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

The effects of the intravenous administration of atropine or magnesium on pancreatic secretion which has been stimulated by secretin and induced hypercalcaemia have been studied in man. In the presence of secretin (0.5 CU/kg.h) the infusion of Ca2+ (0.3 mmol/kg.105 min) resulted in an increase in secretion of enzymes by 100-200%, and in that of Ca2+ and Mg2+ by 50-100% without affecting fluid and bicarbonate secretion. The additional injection of atropine (0.5 mg i.v. and 0.5 mg s.c.) were followed by a prompt fall in enzymes but not in Ca2+ and Mg2+ to the secretin-stimulated values. The additional infusion of Mg2+ (0.12 mmol/kg.45 min) to the Ca2+-infusion did not alter the secretion of enzymes, Ca2+ or Mg2+ compared with the calcium infusion alone. It is suggested that the hypercalcaemic stimulus depends on an intact innervation of the acinar cells. In these experiments the secretion of Ca2+ and Mg2+ seem to originate mainly from extracellular fluxes.
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PMID:Interactions of calcium, magnesium and atropine on exocrine pancreatic secretion in man. 10 22

The influence of magnesium deficiency on cyclic AMP metabolism was investigated in rats on diets of normal and low calcium content. Magnesium deficiency itself did not significantly affect either the basal concentration or the parathyroid hormone-stimulated formation of cyclic AMP in the renal cortex. Magnesium-deficient rats with hypercalcaemia excreted more cyclic AMP in the urine, but similar rats that developed hypocalcaemia on low calcium intake excreted less than their respective controls. The former type of animals also tended to accumulate more cyclic AMP in the renal cortex in response to the injection of a standard dose of parathyroid hormone, whereas rats of the latter type accumulated less. The activity of parathyroid hormone-stimulated renal cortical adenylate cyclase in vitro was increased by magnesium and reduced by calcium under most conditions, but with low concentrations of magnesium small amounts of calcium had a stimulatory effect. These observations suggest that cyclic AMP metabolism is influenced by metabolic disorders developing secondary to magnesium deficiency.
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PMID:Effect of magnesium deficiency and parathyroid hormone on cyclic AMP metabolism in rat renal cortex. 17 79

In contrast to man, the rat exhibits hypercalcemia during the course of magnesium depletion. To investigate the role of the vitamin D (D) endocrine system in the induction of hypercalcemia, circulating D metabolites, the binding properties of the duodenal 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] receptor (VDR), and 45Ca transport studies were undertaken in magnesium-replete rats or after 10 days of magnesium depletion in animals presenting the following D status: D depletion and hypo- or normocalcemia (achieved by oral calcium supplementation), D3 or 1,25-(OH)2D3 repletion. Magnesium depletion did not influence serum calcium in hypo- or normocalcemic D depleted rats, but increased serum calcium in animals receiving D3 (P less than 0.002) or 1,25-(OH)2D3 (P less than 0.0001), suggesting that the D3 endocrine system is necessary to mediate the rise in extracellular calcium and that dietary calcium alone is not sufficient to significantly increase extracellular calcium in the hypomagnesemic rat. The data also show that 25-hydroxyvitamin D formation was not perturbed, but circulating 1,25-(OH)2D3 concentrations were reduced by 10 days of magnesium depletion (P less than 0.0001) even in animals infused with 1,25-(OH)2D3, suggesting increased clearance of the hormone. The kinetic data of the duodenal VDR revealed maximum binding sites ranging from 1018-1500 fmol/mg DNA and Kd ranging from 0.17-0.38 nM, with no significant between-group difference in magnesium-sufficient animals. Ten days of magnesium depletion did not significantly influence VDR affinity in any of the groups, but significantly increased receptor number in hypocalcemic D-depleted rats from 1190 +/- 154 to 2748 +/- 430 fmol/mg DNA (P less than 0.004). Calcium transport studies in D-replete animals indicate that intestinal calcium transport is influenced by the progressive depletion in magnesium, with time-related increases coinciding with the in vivo increase in circulating ionized calcium (day 6 of magnesium depletion). However, despite persistent elevated serum ionized calcium, calcium transport declined only to predepletion levels on days 8 and 10 of magnesium depletion. To investigate the influence of the D3 endocrine system on 45Ca absorption, D-depleted rats sufficient or depleted in magnesium were injected with 1,25-(OH)2D3, either acutely (to reveal its membrane effects) or 16 and 5 h before death (to reveal its genomic effect). The data reveal a reduced response in magnesium-depleted rats to acute 1,25-(OH)2D3 injection (P less than 0.0002), but similar responses when the hormone was injected 16 and 5 h before the experiment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Responsiveness of the intestinal 1,25-dihydroxyvitamin D3 receptor to magnesium depletion in the rat. 131 57

