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Query: UMLS:C0020437 (hypercalcemia)
10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The treatment of rapidly progressive skeletal demineralisation in myelomatosis has been studied with the help of metabolic calcium balance in two patients; In one, osteoporosis accelerated during treatment with melphalan and prednisolone, although he remained normocalcaemic throughout, suggesting that osteoporosis was aggravated by corticosteroid therapy. In the other patient, who was initially hypercalcaemic, conventional treatment produced clinical remission before eventual relapse with more hypercalcaemia and skeletal dissolution. Both patients were then treated with mithramycin alone, and, although neither obtained haematological remission, bone pain was relieved, hypercalciuria and hypercalcaemia were abolished, and calcium balances proved that mithramycin was effective in restoring calcium equilibrium. The results indicate that mithramycin may abolish excessive bone resorption in myelomatosis and that severe bone dissolution may occur in the absence of hypercalcaemia. Regular determination of 24-hour urinary calcium excretion as well as of plasma-calcium is important in monitoring process. Mithramycin should be considered in the early treatment not only of hypercalcaemia but also of severe hypercalciuria, if these complications do not rapidly remit during the first course of conventional myeloma therapy, with or without steroids. Finally, these results add to evidence that a humoral factor may be responsible for osteoclast stimulation in myelomatosis.
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PMID:Treatment of osteolytic myelomatosis with mithramycin. 4 84

The authors treated 17 patients with hypercalcaemia (which in 16 cases resulted from a malignant disease) by means of 1 to 3 daily perfusions of 25 g of mithramycin per kg body weight. In all patients the treatment resulted in reduction in the level of calcaemia. In 12 patients the level of calcaemia was reduced to less than 105 mg/litre; in 16 patients to less than 110 mg/litre. In no patient was the calcaemia reduced to less than 70 mg/litre. The only notable inconvenience of the treatment was vomiting during the perfusion. Mithramycin seems to be the treatment of choice for hypercalcaemia of cancerous origin.
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PMID:[Treatment of hypercalcemia with mithramycin]. 12 91

In 36 patients with neoplastic diseases 72 episodes of hypercalcaemia with serum-calcium levels greater than or equal to 2.75 mmol/l were treated (19 breast carcinoma; 9 bronchial or lung carcinoma; 5 multiple myeloma; 1 each jejunal carcinoid, malignant lymphoma, phaeochromocytoma). Cardinal symptoms were mental, neuromuscular and renal during the hypercalcaemic episodes. Mithramycin is preferred to other methods (infusion of sodium chloride and frusemide, prednisone, sodium-potassium-phosphate infusion) of treating acute or subacute hypercalcaemia. Mithramycin in a single injection of 20-25 microgram/kg body-weight intravenously is usually sufficient to counteract a hypercalcaemic phase for at least 7-10 days, often much longer. There was a highly significant fall in serum-calcium levels from two days onwards after mithramycin injection. Toxic side-effects were minimal and restricted to transitory increase in transaminase levels, initially 5-6 times normal with a maximum on the third day and normalisation on the fifth day after mithramycin administration.
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PMID:[Treatment of hypercalcaemic syndrome in tumour patients, especially with mithramycin]. 14 99

Mithramycin is effective in the treatment of hypercalcemia. The mechanism of its hypocalcemic effect was studied in six patients with hypercalcemia by serum 85Sr or 45Ca kinetic techniques. Mithramycin was given at two dosage levels (25 or 50 microgram/kg iv). Mithramycin at the low dosage had little effect on the rate of bone accretion. However, at both dosage levels, mithramycin caused an upward shift of the slope of the specific activity curve, indicating an inhibitory effect on bone resorption. This effect started 6-12 h after a 25-microgram/kg dose of mithramycin and lasted from 4-6 days. It appears that mithramycin has a preferential effect on bone resorption.
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PMID:Mechanism of the hypocalcemic effect of mithramycin. 15 75

We studied two children with neuroblastoma in whom hypercalcemia developed as the initial manifestation in one and during the course of therapy in the other. Serum parathyroid hormone activity was elevated in the patient in whom the test for it was performed. Mithramycin controlled the hypercalcemia in one patient and tumor resection with radiation therapy and chemotherapy was sufficient for control of this complication in the other.
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PMID:Hypercalcemia associated with neuroblastoma. 15 70

