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

Light microscopic examination of kidney tissue of guinea pigs exposed to 1.5% CO2, 21% O2, and balance N2 for periods as long as 42 days and of rats exposed to the same CO2 concentrations for up to 91 days showed that the incidence of focal kidney calcification increased with length of exposure. Calcification occurred primarily in the tubules of the renal cortex. Another group of guinea pigs were exposed to 1% CO2, 21% O2, and the balance N2 for periods up to six weeks and were later killed at regular intervals, together with control animals of the same litter. In the exposed animals, arterial PCO2 was elevated by 3-4 mmHg and hydrogen ions by about 4 nmol/liter. The standard bicarbonate level was lowered by 1-1.5 mmol, indicating a lack of renal reabsorption of bicarbonate (HCO3), which in turn placed greater stress on the bone buffer system and apparently caused bone calcium and phosphorus mobilization. Bone calcium and phosphorus levels exhibited a cyclic decrease, which resulted in cyclic hypercalcemia and hyperphosphatemia, after one week and six weeks of exposure to 1% CO2. Kidney calcium content increased significantly after two weeks of exposure (27%) and remained at this elevated level during subsequent exposures between the third and sixth weeks. These findings indicate that once the kidney calcification process has started, kidney mineralization is independent of fluctuations in the blood calcium level. A rise in plasma phosphate level that occurred after one day of exposure could have been a precipitating factor in the calcification process. The small but consistent increases in ionized calcium during a 4-week exposure to 1% CO2 may have stimulated the parathyroid, causing an increased blood calcium level that was independent of the two calcium tides in the blood associated with marked bone calcium loss.
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PMID:CO2-induced kidney calcification. 4 51

The effects of calcium-gluconate infusions on renal function were studied in unanesthetised dogs. Each dog was studied during hydropenia and saline infusion. Hypercalcemia, mean serum calcium 3.85 mmol/l (hydropenia) and 3.62 mmol/l (saline infusion), increased fractional excretion of sodium (CNa/CIn), calcium (CCa/CIn), and magnesium (CMg/CIn). The increase was significantly higher in saline-expanded dogs than in hydropenic dogs. Fractional excretion of potassium (CK/CIn) was increased in hydropenia but remained unchanged in saline-expanded animals. Fractional excretion of phosphate (Cp/CIn) was not consistently changed by hypercalcemia. Fractional excretion of chloride (CCl/CIn) was markedly increased in saline-expanded dogs but was not changed in hydropenia. Urine osmolality was reduced in hydropenic dogs but unchanged in saline-expanded dogs. In hydropenic as well as in saline-expanded dogs tubular reabsorption of solute-free water (TcH2O/CIn) increased during the first hour of hypercalcemia. In hydropenic dogs hypercalcemia caused a slight but significant decrease in blood pH, standard bicarbonate, and base excess. In hydropenic as well as in saline-expanded dogs glomerular filtration rate (CIn), renal plasma flow (CPAH), and filtration fraction were unaffected.
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PMID:Renal function in hypercalcemic dogs during hydropenia and during saline infusion. 4 8

Ten uraemic patients on regular haemodialysis were treated with 1alpha-hydroxycholecalciferol (1alpha-H.C.C.) for 5 to 14 months. Five patients who had histological osteitis fibrosa with or without osteomalacia responded well, with resolution of musculoskeletal pain, return of raised serum-alkaline-phosphatase concentrations to normal, resolution of radiological subperiosteal erosions, and improvement in histological signs of osteitis fibrosa and osteomalacia. In these patients 1alpha-H.C.C. proved a safe and effective drug. Five other patients did not improve. Characteristically these patients started with moderately severe histological osteomalacia and minimal, if any, osteitis fibrosa. Proximal myopathy was a prominent symptom and serum-alkaline-phosphatase was normal in four of them. Treatment with 1alpha-H.C.C. resulted in early troublesome hypercalcaemia, and repeat bone histology 5--11 months later showed no improvement. It is suggested that in these patients lack of 1,25-dihydroxycholecalciferol may not have been wholly responsible for the observed osteomalacia, hence 1alpha-H.C.C. alone was ineffective. Phosphate depeltion may have been an important contributing factor.
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PMID:Variable response to long-term 1alpha-hydroxycholecalciferol in haemodialysis osteodystrophy. 5 5

