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

The drug therapies for hypercalcemia of malignancy have been known to be associated with either limited efficacy or cumulative toxicity in patients with advanced renal failure. To establish the guidelines for the use of dialysis and to determine its optimal prescription for hypercalcemia, calcium-free hemodialysis was performed in 6 hypercalcemic patients with renal failure not responding enough to forced saline diuresis. Calcium-free dialysate contained sodium 135, potassium 2.5, chloride 108, magnesium 0.75, bicarbonate 30 mmol/l. Mean hemodialysis time was 160 +/- 27 min and mean Kt/V urea was 0.75 +/- 0.2. Plasma calcium concentrations fell from a mean value of 2.92 +/- 0.21 mmol/l (range 2.55-3.25) to 2.58 +/- 0.16 mmol/l at 1 h of hemodialysis and to 2.16 +/- 0.33 mmol/l (range 1.63-2.53) following 2-3 h of hemodialysis. The ionized calcium (n = 4) decreased from 1.44 +/- 0.14 mmol/l to 0.99 +/- 0.2 mmol/l. No patient showed any hypocalcemic symptoms and signs during hemodialysis. The rate of decrease in plasma calcium did not appear to produce adverse effects in any of the patients. There was a significant positive correlation between the decrease in plasma calcium concentration and the Kt/V urea (y = 1.4x - 0.29, r = 0.92, p < 0.01). We conclude that calcium-free hemodialysis is indicated when the presence of severe renal failure prevents the administration of large volumes of intravenous fluids to hypercalcemic patients. The amount of dialysis (Kt/V urea) can be used to predict the decrease in plasma calcium concentration during calcium-free hemodialysis.
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PMID:Calcium-free hemodialysis for the management of hypercalcemia. 885 91

There is an urgent need for drugs capable of inhibiting renal calcifications, nephrocalcinosis and stones included, in humans. Current anticalcification medication is based mainly on alkalinization of the metabolism using potassium-containing citrate alone, despite the fact that calcium stone patients suffer marginally from both magnesium and potassium deficiency. We investigated the anticalcification efficacy of oral potassium citrate versus the combined administration of this drug and magnesium citrate in the magnesium-deficient rat developing corticomedullary nephrocalcinosis and luminal microliths in the long term. Among other things we employed specific stains for calcium and oxalate, light microscopy and element analysis for renal tissue and calcifications, respectively. In addition, minerals in renal tissue, urine and plasma were determined, as well as the state of extracellular calcium homeostasis. Magnesium deficiency caused pure calcium phosphate tissue deposits, containing no magnesium, but no deposition of calcium oxalate in the tubular lumen; tissue magnesium, calcium and phosphorus were increased, and there was marked potassium wastage via urine; despite mild hypercalcemia other signs of hyperparathyroidism were not found. Alkalinization with the two kinds of medication evoked an increase in urinary pH, citrate, and potassium; however, potassium citrate alone tended to aggravate renal concretions, whereas the combination of this drug with magnesium citrate completely prevented concretions. It was concluded that: (1) magnesium deficiency-induced calcifications are oxalate-free and are not sensitive to mobilization by alkalinization with potassium citrate, which might explain the failure of the drug to prevent stone recurrence in clinical stone patients, and (2) the combination of potassium citrate and magnesium citrate, which shows enormous anticalcification efficacy, deserves high priority in clinical trials aimed at evaluating strategies for the prevention of stones.
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PMID:Reappraisal of the quantity and nature of renal calcifications and mineral metabolism in the magnesium-deficient rat. Effects of treatment with potassium citrate or the combination magnesium citrate and potassium citrate. 987 45

Calcium oxalate uroliths are most commonly encountered in Miniature Schnauzers, Lhaso Apsos, Yorkshire Terriers, Bichons Frises, Shih Tzus, and Miniature Poodles. They are more common in males than females, and more common in older than young dogs. Dogs that form abnormal nephrocalcin are also predisposed to calcium oxalate uroliths. Dietary risk factors for calcium oxalate uroliths include excessive calcium supplementation or excessive calcium restriction, excessive oxalic acid, high protein, high sodium, restricted phosphorus, restricted potassium, and restricted moisture (dry formulations). Dogs with hyperadrenocorticism or hypercalcemia are predisposed to calcium oxalate urolith formation.
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PMID:Epidemiology of canine calcium oxalate uroliths. Identifying risk factors. 1002 54