Magnesium has been a forgotten cation from the therapeutical point of view, given that, although its properties began to be known more than a century ago, its use has been always empirical or isolated. With respect to its use in emergency situations, in addition to correcting its deficit and using it for the treatment of hypercalcemia and hypopotassemia, it is currently recommended as the therapy of choice for the treatment and prevention of several arrhythmias. It can also be used to prevent its deficit, when such deficit is pathological or associated to the ingestion or certain drugs. Given the multiple properties of magnesium, controlled studies are required in order to define its potential therapeutical applications.
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PMID:[Magnesium: therapeutic usefulness in emergency situations]. 150 8

Despite extensive study since the first report of familial benign hypercalcemia (FBH, or hypocalciuric hypercalcemia) in 1972, there is no evidence of the specific abnormal gene product. FBH is highly suitable for either a candidate gene or a reverse genetics approach to localizing the genetic abnormality, because it is inherited in an autosomal dominant pattern, is highly penetrant, does not affect survival, and can be diagnosed in families with readily available measurements. Importantly, several candidate genes have been cloned and mapped. Therefore, we collected blood samples and extracted leukocyte DNA from 94 members of 4 families with well documented FBH (44 affected, 45 unaffected, and 5 unclassifiable). We digested the DNA samples with various restriction endonucleases, conducted standard Southern blotting, and searched for restriction fragment length polymorphisms for the following candidate genes (probe names in parentheses): multiple endocrine neoplasia (MEN) type 1 (pMCMP.1, pHBI59, p3C7, and pTHH26), MEN 2a (MCK2 and cTB14.34), basic fibroblast growth factor (pHFL1-7), (Ca2+,Mg2+)ATPase isoform 4 (hPMCA4), membrane Na/Ca exchanger (cNC28 M-A), PTH (pPTH-LF), and calbindin-D28K (pSKCalb). In addition, we used the anonymous variable number tandem repeat marker pYNH24 to verify pedigree structures by excluding misinheritances. Data were analyzed using the Linkage program. For none of the genes was there significant linkage with the FBH trait; logarithm of odds scores ranged from -1.3 to -26.0 at a recombination fraction of 0.001, and from 0.6 to -5.6 at a recombination fraction of 0.10. We conclude that FBH is unrelated to the MEN syndromes and is not caused by mutations in any of the calcium-regulating or -binding proteins or growth factors studied thus far.
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PMID:Genetic linkage analysis in familial benign hypercalcemia using a candidate gene strategy. I. Studies in four families. 151 76

In the lymphocytes infected in vitro with BLV (bovine leukemia virus) the contents of Ca2+ and Mg2+ were determined using roentgen microanalyser JXA-5 A Joel-form (Japan). In the smears prepared from these cells the activity of enzyme markers of cell membranes i.e. alkaline phosphatase (AP - EC 3.1.3.1), 5'-nucleotidase (5'-NT - EC 3.1.3.5) and adenosine-triphosphatases - Ca2+ and Mg2+ dependent (ATP-ase - EC 3.6.1.3) was determined. The decrease in AP and ATP-assess activity and increase in 5'-NT in the membranes of leukemic lymphocytes were observed. During these changes the increase in Ca2+ and decrease in Mg2+ ions occurred. These processes lead to clear disturbances in the metabolism of cells transformed by the neoplasm. The effect of this phenomenon is probably the opening of calcium canals with the following cytoplasmatic hypercalcemia. It's very destructive for the change in permeability of the membrane of lymphocytes.
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PMID:[The content of Ca2+ and Mg2+ ions and membrane enzyme activity (AP, 5'-NT, ATPases) in the lymphocytes infected in vitro with bovine leukemia virus]. 166 9

The rat Walker carcinosarcoma 256 is an animal model for humoral hypercalcaemia of malignancy (HHM). In this model, the relative contribution of bone and kidney in the hypercalcaemia of tumour-bearing rats was investigated. Daily administration of pamidronate, a bone resorption inhibitor, for 2 days prevented the increased fasting Ca2+ excretion observed in the hypercalcaemic rats, although serum Ca2+ remained high. However, the high serum Ca2+ normalised after the acute injection of ethiofos, an inhibitor of renal Ca2+ reabsorption, which was associated with a marked increase of Ca2+ excretion. Changes in Ca2+ were accompanied by similar changes in Mg2+. The results indicate that altered renal Ca2+ handling has a key role in the hypercalcaemia associated with this HHM model.
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PMID:Relative role of bone and kidney in the hypercalcaemia associated with the rat Walker carcinosarcoma 256. 184 15

