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

There are a variety of water and electrolyte disorders in patients with cancer. These disorders occur during the growth of tumors, generally as a consequence of inadequate intake and absorption of electrolytes, renal failure secondary to tumor or rapid tumor destruction and production of metabolically active substances by the tumor. In this paper, the electrolyte abnormalities associated with cancer were reviewed. Hyponatremia is one of the most common clinical electrolyte abnormalities in advanced cancer. Some patients may have hyponatremia, in spite of increased total body sodium and absence of a defect in water diuresis. This status is designated as "sick cell syndrome" or "essential hyponatremia". In addition, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in association with various tumors has been described. This syndrome is principally due to water retention, but can also be due to continuous urinary loss of sodium, and hypo-osmolality. Hypercalcemia is associated with coexistent primary hyperparathyroidism, prostaglandin (PGE2) or osteoclast-activating factor. It now seems likely that ectopic PTH is rarely the cause of hypercalcemia in nonparathyroid cancer. There are no data supporting the ectopic production of vitamin D-like substance as an important factor in the hypercalcemia of cancer. There are three general categories in which patients with hypercalcemia and cancer may be placed: those with bone metastases, those without bone metastases of solid tumors and those with hematologic malignancies. Hypokalemia is associated with ectopic ACTH- and insulin--producing tumors, and is often found in patients with mucin-secreting, potassium-losing adenocarcinoma of the colon.
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PMID:[Electrolyte abnormalities associated with cancer: a review]. 352 93

Plasma concentrations of vitamin D3 (cholecalciferol) metabolites have been studied in rainbow trout (Salmo gairdneri) adapted to varying environmental calcium concentrations in both fresh water and artificial seawater, and in natural seawater. In vivo, intraarterial injection of tritiated 25-hydroxycholecalciferol was followed by its transformation to a number of metabolites including compounds that cochromatographed on high performance liquid chromatography (HPLC) with 1,25-dihydroxycholecalciferol and 25,26-dihydroxycholecalciferol. Hypercalcaemia and increased environmental calcium were associated with a greater transformation to the compound cochromatographing with 25,26-dihydroxycholecalciferol, while hypocalcaemia and reduced environmental calcium concentrations induced more conversion to the 1,25-dihydroxycholecalciferol-like compound. In vitro, both metabolites were produced by liver but not by kidney preparations, and the difference in conversion ratios observed in vivo associated with changes in plasma calcium were also seen in vitro. It is concluded that the metabolism of 25-hydroxycholecalciferol in the trout can be influenced by calcium status, but at present the physiological importance of this metabolism and the mechanisms and site(s) of action of the metabolites are unknown.
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PMID:Metabolism of 25-hydroxycholecalciferol in a teleost fish, the rainbow trout (Salmo gairdneri). 355 76

We describe 3 patients who developed extreme hypermagnesemia due to ingestion of water of the Dead Sea, which would have been fatal were it not for the protective effects of the accompanying hypercalcemia. We emphasize the clinical features of this condition and the importance and effectiveness of early hemodialysis as the main modality of treatment.
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PMID:Extreme hypermagnesemia due to ingestion of Dead Sea water. 368 88

The mechanism of the concentrating defect of hypercalcemia is explored by examining the effect of concomitant phosphate restriction. Rats were pair fed a normal phosphorus diet, without (group 1) or with dihydrotachysterol (group 2), or a low-phosphorus diet (group 3). Hypercalcemia was comparable in groups 2 (12.1 +/- 0.6 mg/dl) and 3 (11.8 +/- 0.4 mg/dl), but serum phosphate was lower in group 3 than group 2 (3.8 +/- 0.7 vs. 7.1 +/- 1.1 mg/dl, P less than 0.005). Group 2 rats had impaired maximum urinary concentration after 24 h of fluid deprivation (2,441 +/- 450 mosmol/kg H2O, P less than 0.001) compared with group 1 (3,263 +/- 466 mosmol/kg H2O) or group 3 (3,332 +/- 515 mosmol/kg H2O) animals. Polydipsia and polyuria were found in group 2 rats only. Tubular calcium reabsorption was higher in group 2 (83.1 +/- 33.5 mg/24 h, P less than 0.001) than group 1 (47.0 +/- 26.1 mg/24 h) or group 3 (52.8 +/- 19.3 mg/24 h) animals, and medullary calcium concentration was higher in group 2 (7.57 +/- 3.08 nmol/mg dry wt, P less than 0.05) as compared to group 1 (5.04 +/- 1.37 nmol/mg dry wt) or group 3 (5.32 +/- 0.98 nmol/mg dry wt) rats. Total medullary solute concentration was significantly higher in group 3 than group 2 animals. Thus phosphate restriction prevents the defect of urinary concentrating ability of chronic hypercalcemia, probably by decreasing tubular uptake and tissue accumulation of calcium.
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PMID:Prevention of hypercalcemia-induced renal concentrating defect and tissue calcium accumulation. 376 41