The case study presented here illustrates the diagnosis and management of calcium oxalate urolithiasis in a Bichon Frise, a breed at increased risk for this type of stone. If the Bichon Frise had persistent hypercalcemia, we would have evaluated serum concentrations of ionized calcium, parathyroid hormone, and vitamin D to identify an underlying cause. Because his urine was alkaline, additional potassium citrate was not provided. Likewise, as a fortified diet was fed to him, vitamin B6 therapy was not considered. This case study illustrates the benefits of radiographic evaluation immediately following surgery and during follow-up examinations. If we had postponed radiographs until the patient developed clinical signs, additional surgical procedures may have been required.
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PMID:Canine calcium oxalate urolithiasis. Case-based applications of therapeutic principles. 1002 55

Polydextrose (CAS no. 68424-04-4) is a water-soluble polymer of glucose that provides to foods the bulk and texture of sucrose. There are two main forms of polydextrose, an acidic form (PD-A) and a neutralized potassium salt (PD-N). Polydextrose is resistant to mammalian metabolic and microbial degeneration, rendering it both low in caloric value and non-cariogenic. Little polydextrose is absorbed intact although some is metabolized by caecal/colonic bacteria. At high enough levels of ingestion, this bacterial metabolism results in flatus, bloating, loose stools and ultimately a frank diarrhoea. Microbial metabolism also produces some volatile fatty acids that are absorbed by the animal and have calorigenic value. The species and dose threshold for persistent loose stools/watery diarrhoea determines the degree of electrolyte loss by the animal. In the dog, an obligate carnivore, sodium-sparing activity by the kidney and concomitant and obligatory calcium reuptake result in a well-defined aetiology of hypercalcaemia and subsequent nephrocalcinosis, particularly for PD-N. Of the species tested, the dog was the most sensitive to this carbohydrate with a no-effect level of 2000 mg/kg body weight/day. Omnivores, including the rat, mouse and monkey, have a no-effect level ranging from 2500 to 10,000 mg/kg body weight/day. No toxicity has been demonstrated in man, although the dose for laxation (to be distinguished from diarrhoea) is approximately 90 g/day (v. sorbitol at 70 g/day). Polydextrose did not show any reproductive toxicity, teratology, carcinogenesis, mutagenicity or genotoxicity. Polydextrose has been approved for food additive use (21 CFR 172.841) in the US, and an "ADI not specified" by the Joint WHO/FAO Expert Committee on Food Additives (JECFA, 1987). It has been approved in over 50 countries around the world and has been used extensively in the diet for over15 years. Specification monographs are published in the Food Chemicals Codex (FCC) (NAS, 1996) and the FAO Compendium (JECFA, 1995). This review provides an overview of the studies and salient data, not previously reported in the scientific literature, which had been submitted to regulatory agencies in support of these approvals.
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PMID:A review of the studies of the safety of polydextrose in food. 1022 45

The purpose of this present study was to assess the prevalence of hypermagnesaemia in a hospital population. Furthermore, the relationship between hypermagnesaemia and other common electrolyte disturbances such as hypo- and hypercalcaemia, hypo- and hyperkalaemia and hypo- and hyperphosphataemia was studied. Twenty-seven percent of magnesium requests showed a serum magnesium concentration equal to, or greater than, 1.0 mmol/l. Hyperkalaemia (a plasma potassium concentration of equal to, or greater than, 5.0 mmol/l) was found in 18% of the patients with hypermagnesaemia and 25 % of these patients showed hyperphosphataemia (a plasma phosphate concentration of equal to, or greater than, 1.5 mmol/l). Of the serum magnesium requests, hypermagnesaemia was particularly common on the intensive care (23%) and the renal unit (43%). Hypermagnesaemia was also seen in patients undergoing cardiothoracic surgery (17 %) and who had an acute myocardial infarction (8 %). Seventy-three percent of patients with a plasma magnesium of greater than 1.0 mmol/l showed abnormal renal function. However, it was rare to find a serum magnesium of greater than 2.0 mmol/l (less than 1% of magnesium requests).
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PMID:A study of hypermagnesaemia in a hospital population. 1036 17