The pathogenesis of familial benign hypercalcemia (FBH) is unknown. Possible explanations for the disorder include a set-point error in parathyroid gland regulation and intrinsic renal hyperreabsorption of calcium. Thus, FBH may involve an alteration in cellular calcium transport, especially in renal and parathyroid cells. A primary mediator of cellular calcium transport is (Ca2+,Mg2+)ATPase. Therefore, we examined in detail the kinetics of (Ca2+,Mg2+)ATPase activity in erythrocyte plasma membranes from 11 patients with FBH from 7 families, 5 patients with untreated primary hyperparathyroidism, and equal numbers of age- and sex-matched normal subjects. (Ca2+,Mg2+)ATPase activity was measured in isolated membranes as a function of free calcium (0.05-300 mumol/L) in the presence or absence of calmodulin (600 nmol/L) and as a function of calmodulin (0-1800 nmol/L). We found no significant differences in calcium- or calmodulin-dependent (Ca2+,Mg2+)ATPase kinetics between patients with FBH or primary hyperparathyroidism and their age- and sex-matched normal subjects. None of the kinetic parameters was correlated with serum calcium or serum PTH values. We postulate that a mechanism other than a global defect in (Ca2+,Mg2+)ATPase activity is responsible for the hypercalcemia in patients with FBH.
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PMID:Kinetics of erythrocyte plasma membrane (Ca2+, Mg2+)ATPase in familial benign hypercalcemia. 252 97

A major unanswered question in central nervous system physiology concerns the mechanism by which cerebrospinal fluid (CSF) Ca2+ homeostasis is maintained in the face of hypo- or hypercalcemia. To address this question, we sought and found a protein of Mr approximately 140,000 in choroid plexus plasma membranes that forms a phosphorylated intermediate with characteristics of a plasma membrane Ca2+-pump. A choroid plexus plasma membrane protein of this molecular weight also bound to a monoclonal antibody prepared against the human erythrocyte plasma membrane Ca2+-Mg2+ ATPase Ca2+-pump. When this monoclonal antibody was used for immunohistochemical localization, the plasma membrane Ca2+-pump was found primarily in the CSF-facing membranes of choroid plexus cells from rats, cats, and man. The localization of a plasma membrane Ca2+-pump in the CSF-facing membranes of the choroid plexus suggests that the choroid plexus, by mechanisms including this pump, may regulate CSF Ca2+ concentrations.
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PMID:Cerebrospinal fluid calcium homeostasis: evidence for a plasma membrane Ca2+-pump in mammalian choroid plexus. 252 46

Although relatively common, aberrations in divalent cation homeostasis may be overlooked in Emergency Department patients. The intracellular concentration of ionized calcium is the major regulator of cellular function. Patients may present with signs and symptoms of deranged calcium homeostasis that range from the mild and nonspecific to the truly life threatening. Critically ill patients may develop profound, life-threatening hypocalcemia either as a result of their underlying illness or as a complication of resuscitation. Patients with hypercalcemia may present with symptoms that are so vague and nonspecific that the diagnosis may not be considered. An understanding of the pathophysiology of calcium metabolism allows the emergency physician to identify patients at risk for abnormal calcium homeostasis, and to intervene in an appropriate manner. Magnesium is an essential cofactor in a host of important biochemical reactions. Magnesium deficiency is fairly common in certain groups of patients and can cause serious complications. The diagnosis is often difficult to make in the Emergency Department setting. The emergency physician should be aware of clinical situations that predispose to magnesium deficiency and be prepared to institute empiric therapy if indicated. Severe hypermagnesemia is rather uncommonly encountered in the Emergency Department. The magnesium ion is an effective calcium channel blocker, and patients with severe hypermagnesemia develop profound cardiovascular and neuromuscular dysfunction as a result. In pharmacologic doses, magnesium's unique calcium channel antagonism may be clinically useful, and there is growing interest in its potential use as an antiarrhythmic, anticonvulsant, and smooth muscle relaxant.
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PMID:Disorders of calcium and magnesium metabolism. 268 Apr 66


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