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

Paget's disease of bone is often discovered incidentally, but can have extensive metabolic and local mechanical complications. Treatment is not required for all patients and should only be undertaken for certain indications, and with a clear understanding of the three types of drugs available. Bone pain unmanageable with analgesics and pathologic fractures are the most common indications, while neurologic symptoms, hypercalcemia and congestive heart failure are less frequent ones. Calcitonin or mithramycin is used for the more urgent indications, and calcitonin or the diphosphonate, etidronate sodium (EHDP), for the more chronic ones. The drugs are generally efficacious and well tolerated.
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PMID:Paget's disease of bone: clinical features and treatment. 315 5

This is a comparative study of the glycoprotein hormone, teleocalcin, from the corpuscles of Stannius of sockeye (Oncorhynchus nerka) and coho (O. kisutch) salmon. Coho teleocalcin was purified by the same procedures used previously to obtain sockeye teleocalcin and was obtained in a comparable yield. Both salmon teleocalcins had the same molecular weight as estimated by sodium dodecyl sulfate-electrophoresis and both appeared to have the structure of disulfide-linked oligomers. The two hormones were similar on the basis of amino acid and carbohydrate composition and shared 95% homology in the first 40 residues on the N-terminal. The salmon teleocalcins also shared 80% homology with the predicted 1-40 N-terminal sequence from Australian eels (Anguilla australis). Both teleocalcins had potent inhibitory effects on gill calcium uptake in intact rainbow trout (Salmo gairdneri). However, these effects were observed only at the peak in the calcium uptake cycle that is displayed by this species. In North American eels (A. rostrata), the acute administration of both teleocalcins caused significant inhibition of gill calcium uptake without any concomitant changes in plasma calcium levels or other plasma electrolytes. In 4- and 7-day stanniectomy (STX) eels, the acute administration of coho teleocalcin significantly reduced or completely abolished the accelerated gill calcium transport that occurs postoperatively, with no concomitant changes in plasma electrolytes or post-STX hypercalcemia. These experiments provide further evidence that teleocalcin is a regulator of gill calcium transport and has no acute hypocalcemic effects in fish.
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PMID:Comparative biochemistry and physiology of teleocalcin from sockeye and coho salmon. 319 44

The efficacy of intravenous aminohydroxypropylidene bisphosphonate as treatment for the hypercalcemia of malignancy was examined in a phase II multicenter study in 132 patients with a large variety of primary tumors. This provided an opportunity for an analysis of the separate influences of bone resorption and renal calcium handling on the genesis and maintenance of hypercalcemia. The results demonstrated that increased bone resorption is the major contributory factor and that inhibition with bisphosphonate normalizes the serum calcium concentration within five days in more than 90 percent of patients. Hypercalcemia is sustained by an inability of the kidney to deal efficiently with a chronically increased calcium load. This is influenced by the requirements of volume regulation in the presence of a sodium diuretic effect of hypercalcemia and is very sensitive to induced variations of sodium load. In addition, in a minority of patients, direct renal actions of tumor-derived humoral factors adversely reduce the ability to excrete calcium. For optimal treatment of tumor-induced hypercalcemia, bisphosphonate treatment should be combined with intravenous administration of saline solution.
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PMID:Role of bone and kidney in tumor-induced hypercalcemia and its treatment with bisphosphonate and sodium chloride. 330 Mar 3

