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 17-year-old girl was immobilized in traction for 3 months and in a spica cast for 6 weeks for fractures of the femur and pelvis. Seven weeks after injury and after her acute renal failure had resolved, serum calcium rose and remained elevated for the duration of her immobilization. Conservative treatment by hydration, diuresis, and later tilttable therapy failed to relieve her hypercalcemia. Only after mobilization did the serum calcium levels return to normal and the symptoms abate. Administration of recently developed medical methods of management of hypercalcemia may have prevented this complication.
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PMID:Immobilization hypercalcemia: a case report and review of the literature. 13 82

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

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

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

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

The role of dialysis in the treatment of patients with severe hypercalcemia is uncertain. The fourteen previously reported cases of hypercalcemia treated with either peritoneal or hemodialysis have been reviewed. Two additional patients treated with hemodialysis are described in this report. Because the use of large volumes of intravenous fluids was contraindicated, each of the patients received a low calcium bath (0-1 mEq calcium per liter) hemodialysis for three and a half hours. After dialysis, the serum calcium fell to normal in both and remained normal thereafter with treatment of the underlying disease (multiple myeloma in one and vitamin D intoxication in the other). Hemodialysis can clear up to 682 mg of calcium per hour as compared to 124 mg per hour for peritoneal dialysis and 82 mg per hour with forced saline diuresis. Low calcium bath hemodialysis is indicated when the presence of renal and/or cardiac failure prevents the administration of large volumes of intravenous fluids to hypercalcemic patients.
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PMID:Role of dialysis in the treatment of severe hypercalcemia: report of two cases successfully treated with hemodialysis and review of the literature. 16 Aug 52

A test was developed to diagnose various forms of hypercalciuria. A two-hour urine sample after an overnight fast and a four-hour urine sample after 1 g of calcium by mouth were tested for calcium, cyclic AMP and creatinine. The 24 patients with absorptive hypercalciuria had normocalcemia and normal fasting urinary calcium (less than 0.11 mg per milligram of urinary creatnine). Urinary calcium was high (greater than or equal to 0.2 mg per milligram of creatinine) after a calcium load. Of the 28 patients with primary hyperparathyroidism (resorptive hypercalciuria), 25 had hypercalcemia and 21 had high fasting urinary calcium. Urinary cyclic AMP, elevated in 30 per cent of fasting patients, was high (greater than 4.60 mu moles per gram of creatinine) in 82 per cent of cases after calcium load. Six patients with renal hypercalciuria had normocalcemia, high fasting urinary calcium, and high (greater than 6.86 mu moles per gram of creatinine) or high-normal fasting urinary cyclic AMP was normal. This simple test should facilitate the differentiation of various causes of hypercalciuria.
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PMID:A simple test for the diagnosis of absorptive, resorptive and renal hypercalciurias. 16 60

The long-term effects of the vitamin D metabolite, 25-hydroxycholecalciferol (25-HCC), were evaluated in 2 children with hypophosphatemic vitamin D-resistant rickets. Serial total balance studies demonstrated an apparent lack of correlation between the effects of the vitamin on intestinal absorption of calcium and phosphorus and both the onset of healing in 1 of the 2 patients treated with 5,000 to 7,500 u of the metabolite and the absence of demonstrable radiologic improvement in another patient in whom the final dosage was 20,000 u. per day. At first, the metabolite induced a positive calcium balance in both patients resulting largely from a reduction in intestinal calcium excretion. Despite a continued positive calcium balance, 1 of the 2 patients did not demonstrate further healing, while in the other patient healing was noted even when total calcium balance was negative. Serum phosphate levels did not return to normal in either patient, nor was phosphate excretion altered by 25-HCC. Serum alkaline phosphatase remained elevated in both. Serum immunoassayable parathyroid hormone levels were consistently normal to high-normal in the 2 patients throughout more than 24 months of observation. No instances of hypercalcemia and only occasional hypercalciuric episodes were noted.
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PMID:Long-term therapy of viramin D-resistant richets with 25-hydroxycholecalciferol. 16 13

This review considers the most recent developments concerning the metabolism and homeostasis of calcium and phosphorus. The kinetics of the distribution of calcium, theories of calculus formation, hypercalcemia and hypocalcemia are discussed, as well as the role of parathyroid hormone, thyrocalcitonin and 1,25 dihydroxy Vitamin D(3) in maintaining calcium levels and skeletal integrity. In addition, the role of calcium in enzyme activation and inhibition, muscle and nerve function, and intracellular metabolism are considered.
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PMID:Recent advances in calcium and phosphorus metabolism. 16


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