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

The effect of hypomagnesemia on renal concentrating ability was assessed in rats fed diets either low in magnesium or low in magnesium and calcium for 30 days. The rats fed a low-magnesium diet became hypomagnesemic (0.26 +/- 0.03 versus 1.53 +/- 0.04 mEq/L in controls), hypercalcemic (5.96 +/- 0.04 versus 5.22 +/- 0.11 mEq/L in controls), and hypokalemic (3.1 +/- 0.1 versus 4.2 +/- 0.4 mEq/L in controls) with decreased muscle content of potassium. Despite being hypomagnesemic, hypercalcemic, and potassium depleted, the rats had normal renal concentration ability (2499 +/- 65 versus 2415 +/- 119 mOsm/kg H2O in control). Those rats fed a diet low in both magnesium and calcium became hypomagnesemic (0.41 +/- 0.08 versus 1.53 +/- 0.04 mEq/L in controls) but were hypocalcemic. They also had normal renal concentrating ability (2399 +/- 109 versus 2415 +/- 119 mOsm/kg H2O in controls). It is concluded that hypomagnesemia does not decrease renal concentrating ability in rats. Furthermore, a normal concentrating ability demonstrated in hypomagnesemic rats, in spite of hypercalcemia and potassium depletion suggests that hypomagnesemia may ameliorate the deleterious effects of hypercalcemia and/or potassium depletion on renal concentrating ability.
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PMID:The effect of hypomagnesemia with or without associated hypercalcemia on renal concentrating ability in rats. 665 59

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

To investigate the effect of nifedipine on hypercalcemic electrocardiographical alterations, steadily increasing hypercalcemia was induced in guinea-pigs by continuous calcium gluconate infusion until cardiac arrest occurred. During the experimental time the electrocardiograms were continuously recorded and compared in animals with and without pretreatment by nifedipine (Adalat). The hypercalcemia-induced electrocardiographical alterations intensified during increasing serum calcium levels. Ascending serum potassium and magnesium levels indicated increasing cell damage with a leak of these mainly intracellular ions. Pretreatment by nifedipine did not significantly influence the hypercalcemia-induced bradycardia and augmentation of the P-Q interval except a small and transient effect during relatively low calcium levels. The drug, however, exerted a distinct normalizing effect on hypercalcemic reduction of the S-T segment and the Q-T interval despite of an unaltered development of hypercalcemia. Accordingly, the cellular potassium and magnesium leaks were markedly reduced and the survival time during calcium infusion was significantly prolonged after nifedipine pretreatment. These electrophysiological data are in agreement with our previous cytochemical studies, which showed a protective effect of nifedipine against hypercalcemia-induced overloading of the cellular calcium depots in myocardial cells. Whether this cardio-protective effect of nifedipine during hypercalcemia can be used therapeutically in hypercalcemic crisis, has to be examined in clinical studies.
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PMID:Electrocardiographic evidence for a cardioprotective effect of nifedipine during experimental hypercalcemia. 707 50

To evaluate the efficacy and safety of a simple approach to intravenous (IV) phosphorus therapy, ten adult patients with severe hypophosphatemia (less than or equal to 1 mg/dL) and normal renal function were studied prospectively. They were treated with a solution containing 9 mmole of phosphorus as monobasic potassium phosphate (KH2PO4), infused continuously every 12 hours. Serum phosphorus, potassium, and calcium levels and urinary excretion of phosphorus were measured every 12 hours. The serum phosphorus level was significantly improved at 12 hours, more than 1 mg/dL in all patients at 36 hours, and normal in six patients at 48 hours. The serum potassium level was never above normal, and serum calcium levels declined in only one patient. Administration of 9 mmole of phosphorus as KH2PO4 every 12 hours is both safe and efficacious IV therapy for severe hypophosphatemia in the adult patient with normal renal function and without hyperkalemia or hypercalcemia.
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PMID:Efficacy of intravenous phosphorus therapy in the severely hypophosphatemic patient. 723 7