Three patients are described who were examined with the bone-seeking substance 99mTc-E.H.D.P. The abnormalities discovered were ascribed to metastatic calcification in the lungs. The patients suffered from three quite different conditions, but in each there was hypercalcaemia. One patient had chronic renal insufficiency with secondary hyperparathyroidism, in the other cases the cause of the hypercalcaemia could not be determined. In one patient, it was possible to confirm the diagnosis of pulmonary calcinosis histologically. Previously published cases indicate that it is possible to demonstrate lung calcification by using Tc-phosphate compounds, particularly 99mTc-E.H.D.P. This is important, since it is often not possible to demonstrate it radiologically. It further demonstrates that the accumulation of 99mTc-E.H.D.P. is dependent on active bone metabolism.
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PMID:[The diagnosis of pulmonary calcinosis by scintigraphy (author's transl)]. 13 Oct 61

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

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 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

A case of watery diarrhea, hypokalemia and hypercalcemia associated with an islet cell tumor was described. A 62-year old man exhibited frequent watery diarrhea and hypokalemia for two years. He had no peptic ulcer and serum gastrin level was normal. His serum calcium was abnormally high and serum phosphate was lowered. He had secretin-like activity in his plasma. Autopsy revealed a small islet cell tumor in the pancreas and several metastatic masses in the liver. Microscopic examination revealed the tumor cell was not beta, alpha nor D cells. By electron microscopy the secretion granules of the tumor cell resembled those of S, M and T cells. It was not possible to decide which of the tree cell types was responsible for the pancreatic cholera.
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PMID:A case of watery diarrhea, hypokalemia and hypercalcemia associated with nonulcerogenic islet cell tumor of the pancreas. 17 23

To determine the functional capabilities of the parathyroid glands, 17 EDTA infusions were given to 11 children (ages 1 month to 12 years) and to two mothers of four of the children. Serum ionized Ca fell from 4.1 mg/dl to 3.4 mg/dl. Excessive parathyroid hormone responses were elicited during seven of nine EDTA infusions in five children and in one adult with hypophosphatemic rickets, during the active phase of rickets. In four of five subjects with problems related to hypercalcemia, borderline low or undetectable PTH responses were elicited. Three relatively normal PTH responses were obtained, two in an infant after phosphate-induced hypocalcemic tetany was corrected, and one in a child with a malabsorption syndrome. The renal tubular reabsorption of phosphate was inversely related and the urinary cyclic AMP excretion was positively related to the PTH response. Thus EDTA infusions in infants and children might be useful in the identification of hyper-, normo-, or hypoparathyroid states and would be of value in defining the functional condition of the parathyroid glands in children with deranged Ca or P metabolism.
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PMID:Parathyroid function tests with EDTA infusions in infancy and childhood. 17 44

A review is given of the literature concerning the so-called plant induced calcinosis in animals (tabel I), i.e. diseases which in their patological-anatomical appearance show great similarities with vit. D-intoxication. The etiology of the diseases are discussed in view of the last 5--10 years rapid development of knowledge concerning vit. D3 metabolism. It is pointed out that the most recent results indicate that enzootic calcinosis is caused by a 1,25-dihydrocholecalciferol-glycoside, which is hydrolysed in the intestinal tract. By this reaction 1.25 (OH) 2 cholecalciferol--the biological active metabolite of vit. D3 -- is set free, and thus able to act directly on the intestinal absorption mechanism. By this reaction the point of calcium metabolism regulation is essentially by-passed and calcium and phosphate absorption proceeds essentially out of control, causing hypercalcaemia, hyperphosphataemia, hypersecretion of calcitonin and calcinosis.
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PMID:[Enzootic calcinosis and other plant induced calcinoses (author's transl)]. 19 May 89


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