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)

White Leghorn chick embryos were injected on the 15th day of incubation with 70 to 300 pmoles 1,25-(OH)2D3. All doses produced hypercalcemia; with the highest dose, the concentration of calcium in serum started to rise 4 h after the injection, reached a peak 20 h after, and was still high 48 h after. Twenty hours after the injection of the same dose, the concentration of inorganic phosphorus in the serum was significantly lower than in the corresponding controls. The tibias from 17-day-old chick embryos injected with 300 pmoles on day 15 were shorter, lighter, and had a lower ash content than those from controls. Histological signs of resorption appeared to be reduced with respect to controls, but no precise quantitation was conducted. The fact that hypercalcemia was not accompanied by hyperphosphatemia may suggest that the vitamin stimulates resorption of calcium from the shell, which is mainly formed by calcium carbonate rather than from the bone from which calcium and phosphate are usually resorbed together.
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PMID:Effects produced by the administration of high doses of 1,25-dihydroxycholecalciferol to the chick embryo. 57 6

Patients with severe symptomatic renal osteodystrophy were treated with either 1,25(OH)2D3 or 1 alpha(OH)D3. In 39 instances, there was either reversal of symptoms and/or a marked fall in plasma alkaline phosphatase. Bone biopsies showed improvement of either osteomalacia or osteitis fibrosa, and serum iPTH often fell. In thirteen patients, no improvement occurred. In seven patients, bone biopsy disclosed osteomalacia, and serum iPTH was normal or only slightly elevated. Thus, there was a defect in mineralisation. apparently unrelated to the lack of 1,25(OH)2D3 and in the absence of evidence of phosphate depletion. The other 'treatment failure' group showed osteitis fibrosa on biopsy and iPTH levels were markedly elevated. They are presumed to have marked secondary hyperparathyroidism. These 'treatment failure' groups had higher pre-treatment levels of serum Ca and Mg than in those showing a favourable response; also, hypercalcaemia developed rapidly during 1,25(OH)2D3 treatment. Thus, 1,25(OH)2D3 is efficacious in treating symptomatic osteodystrophy in many uraemic patients, and in other patients, it may help identify bone disease of other, as yet unknown, pathogenesis.
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PMID:Use of 1,25(OH)2-vitamin D3 to separate 'types' on renal osteodystrophy. 60 Sep 61

Scintiscanning to detect the uptake of bone-seeking radioactive isotopes by soft tissue is a promising technique for the in vivo study of visceral calcification. Visceral uptake of such radioisotopes was studied in 40 patients: 22 undergoing long-term dialysis, 9 with malignant disease and hypercalcemia and 9 with primary hyperparathyroidism and hypercalcemia.Fifteen patients, 11 undergoing dialysis and 4 with malignant disease, had radioisotope uptake in the lungs, and 5, 3 undergoing dialysis and 2 with malignant disease, had uptake in the stomach. None of the patients with primary hyperparathyroidism had visceral uptake, nor did the patients with uptake have radiologic evidence of pulmonary or gastric calcification. The dialysis patients with visceral uptake had a mean calcium x phosphate product of 84.3 +/- 23.7 (standard deviation), which was significantly greater (P < 0.001) than that of patients without such uptake (59.2 +/- 14.0). Similarly, in patients with malignant disease and visceral uptake the Ca x P product was 72.2 +/- 6.4 - significantly greater (P < 0.005) than that of patients without such uptake (49.3 +/- 6.7).These findings indicate that scintiscanning for the visceral uptake of a bone-seeking radioisotope is a simple and effective technique for the in vivo study of visceral calcification. An elevation in the Ca x P product seems to be the single most important factor in the production of visceral calcification.
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PMID:Detection and pathogenesis of visceral calcification in dialysis patients and patients with malignant disease. 62 Mar 83

An unusual finding of systemic calcinosis in a patient with a nonparathyroid malignant neoplasm stimulated us to do a sclinicopathologic review of similar cases at our institution in the past seven years. Of 3,268 autopsies performed from 1968 to 1975, a total of 17 cases of calcinosis were found, 11 with solid tumors and 6 with hematopoietic neoplasms. Calcinosis was most prominent in the lung, kidney, heart, and stomach and was rarely discovered prior to death. Eighty-two percent of the patients had hypercalcemia and 53% had associated bony metastatic disease. Corticosteroid or phosphate treatment for the hypercalcemia may have contributed to the tissue deposition of calcium. Significant hepatic, renal, metabolic, and pulmonary dysfunctions were also associated with this disorder. Thirty-six percent of the patients had hypercalcemia without skeletal involvement; tumor-produced parathormone-like substances may be responsible for these calcium abnormalities. Calcinosis was a significant complication of neoplastic disease in these patients and contributed to morbidity and mortality.
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PMID:Calcinosis in nonparathyroid malignant disease: an unusual case report and clinicopathologic review of 17 cases. 62 63