The effects of treatment with bendroflumethiazide (2.5 mg twice daily with potassium supplements) on mineral metabolism were evaluated in 111 patients followed for a minimum period of one year. The urinary calcium decreased with approximately 30% irrespective of the pretreatment levels and remained on this lower level during follow-up. This reduction of urinary calcium was associated with a reduction of the intestinal calcium absorption. The serum calcium increased slightly in most of the patients and in 10% of them hypercalcaemia could be demonstrated at some time. In most of these cases the hypercalcaemia was slight and temporary and when sustained rapidly reversed upon withdrawal of therapy. Initially the urinary magnesium excretion increased but after two years' treatment the values were no longer raised. The serum magnesium levels showed a continued decrease during follow-up but in muscle biopsies, performed after three years treatment, no magnesium deficiency was evident. During treatment also the fasting urinary calcium was reduced, suggesting reduced bone resorption, but urinary hydroxyproline was unchanged. The serum PTH levels appeared unchanged during follow-up. Thiazides appear to cause a persisting reduction of calcium excretion, which is compensated by reduced intestinal uptake, whereas parathyroid function is unaffected. Although there was a gradual decline of serum magnesium, magnesium deficiency was not demonstrated.
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PMID:Calcium and magnesium metabolism during long-term treatment with thiazides. 732 48

Thirty patients with drug associated acute nontraumatic rhabdomyolysis were evaluated. Acute renal failure, oliguric (ORF) in ten and nonoliguric (NORF) in another ten patients, was observed. The remaining ten patients did not develop renal failure (NRF). To identify factors that may have contributed to this clinical diversity, these three groups were compared. Data from 51 patients reported in the literature were also included in the analysis. The patients with ORF were slightly younger than patients with NORF. They had higher incidence of muscle swelling and higher serum potassium. ORF was more severe, lasted longer, and required more dialysis than NORF. The group of patients with renal failure had higher incidence of coma and more patients with very high muscle enzyme elevation than NRF patients. Hypercalcemia, a unique complication of rhabdomyolysis, was reported in 22 patients. It was not seen in patients without renal failure. There were no differences in age, incidence of coma, muscle swelling, and muscle enzyme between those who did and those who did not develop hypercalcemia. Sixteen patients with nerve entrapment had higher incidence of coma and muscle swelling than the rest of the patients.
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PMID:Acute drug-associated rhabdomyolysis: an examination of its diverse renal manifestations and complications. 743 19

Hyperphosphataemia plays a key role in the pathogenesis of renal osteodystrophy, and phosphate-binding agents are required in many chronic dialysis patients. Aluminium hydroxide and calcium carbonate are well-established phosphate binders, but their use is associated with toxicity or poor efficacy. Calcium acetate is known to be a potent phosphate binder, and has recently been used successfully in chronic dialysis patients. In this randomized cross-over trial in 31 chronic haemodialysis patients, equimolar doses of calcium acetate and calcium carbonate were administered for 6 weeks each. Compliance was estimated from tablet counts, and biochemical parameters were measured at the end of each treatment period. Of the 31 patients 23 completed both treatment arms; of the remainder, three withdrew due to adverse symptoms, hypercalcaemia necessitated treatment withdrawal in two, and three died. Non-compliance was significantly higher with acetate (18.3% tablets not taken) than with carbonate (8.7%). Serum phosphate was significantly lower after treatment with acetate (1.51 mmol/l) than with carbonate (1.80), as was the Ca x PO4 product (3.59 vs 4.18 respectively) and PTH (17.8 vs 25.4 pmol/l respectively). Serum calcium was significantly higher after acetate therapy (2.40 vs 2.32 mmol/l). No significant difference was found for sodium, potassium, bicarbonate, urea, creatinine, and haemoglobin. This study confirms that the treatment of hyperphosphataemia is more effective with calcium acetate than with calcium carbonate. For the first time an associated beneficial effect on secondary hyperparathyroidism has also been demonstrated. Patient tolerability of calcium acetate was considerably poorer, probably due in part to tablet formulation and bulkiness, as well as possible direct gastrointestinal effects of the acetate salt.
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PMID:Calcium acetate versus calcium carbonate as phosphate-binding agents in chronic haemodialysis. 780 Feb 11