Increased QT dispersion (QT(d)) has been associated with increased risk for ventricular arrhythmias. Pathologic extracellular electrolyte concentrations may result in ventricular arrhythmias. The aim of this study was to evaluate the effect of electrolyte abnormalities on QT(d). Ten consecutive patients with isolated electrolyte abnormalities were selected for each of the following groups: hypokalemia, hyperkalemia, hypercalcemia, hypocalcemia, hypomagnesemia, and normal controls. Standard 12-lead electrocardiography was performed for each patient and average QT, JT, and RR intervals were calculated for each lead. Dispersion of QT, JT (JT(d)), and QTc (QTc(d)) intervals were calculated as the range between the longest and shortest measurements. Compared with controls, only patients with hypokalemia had a greater QT(d) (115 +/- 31 vs. 49 +/- 15 ms), JT(d) (116 +/- 34 vs. 52 +/- 12 ms), and QTc(d) (141 +/- 40 vs. 58 +/- 1 ms), (P < 0.05). In an experimental substudy, seven rats were maintained on K(+) and seven on Mg(2+)-free diet followed by normal diet. Experimental hypokalemia significantly increased QT(d) (10 +/- 4 to 37 +/- 7 ms), and QTc(d) (32 +/- 6 to 79 +/- 27 ms) (P < 0.05), whereas hypomagnesemia did not. Restoration of serum potassium resulted in normalization of dispersion (QT(d), 14 +/- 2; QTc(d), 34 +/- 6 ms). Hypokalemia increases the dispersion of ventricular repolarization that may be responsible for arrhythmias. Even though hyperkalemia, hypocalcemia, and hypercalcemia are known to affect ventricular repolarization, our study shows that they are not associated with increased dispersion.
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PMID:Influence of electrolyte abnormalities on interlead variability of ventricular repolarization times in 12-lead electrocardiography. 1130 65

A 43-year-old man with refractory myeloma underwent allogeneic bone marrow transplantation from his HLA-matched sibling. He was conditioned with TBI (12 Gy) followed by melphalan (140 mg/m(2) ). Immediately after conditioning was initiated, he began complaining of severe lumbago, and the level of serum calcium rose from 2.25 to 3.34 mmol / l. However, the biochemical markers for tumor-lysis syndrome such as potassium, uric acid, and lactic dehydrogenase remained unchanged. Hydration with saline and pamidronate were started, but he developed acute renal failure requiring hemodialysis for 3 weeks. His plasma parathyroid hormonerelated protein (PTHrP)-NH2-terminal (3.9 pmol/l) and serum PTHrP-C-terminal (125.0 pmol / l) levels markedly increased immediately after conditioning. These results suggested that the increased release of PTHrP from myeloma cells, which resulted from destruction of myeloma cells by conditioning, was the primary contributes to the occurrence of hypercalcemia. We should be aware of the occurrence of hypercalcemia when high-dose therapy is to be given to patients with refractory myeloma.
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PMID:Hypercalcemia after High-Dose Chemoradiotherapy for Refractory Multiple Myeloma; Subject Heading. 1139 24

The authors investigated the effect of long-term lithium administration on intracellular calcium mobilization. The subjects were 13 women with bipolar affective disorder stabilized on lithium and 12 matched healthy controls. Total and ionized serum calcium, intracellular calcium ion concentration, plasma parathyroid hormone (PTH) and tyrotropin (TSH), serum electrolytes and cyclic AMP (cAMP) activity in platelets were measured. The serum electrolytes sodium, potassium and creatinine and plasma PTH and TSH were all within normal ranges in patients and controls and no differences were found between the two groups. No difference was found in basal and prostaglandin E1 (PGE1)-stimulated cAMP generation in platelets between patients and controls. However, total serum calcium and ionized serum calcium levels were higher in patients than in controls and there was a significant correlation between these two measures. In the patient group, serum lithium concentration correlated positively with stimulated levels of intracellular calcium in platelets. In the present study, no distinct hyperparathyroidism was found in lithium-treated patients. However, our findings indicate that lithium administration affects calcium metabolism in patients with bipolar affective disorder inducing mild hypercalcemia and a dose-dependent normalized calcium mobilization. Furthermore, our results did not support the hypothesis that lithium's primary site of action in bipolar illness may be on signal transduction mechanisms.
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PMID:Calcium homeostasis in long-term lithium-treated women with bipolar affective disorder. 1245 27

Even small losses of gastrointestinal secretions when combined with reduced intake of electrolytes may seriously disturb electrolyte balance. Knowledge of the ionic composition of secretions lost is essential in planning therapy. Loss of gastric contents usually results in excessive loss of chloride; in achlorhydria this is not the case. Loss of sodium and potassium may be large in either case and is often underestimated. Small bowel obstruction results in a more balanced loss of electrolyte which may not affect acidbase balance greatly. In diarrhea loss of base predominates, and may result in a large potassium deficit. Steatorrhea due to nontropical sprue results in large fecal losses of sodium, potassium and chloride, in addition to the large calcium and phosphorus loss. In chronic peptic ulcer excessive ingestion of milk and absorbable alkalies may result in hypercalcemia, azotemia and alkalosis, without hypercalciuria. Since renal function is usually adequate in the milder gastrointestinal disturbances, electrolyte and fluid replacement should be started early, and can be guided by generally available laboratory tests, the carbon dioxide combining power and serum chloride levels, provided the predominate ionic loss is known and potassium deficiency remedied. If this is done, development of serious fluid and electrolyte deficits can usually be prevented.
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PMID:Electrolyte balance in gastrointestinal disease. 1326 Sep 27


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