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.
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PMID:Mechanism of lithium-induced hypercalciuria in rats. 62 44

Parathyroid hormone (PTH), creatinine, calcium and phosphate blood levels were repeatedly measured in 5 patients with acute renal failure. 1 patient developed hypercalcemia during the recovery phase of the illness. PTH was elevated in all cases before starting hemodialysis treatment and returned to normal when renal function recovered. Calcium and PTH were inversely correlated in 3 patients including the patient with transient hypercalcemia. These data show that parathyroid function in acute renal failure is closely related to changes in renal function and the hypercalcemia, when occurring, is not necessarily due to parathyroid hyperactivity.
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PMID:Parathyroid hormone and calcium blood levels in acute renal failure. With special reference to one patient developing transient hypercalcemia. 63 17

The influence of hypercalcemia on renal function was studied retrospectively in 13 patients suffering from primary hyperparathyroidism, sarcoidosis, vitamin D intoxication, malignant lymphoma or chronic lymphatic leucemia. Different kinds of treatment, depending upon the primary disease, often induced a rapid fall in the serum calcium concentration. The serum creatinine concentration always fell simultaneously. The serum phosphate concentration fell in all but two patients. Changes in serum calcium and serum creatinine correlated significantly (p less than 0.001), as did changes in serum calcium and serum phosphate concentrations (p less than 0.05). Serum calcium/serum creatinine and serum calcium/serum phosphate ratios were significantly higher in patients with primary hyperparathyroidism than in patients with hypercalcemia of non-hyperparathyroid origin (p less than 0.01, p less than 0.001). This suggests a different effect of calcium on the glomerular filtration rate in hyperparathyroid and non-hyperparathyroid patients, the latter group being more sensitive to the influence of hypercalcemia. Possible explanations for this difference, such as a protective effect of PTH on the glomerular filtration, are discussed.
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PMID:Reversible renal failure caused by hypercalcemia. A retrospective study. 64 44

Hypercalcemia causes lethargy and coma in patients with head and neck cancer. It is important to realize that coma may be due to hypercalcemia and need not be a terminal event in the progress of the tumor. Also, the development of hypercalcemia in a previously normocalcemic patient requires investigation as to the cause of the hypercalcemia. I report two cases of comatose patients, hypercalcemic from bony metastases from tongue cancer, in whom treatment by furosemide and intravenous fluid diuresis, prednisone, sodium phosphate, and mithramycin produced worthwhile remissions. Hypercalcemia may be due to (1) bony metastases, (2) pseudohyperparathyroidism, (3) unrelated associated parathyroid tumors, or (4) a second primary tumor. Even with treatment, hypercalcemia is a bad prognostic sign in patients with head and neck cancer.
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PMID:Hypercalcemia and head and neck cancer. Bony metastases from tongue cancer. 69 40

Six patients with chronic renal failure on regular dialysis treatment were given low doses (0.5--1.0 microgram/day) of 1alpha-hydroxyvitamin D3, monitoring the serum calcium, inorganic phosphate, immunoreactive parathyroid hormone concentration (IPTH) and alkaline phosphatase activity. The serum calcium rose in all patients after 7 days' treatment, in some subjects to hypercalcemic range; this effect persisted 6--14 days after withdrawal of 1alpha-hydroxyvitamin D3. The elevated serum IPTH rose in the first days of treatment, but later decreased to normal values. It is suggested that active vitamin D metabolites are necessary for normal response of parathyroid glands to variation in serum calcium. Low-dose 1alpha-hydroxyvitamin D3 treatment appears to be a promising method of correcting hypocalcemia and secondary hyperparathyroidism in chronic renal failure. Careful control of serum calcium is necessary, as hypercalcemia may occur even after minute doses of 1alpha-hydroxyvitamin D3.
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PMID:Effects of 1alpha-hydroxyvitamin D3 on serum calcium and immunoreactive parathyroid hormone in patients with chronic renal insufficiency. 70 Sep 46

Plasma concentrations of calcium fractions, proteins, phosphate and magnesium were measured before, during and after cardiopulmonary bypass in 15 patients undergoing cardiac surgery. When calcium chloride was added to a pump priming solution which contained little or no blood, the concentrations of all calcium fractions were significantly greater after bypass than before, with a mean ionized calcium concentration of 1.52 mmol litre-1 plasma water, 30 min after completion of bypass. This iatrogenic hypercalcaemia was increased significantly by the administration of more than 10 mg kg-1 calcium chloride in the first 30 min after bypass. Other plasma constituents showed the dilutional effect of the pump prime during bypass and only the magnesium concentration failed to return towards normal values after operation.
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PMID:Changes in ionized calcium and other plasma constituents associated with cardiopulmonary bypass. 70 63


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