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 patient with metastatic islet cell carcinoma of the pancreas, recurrent peptic ulcer disease, and hypergastrinemia (Zollinger-Ellison syndrome) developed symptomatic hypercalcemia and renal insufficiency; she was treated with streptozotocin after parathyroidectomy failed to control her hypercalcemia. Shortly after somewhat less than the usual recommended dose of streptozotocin was administered, the serum calcium concentration fell to near normal with complete resolution of symptoms. Seven months after therapy, mild hypocalcemia, consistent with her degree of renal impairment was noted. However, mild hypercalcemia recurred 13 months after therapy. Shortly after streptozotocin therapy, the mean serum gastrin concentration fell to near normal with radiographic disappearance of the anastomotic ulcer. At 7 and 13 months after therapy, serum gastrin levels were normal. Streptozotocin therapy was accomplished without major complications; specifically, without a detrimental effect on the creatinine clearance. Thus, although hypercalcemia in patients with pancreatic islet cell tumors is often due to associated primary hyperparathyroidism, in some patients it may be due to secretion of a hypercalcemic substance from the tumor and may respond to streptozotocin. Similarly, hypergastrinemia in patients with islet cell tumors may also respond to streptozotocin.
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PMID:Pancreatic islet cell carcinoma with hypercalcemia and hypergastrinemia: response to streptozotocin. 13 70

Normally, in 99mTc-diphosphonate-skeletal scintigrams the kidneys are delineated with the same intensity as the lumbar spine; This is not the case in patients with reduced renal function. In a series of 20 patients with varying degrees of renal insufficiency, a continuous decrease in the renal intensity with increasing serum creatinine was seen: clearly recognizable decreased renal intensity in patients with serum creatinine over 2 mg%, and no visualization of the kidneys in patients with serum creatinine over 8 mg%. This effect is intensified through a simultaneously existing hypercalcemia has the opposite effect, i.e., the intensity decrease is partially prevented. In patients with normal renal function a hypercalcemia even leads to an increased renal intensity. As a further cause for excessive renal intensity, an increased parenchymal transit time was found in the radionephrography in 5 out of 11 patients with normal serum creatinine in whom the increased renal intensity in the skeletal scintigram was a chance finding.
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PMID:[Role of renal function and calcemia in demonstration of kidneys in 99mTc-diphosphonate skeletal scintigrams (author's transl)]. 13 43

Dichloromethylene diphosphonate (Cl2MDP) antagonized the action of vitamin D on bone in thyroparathyroidectomized rats by reducing the metabolic activity of osteoblasts and osteocytes and decreasing the number of osteoclasts. Ultrastructurally, osteoblasts in Cl2MDP-treated rats were interpreted to be less active in bone matrix synthesis. Osteocytes in Cl2MDP-treated rats were interpreted ultrastructurally to be inactive; there was no evidence of bone resorption when compared to osteocytes in rats given vitamin D alone. Abnormal osmiophilic densities in the pericellular bone matrix of rats given vitamin D alone were not present in rats given vitamin D and Cl2MDP. The ultrastructure of osteoclasts was unaltered by Cl2MDT. These cellular changes were associated with a decrease in serum calcium and increase in bone ash and magnesium concentration in rats given high levels (10 mg/kg) of Cl2MDP. Bone adenosine triphosphatase and alkaline phosphatase activities were not affected by Cl2MDP. These results suggest that Cl2MDP may limit the hypercalcemia of hypervitaminosis D by directly inhibiting bone cells in addition to its physicochemical action.
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PMID:Interaction of dichloromethylene diphosphonate and vitamin D on bone of thyroparathyroidectomized rats. 14 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

Three patients with malignant disease received the usual recommended doses of mithramycin and calcitonin, either concurrently or concomitantly, because of severe life-threatening hypercalcemia. All three patients developed severe, symptomatic hypocalcemia. The mechanisms for this phenomenon are discussed. A possible synergism between calcitonin and mithramycin may prove to be hazardous in such patients and this possibility must be kept in mind when these agents are being considered as a combination treatment for hypercalcemia.
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PMID:Symptomatic hypocalcemia following combined calcitonin and mithramycin therapy for hypercalcemia due to malignancy. 15 45

The ingestion of vitamin A, which is often prescribed for the treatment of acne, may lead to hypervitaminosis A. This syndrome has a wide spectrum of clinical features, hypercalcaemia being of special note since it has been reported in 4 previous cases only. Hypervitaminosis A has been described as resulting from excess ingestion of vitamin A for prevention of sunburn and treatment of minimal brain dysfunction. With the present glut of health foods, this condition should be borne in mind when patients present with symptoms of hypercalcaemia and liver dysfunction.
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PMID:Acne, hypervitaminosis A and hypercalcaemia. A case report. 15 90

Analysis of calcium tolerance in suggested to represent a valuable diagnostic aid in osteoporosis, particulary in the menopause. The serum calcium level was found to exceed 11.0 mg/dl 60 min after the intravenous injection of 3.6 mg per kg body weight of Ca++ in all patients with osteoporosis, while the level was normal at that point of time in every subject without osteoporosis, including patients with bone disease other than osteoporosis. Administration of norandrosterone decanoate or dehydroepinandrosterone to patients with menopausal osteoporosis resulted in normalization of the post-load hypercalcaemia. Calcium tolerance of menopausal patients without osteoporosis was not affected by dehydroepiandrosterone.
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PMID:Effect of intravenous calcium load on the serum calcium level in postmenopausal osteoporosis (a study of the pathogenesis, and diagnostic use of the test). 15 1

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

Hypercalcemia calls first for supportive measures, eg, adequate hydration, movement or mobilization of the patient to the greatest amount tolerated, and reevaluation of drugs being taken. When immediate lowering of the serum calcium level is not clinically mandatory, oral administration of furosemide, corticosteroid, or phosphorus should be considered. In acute emergencies, saline loading and parenteral furosemide therapy should be tried first, except in a patient with renal failure and congestive heart failure, in whom peritoneal dialysis or hemodialysis should be used instead. Calcitonin can be given for the first 12 to 24 hours to lower serum calcium concentration until a definitive management plan is formulated. Corticosteroid, if not contraindicated, should be started as soon as possible. In severe primary hyperparathyroidism with hypophosphatemia, phosphorus can be given intravenously until oral phosphate therapy can be established. Surgery, of course, should be performed as soon as possible. In most cases of neoplasia, mithramycin given according to a recommended schedule is safe and frequently effective. In desperate cases, additional use of prostaglandin synthesis inhibitors probably now is justified by empirical observations. All of these therapeutic measures are used only to stabilize electrolyte balance so that the primary cause of the hypercalcemia can be treated.
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PMID:Management of hypercalcemia. 15 84


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