Two cases of paraneoplastic hypercalcemia secondary to ovarian tumors are presented. Both cases were secondary to ectopic parathormone (PTH) production. Other mediators postulated to cause this syndrome are prostaglandins, vitamin D-like sterols, non-vitamin D sterols, vitamin A, cortisol, and "osteoclast-activating factor.' The key treatment modalities for acute hypercalcemia are hydration and diuresis with furosemide; phosphates, steroids, antiprostaglandins, and hemodialysis may also be of value. Calcitonin is theoretically the most attractive treatment modality, but the rapid development of resistance limits its use to acute management. Mithramycin is most effective for long-term palliation of hypercalcemia if tumor-directed therapy is unsuccessful. Review of the literature confirms the previously made observation that mesonephromas are disproportionaately represented in association with this syndrome.
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PMID:Paraneoplastic hypercalcemia in ovarian tumors. 49 33

The use of intravenous procaine in the treatment of hyperpyrexia in a patient with hyperparathyroidism has not been previously reported. A case of metastatic malignant melanoma precipitating the syndrome of hypertonicity of muscle, hyperpyrexia, acidemia, hypercalcemia and elevated serum parathormone levels is presented. Mithramycin was used in an attempt to reduce elevated serum calcium concentrations. The use of intravenous procaine in "caffeine rigor" and malignant hyperthermia due to succinylcholine and halothane formed the basis for its trial in this case. The relationship between cyclic AMP and calcium ions is discussed in postulating mechanism of procaine action.
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PMID:The use of procaine in acquired malignant hyperthermia in a patient with malignant melanoma metastatic to the parathyroid gland: a case report. 99 Sep 78

A patient with acute primary hyperparathyroidism treated with mithramycin preoperatively, underwent neck exploration and two enlarged parathyroid glands were excised: one huge adenoma (6g) and another smaller gland. Mithramycin was administered preoperatively to lower life-threatening hypercalcaemia, and parathyroid slices from the huge adenoma removed at surgery were submitted in vitro to various calcium concentrations in the media to determine the influence of calcium on parathyroid adenoma secretory pattern in acute primary hyperparathyroidism. Mithramycin induced a significant decline in calcium levels and significant elevations of calciotrophic hormones (intact PTH, mid-region specific PTH, calcitonin and calcitriol). Significant suppression in PTH output in vitro was achieved by increasing calcium levels in the media. These results exclude autonomous PTH secretion (non-calcium dependent) as a possible aetiology of acute primary hyperparathyroidism. We suggest that a sudden increase in the set-point of the diseased parathyroid cells in the presence of a huge cell mass accounts, in large part, for both the marked hypercalcaemia and elevated PTH levels in this patient.
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PMID:Non-autonomy of parathyroid hormone secretion in acute primary hyperparathyroidism. 128 27

Two cases of rhabdomyolysis with renal failure followed by hypercalcaemia are reported. Both had major hyperphosphataemia and hypocalcaemia, requiring haemodialysis. Hypercalcaemia developed during the diuretic phase, when renal function was still abnormal, and before phosphate blood levels had returned to normal. Soft tissue calcifications occurred in one of the patients. The pathogenesis and treatment of this condition are discussed. Increased levels of serum calcitriol may play an important role in the genesis of hypercalcaemia, which may last for several months. Giving calcium salts and or vitamin D to these patients during the hypocalcaemic phase is dangerous, and should be avoided. The usual treatment for hypercalcaemia my remain ineffective. Mithramycin can lower the serum calcium concentration but the new diphosphonates (sodium etidronate) are very effective in the treatment of this hypercalcaemia. However, in serious or urgent cases, hypocalcaemic haemodialysis may be required, with the simultaneous administration of calcitonin and diphosphonates.
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PMID:[Severe hypercalcemia after rhabdomyolysis and acute renal failure]. 150 21

Thirty-nine patients with cancer-associated hypercalcaemia were randomly allocated to receive aminohydroxypropylidene diphosphonate (APD), mithramycin, or corticosteroids and salmon calcitonin. Corticosteroids/calcitonin had the fastest calcium-lowering effect, owing mainly to an acute reduction in renal tubular calcium reabsorption; continued therapy over 9 days failed to suppress accelerated bone resorption, however, and most patients remained hypercalcaemic. Mithramycin also substantially reduced serum calcium within 24 h. A further dose on day 2 generally controlled hypercalcaemia until day 6 by reducing both bone resorption and renal tubular calcium reabsorption. By day 9, however, about 50% of the mithramycin-treated patients had started to relapse as bone resorption increased again. With APD serum calcium levels fell more slowly but progressively owing to effective suppression of bone resorption; by day 9 the control of hypercalcaemia was significantly better than in the other treatment groups. Symptoms of hypercalcaemia were greatly relieved, especially by APD.
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PMID:Comparison of aminohydroxypropylidene diphosphonate, mithramycin, and corticosteroids/calcitonin in treatment of cancer-associated hypercalcaemia. 286 17


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