathologic lung uptake of Ga-67 citrate.
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PMID:Abnormal lung and liver uptake of gallium-67 and technetium-99m MDP in hypercalcemia of lymphoma with metastatic pulmonary calcification. 352 9

Abnormal accumulation of Tc-99m MDP in the lungs and stomach was observed in a patient with multiple myeloma and refractory hypercalcemia. There was no roentgenographic evidence of calcification. At postmortem examination, the presence of amyloid deposits was confirmed in both organs, while the corresponding metastatic calcification was demonstrated only in the gastric mucosa. It seems likely that, in our case, soft-tissue localization of bone-seeking agent was attributable to the presence of amyloid deposits rather than metastatic calcification. No cases showing the combined occurrence of amyloid deposition and metastatic calcification in soft-tissues have previously been demonstrated to concentrate bone-seeking agent.
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PMID:Soft-tissue uptake of technetium-99m MDP in multiple myeloma. 381 90

30 patients with disorders of calcium metabolism were treated with dichloromethylene diphosphonate (C1(2)MDP, or clodronate disodium), an inhibitor of bone resorption. 13 patients with Paget's disease of bone were given C1(2)MDP by mouth (1.6 g/day). Serum-alkaline-phosphatase and urinary hydroxyproline fell to normal or near-normal within 3-7 months, and there was a clinical improvement in all but 1 patient. C1(2)MDP (0.8-3.2 g/day) also reduced plasma-calcium and urinary calcium in 17 patients with hypercalcaemia due to primary hyperparathyroidism or secondary to malignant disease. C1(2)MDP seems to be an effective oral drug for inhibiting excessive bone resorption in man.
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PMID:Effect of dichloromethylene diphosphonate in Paget's disease of bone and in hypercalcaemia due to primary hyperparathyroidism or malignant disease. 610 89

Diphosphonates were administered intravenously to 4 patients with myeloma-induced hypercalcaemia. All patients received EHDP 4.3 mg/kg/day for 3 to 8 days. One of them, whose hypercalcaemia recurred, was later treated with Cl 2 MDP 5 mg/kg i.v. for 8 days. In 2 patients EHDP infusions were followed by EHDP administered orally (5 mg/kg/d) for 3 weeks, after which transiliac bone biopsy was performed. In all patients calcemia fell from 130 +/- 14 to 99 +/- 4 mg/l at the end of the intravenous treatment, with parallel decrease in calciuria. Histomorphometric analysis of the bone biopsies showed few osteoclasts but massive infiltration with plasmocytes. In one case, EHDP probably induced a deficit in mineralization. Intravenous diphosphonates therefore proved to be rapidly effective in the treatment of hypercalcaemia due to malignancy. However prolonged administration of EHDP in high doses is not recommended, as it may result in osteomalacia.
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PMID:[Treatment of hypercalcemia of myelomatous origin with intravenous diphosphonates]. 622 88


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