Hypophosphatemia and hyperphosphaturia characteristically occur in patients with humoral hypercalcemia of malignancy (HHM). To determine if a tumor product causes these abnormalities in phosphate metabolism, rather than, for example, hypercalcemia, we investigated the effect of partially-purified adenylate cyclase-stimulating activity (ACSA) from human and animal HHM-associated tumors on sodium-dependent phosphate transport (Na PiT) in a PTH-responsive renal epithelial cell line. Thirty minute exposure to 7 X 10(-10) MbPTH (1-34) equivalents of ACSA from the human and animal tumors, reduced NaPiT by 20% and 14%, respectively. We also recently isolated an adenylate cyclase-stimulating protein (hACSP) from two human tumors associated with HHM and identified a cDNA clone for this protein which encodes a 141 amino-acid peptide. Based on the deduced amino-acid sequence, we synthesized tyr36 (1-36) hACSP. This synthetic peptide induced a 22% decrease in the initial rate of NaPiT by the epithelial monolayer. Its inhibitory activity was roughly equipotent to that of bPTH (1-34). We conclude that the ACSP derived from HHM-associated tumors decreases phosphate transport in renal epithelial cells. This peptide appears to play a key role in mediating the changes in phosphate metabolism in this syndrome.
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PMID:Synthetic and partially-purified adenylate cyclase-stimulating proteins from tumors associated with humoral hypercalcemia of malignancy inhibit phosphate transport in a PTH-responsive renal cell line. 333 17

After 7 days in air on wet filter paper mudskippers had normal body weight and normal levels of plasma sodium, potassium, and phosphate. They were, however, significantly hypercalcemic. The hypercalcemia could be reduced by the daily intraperitoneal injection of synthetic eel calcitonin (1.67 microgram kg-1 day-1) and this effect was dose dependent with a maximal response at a dose of 3.33 micrograms kg-1 day-1. Calcitonin had no effect on plasma calcium levels of fish held in water but did induce significant hyperphosphatemia whether the fish were held in water or in air on wet filter paper with this effect being greater under the latter conditions. The hypocalcemic action of calcitonin was restricted to conditions under which the fish displayed patent hypercalcemia. Under no conditions did calcitonin produce significant hypocalcemia so it appears that the action of synthetic eel calcitonin in the mudskipper, Periophthalmodon schlosseri, is dependent upon the presence of excess plasma calcium and is thus more accurately described as being anti-hypercalcemic rather than hypocalcemic.
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PMID:Effects of calcitonin on plasma calcium and phosphate in the mudskipper, Periophthalmodon schlosseri (Teleostei), in water and during exposure to air. 338 5

Hypercalcemia is associated with impaired urinary concentrating ability. To explore the mechanism(s) by which hypercalcemia impairs chloride transport in the loop of Henle, we carried out in vivo microperfusion of the loop segment in Sprague-Dawley rats rendered acutely hypercalcemic (12.1 +/- 0.1 mg/dliter) by calcium gluconate infusion. Control rats were infused with sodium gluconate and had normal plasma calcium (8.0 +/- 0.2 mg/dliter). Compared to control, fractional chloride reabsorption was decreased (61 +/- 4 to 50 +/- 3%; P less than 0.05) and early distal chloride increased 74 +/- 6 to 98 +/- 3 mEq/liter (P less than 0.001) in hypercalcemia. During hypercalcemia, infusion of verapamil failed to increase fractional chloride reabsorption (49 +/- 4%; P less than 0.05) or decrease early distal chloride (95 +/- 2; P less than 0.05) toward control values. Similarly, indomethacin did not improve fractional chloride reabsorption (48 +/- 4%; P less than 0.05) or distal chloride concentration (93 +/- 7; P less than 0.05). In control rats infused with Ringers HCO3, the addition of calcium 8.0 mEq/liter to the perfusate increased early distal calcium (9.22 to 3.11 mEq/liter) but was associated with no change in fractional chloride reabsorption (-6 +/- 6%) and a slight decrease in early distal chloride (-9 +/- 3 mEq/liter; P less than 0.05). These data are consistent with the hypothesis that an elevated plasma, not luminal calcium, concentration impairs chloride reabsorption in the loop segment, primarily the ADH-stimulated component. This may have an important role in the urinary concentrating defect of hypercalcemia.
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PMID:Role of the loop segment in the urinary concentrating defect of hypercalcemia. 348 71