The association of hypercalcemia and acute pancreatitis had been experimentally reproduced in cats by local infusions of the divalent cation calcium whereas the monovalent cation potassium did not induce any pancreatic pathology. The purpose of the present study was therefore to investigate the role of further divalent cations in order to determine the relevance of ion valency for pancreatitis induction. Anesthetized male SIV-rats received divalent cations, of which a role in the pancreas had already been reported in the literature, through retrograde infusions into the splenic artery at a dose of 0.6 mmol/kgh for 3 hours and at a flow of 0.5-1.0 ml/h. The pancreas was then removed for morphologic studies. In the animals treated with calcium and manganese, pancreas showed a hemorrhagic necrosis of the acinar lobuli with leucocytic infiltrates. The barium treated animals spontaneously died after 49 +/- 15 minutes and revealed acute pancreatitis in the perfused, but not in the residual pancreas. Zinc at the initial dose induced an immediate heparin-refractory blood-clotting with subsequent ischemic necrosis whereas a lower dosis (0.002 mmol/kgh) led to an acute pancreatitis as seen after calcium. The magnesium treated animals and the controls did not reveal any pathology. We conclude that some divalent cations may induce an acute pancreatitis, but that the induction is not dependent on the cation valency.
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PMID:[Acute pancreatitis after local infusion of divalent cations]. 837 61

Interleukin-1 (IL-1) is a monokine that exerts multiple biological activity, including immunity and inflammation. Moreover, IL-1 is involved in Ca2+ release causing hypercalcemia and bone resorption. Recently, a 22 kDa natural inhibitor to IL-1 called interleukin-1 receptor antagonist (IL-1ra) has been described in human fluids, which specifically binds IL-1 alpha or IL-1 beta receptors. In this study, we found that experimental granuloma induced by subcutaneous injections (0.2 ml) of potassium permanganate (KMnO4) 1:40 saturated crystal solution, after 7 days was strongly inhibited in size, weight and calcium content (measured as dry ash weight by incineration of granuloma tissue) compared with untreated controls, in mice treated intraperitoneally with IL-1ra (20 micrograms/bolus) given twice; the first at the same time of the induction of the granuloma and the second 24 hours later. In addition, leukotriene B4 and prostaglandin E2 were also inhibited in fresh granuloma of mice treated with IL-1ra. Taken together, these findings conclude for the first time, that the accumulation of calcium in chronic inflammatory states is strongly inhibited by IL-1ra, which decreases tissue calcergy and can potentially be useful for the treatment of calcium-related inflammatory diseases and malignancy-associated hypercalcemia.
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PMID:Interleukin-1 receptor antagonist inhibits calcium accumulation in in vivo chronic granuloma induced by potassium permanganate. 838 44

A 5-month-old sexually intact male Chesapeake Bay Retriever was evaluated for lameness of 2 weeks' duration and lymphocytosis. Acute lymphoblastic leukemia was diagnosed on the basis of results of cytologic and cytochemical evaluation of a bone marrow aspirate. Serum biochemical abnormalities included hypercalcemia and hyperkalemia. Hypercalcemia was likely paraneoplastic; hyperkalemia was believed to be a result of release of potassium from large numbers of lymphocytes in vitro (pseudohyperkalemia). The dog was euthanatized, and necropsy revealed infiltration of the hepatic vasculature and sinusoids, renal parenchyma, mesenteric and peripheral lymph nodes, bone marrow, and iridial tissue with neoplastic cells. Unique features of this case include the young age of the dog and the hypercalcemia and hyperkalemia associated with acute lymphoblastic anemia.
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PMID:Acute lymphoblastic leukemia, hypercalcemia, and pseudohyperkalemia in a dog. 856 80


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