To assess the consequences of hypercalcemia on systemic and renal hemodynamics, vasoactive hormones, and water and electrolyte excretion in intact, conscious mongrel dogs, measurements in 10 dogs receiving 100 mg/kg calcium gluconate and 10,000 U/kg vitamin D daily for 2 weeks were compared with measurements made in 10 time-control dogs not receiving calcium or vitamin D. Hypercalcemia induced by dietary supplementation with calcium and vitamin D resulted in profoundly reduced glomerular filtration rate (40 vs 78 ml/min in controls; p less than 0.005), estimated renal plasma flow (145 vs 267 ml/min in controls; p less than 0.005), and renal blood flow (254 vs 441 ml/min in controls; p less than 0.005). Renal resistance was significantly increased in the hypercalcemic dogs (0.57 +/- 0.07 vs 0.28 +/- 0.01 mm Hg/ml/min; p less than 0.005). Hypercalcemia also resulted in increased fractional excretion of water (4.8 vs 1.4% in controls; p less than 0.005), sodium (1.4 vs 0.6% in controls; p less than 0.005), calcium (1.7 vs 0.7% in controls; p less than 0.01), and magnesium (10.2 vs 4.1% in controls; p less than 0.005). Systolic blood pressure (160 vs 172 mm Hg in controls; p less than 0.05) and stroke volume were lower (0.024 vs 0.036 L/beat in controls; p less than 0.005) in hypercalcemic dogs, presumably because of the diuresis, while total peripheral resistance was higher (36 vs 31 mm Hg/L/min; p less than 0.05) in controls. Magnesium levels were significantly lower in the experimental group (1.3 vs 1.7 mg/dl in controls; p less than 0.0005). Aldosterone levels, plasma renin activity, and urinary prostaglandin excretion were not significantly affected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systemic and renal vascular responses to dietary calcium and vitamin D. 377 Aug 72

Sodium-retaining activity of chum salmon prolactin (PRL) was examined in several euryhaline teleosts. Chum PRL was 100 times more potent than ovine PRL in maintaining plasma sodium levels in the hypophysectomized killifish, Fundulus heteroclitus, transferred from 50% seawater to fresh water. The effects of PRLs were parabolic, high doses of the hormones being less effective than low doses. When injected into seawater-adapted fry of the ayu, Plecoglossus altivelis, or into juvenile rainbow trout, Salmo gairdneri, adapted to 50% seawater, a dose-dependent increase in plasma sodium was observed. Chum PRL was 2-10 times more active than ovine PRL, and the effects in the ayu were also parabolic. An increase in plasma sodium also occurred when the PRLs were injected into the seawater-adapted eel, Anguilla japonica; the chum and ovine PRLs were equipotent, and hypercalcemia was also observed. In contrast, both chum and ovine PRLs were without effect on plasma sodium levels of chum salmon fry, either when injected into seawater-adapted fish kept in seawater or into fish subsequently transferred to fresh water. The absence of an effect of PRLs in chum salmon fry seems to be due, at least in part, to their good osmoregulatory ability during the period of seaward migration; effects of the exogenously administered PRLs may be compensated for by other hormones responsible for their hydromineral balance.
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PMID:Sodium-retaining activity of chum salmon prolactin in some euryhaline teleosts. 378 Dec 35

Twelve cases representing variants of peripheral T malignant lymphoma were described for the first time in this country. Rosette test and immunocytology were crucial for their identification. Convoluted nuclei were a dominant histologiial feature as well as a voluminous water-clear cytoplasm which kept being surprisingly well demarked. Basic features were analogous to the Far East cases. Nevertheless, hypercalcemia and substantial pulmonary lesion were not observed.
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PMID:[Peripheral T-malignant lymphoma (PTML)]. 387 12

Ovine prolactin stimulated the net uptake rate of Ca2+ from the water by 96%, produced frank hypercalcemia, and increased total bone calcium content in fed rapidly growing freshwater male tilapia, Oreochromis mossambicus. It did not, however, alter the size of the readily exchangeable bone calcium pool. The increase in calcium accumulation resulted from an increase in whole-body Ca2+ influx and a decrease in Ca2+ efflux. It is concluded that prolactin exerts an important control over Ca2+ exchange between the fish and its environment and that through its hypercalcemic action prolactin indirectly facilitates bone mineralization.
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PMID:Effects of ovine prolactin on calcium uptake and distribution in Oreochromis mossambicus. 394 34

Neonatal primary hyperparathyroidism is rare but must be evoke during respiratory distress with thoracic deformity and hypercalcemia. The plasma immunoreactive parathyroid hormone level allows the diagnostic. This case, with diffuse hyperplasia of water-clear cells type, develops rickets of vitamin D deficiency before surgery. A large parathyroidectomy (7/8) was performed and the child is normo-calcemic 2 years after. The time of surgery is function of calcium level.
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PMID:[Neonatal primary hyperparathyroidism caused by clear cell hyperplasia]. 402 15

A possible association between the impairment of urinary concentrating ability and an impairment of the vasopressin-dependent cyclic AMP system in hypercalcemia was investigated in rat kidneys both in vivo and in vitro. The increases of urinary osmolality and negative free water clearance and the increase of urinary cyclic AMP excretion by vasopressin injection were significantly less in the hypercalcemic rats than in the control rats. The increase of cyclic AMP concentration by vasopressin in renal medullary tissue was significantly less in the slices obtained from the hypercalcem'c rats than in those obtained from the control rats. The activation of adenylate cyclase by vasopressin was significantly less in the group with an increased concentration of calcium in media than the control group, but phosphodiesterase activity was not affected by calcium concentration in the media. These data suggest that the impaired urinary concentrating ability in hypercalcemic kidneys is due at least in part to the direct inhibitory effect of calcium on the vasopressin-dependent cyclic AMP system at the level of adenylate cyclase in renal medulla.
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PMID:Pathogenic role of cyclic AMP in the impairment of urinary concentrating ability in acute hypercalcemia. 437 61


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