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

The control of hyperphosphatemia in dialysis patients is frequently achieved using aluminium hydroxide (A1(OH)3) and/or calcium carbonate (Ca CO3). However, this effect is counterbalanced by risk of aluminium intoxication and hypercalcemia. An alternative to the use of these phosphate binders is the prescription of magnesium hydroxide (Mg(OH)2) in association with a magnesium free dialysate. 19 patients with subtoxic plasma aluminium concentration received such a therapy. 9 months after starting the essay 4 patients had been excluded for digestive intolerance (3 cases) and neuro-psychic symptoms related to hypermagnesemia (1 case) after therapy with maximal doses of 6 to 12 g/d. Plasma inorganic phosphorus was decreased from 2.47 +/- 0.32 to 1.86 +/- 0.40 mmol/l (P less than 0.05) and plasma aluminium from 3.03 +/- 0.93 to 1.52 +/- 0.15 mumol/l (P less than 0.05). The results have been obtained without any significant increase in plasma and red cell magnesium levels. Metabolic alkalosis has been observed in association with the increase of ion exchange resin (sodium polystyrene sulfonate: Kayexalate) to treat progressive hyperkalemia. With the exception of possible metabolic effects occurring on a long term basis, Mg(OH)2 in association with magnesium-free dialysate seems of value to treat dialysis hyperphosphatemia.
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PMID:[Magnesium hydroxide treatment of hyperphosphatemia in chronic hemodialysis patients with an aluminum overload]. 361 5

The theoretical tubular maximum for calcium reabsorption was calculated and its usefulness assessed in the diagnosis and differential diagnosis of primary hyperparathyroidism and familial hypocalciuric hypercalcaemia. The sensitivity of the test in the diagnosis of primary hyperparathyroidism was only 12%. The theoretical tubular maximum for calcium reabsorption was recalculated after correction of calcium concentration in plasma for albumin concentration and for urinary sodium excretion. Despite these corrections, the sensitivity improved to only 44%. This contrasts with a sensitivity of 80% for the plot of fasting calcium excretion against calcium concentration in plasma in primary hyperparathyroidism. The calculation of theoretical tubular maximum for calcium reabsorption cannot be recommended as a useful test for distinguishing between primary hyperparathyroidism and familial hypocalciuric hypercalcaemia. The simple calculation of fractional excretion of calcium was a better test in distinguishing familial hypocalciuric hypercalcaemia from primary hyperparathyroidism.
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PMID:Tubular maximum for calcium reabsorption: lack of diagnostic usefulness in primary hyperparathyroidism and familial hypocalciuric hypercalcaemia. 362 96

The relation between urinary sodium excretion (NaE) and renal tubular calcium reabsorption (TmCa/GFR) was assessed in patients with hypercalcaemia associated with malignancy and primary hyperparathyroidism. On acute saline loading of seven normally hydrated patients with primary hyperparathyroidism and five patients with malignancy, raised values of TmCa/GFR were reduced to normal in most cases, in association with increases in NaE. The reduction in TmCa/GFR, which occurred, may have been due to a reduction in proximal tubular calcium reabsorption associated with sodium: this would have obscured the effect of humorally mediated increases in distal tubular calcium reabsorption, which are stimulated either by parathyroid hormone or by a putative humoral mediator in hypercalcaemia of malignancy. In patients who were normally hydrated NaE and TmCa/GFR were not significantly correlated. When data were included from patients who were dehydrated and from those undergoing acute saline loading, significant inverse correlations between NaE and TmCa/GFR were observed both in primary hyperparathyroidism (r = -0.49; p less than 0.02) and malignancy (r = -0.60; p less than 0.001). In clinical practice changes in TmCa/GFR associated with sodium seem to be of minor importance under normal circumstances, but they become evident at the upper and lower extremes of urinary sodium excretion. In clinical studies of renal calcium handling urinary sodium excretion must also be assessed, as interpreting TmCa/GFR data is difficult in states of excessive sodium loading or depletion.
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PMID:Influence of urinary sodium excretion on the clinical assessment of renal tubular calcium reabsorption in hypercalcaemic man. 372 17


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