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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 calcium-gluconate infusions on renal function were studied in unanesthetised dogs. Each dog was studied during hydropenia and saline infusion. Hypercalcemia, mean serum calcium 3.85 mmol/l (hydropenia) and 3.62 mmol/l (saline infusion), increased fractional excretion of sodium (CNa/CIn), calcium (CCa/CIn), and magnesium (CMg/CIn). The increase was significantly higher in saline-expanded dogs than in hydropenic dogs. Fractional excretion of potassium (CK/CIn) was increased in hydropenia but remained unchanged in saline-expanded animals. Fractional excretion of phosphate (Cp/CIn) was not consistently changed by hypercalcemia. Fractional excretion of chloride (CCl/CIn) was markedly increased in saline-expanded dogs but was not changed in hydropenia. Urine osmolality was reduced in hydropenic dogs but unchanged in saline-expanded dogs. In hydropenic as well as in saline-expanded dogs tubular reabsorption of solute-free water (TcH2O/CIn) increased during the first hour of hypercalcemia. In hydropenic dogs hypercalcemia caused a slight but significant decrease in blood pH, standard bicarbonate, and base excess. In hydropenic as well as in saline-expanded dogs glomerular filtration rate (CIn), renal plasma flow (CPAH), and filtration fraction were unaffected.
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PMID:Renal function in hypercalcemic dogs during hydropenia and during saline infusion. 4 8

In 36 patients with neoplastic diseases 72 episodes of hypercalcaemia with serum-calcium levels greater than or equal to 2.75 mmol/l were treated (19 breast carcinoma; 9 bronchial or lung carcinoma; 5 multiple myeloma; 1 each jejunal carcinoid, malignant lymphoma, phaeochromocytoma). Cardinal symptoms were mental, neuromuscular and renal during the hypercalcaemic episodes. Mithramycin is preferred to other methods (infusion of sodium chloride and frusemide, prednisone, sodium-potassium-phosphate infusion) of treating acute or subacute hypercalcaemia. Mithramycin in a single injection of 20-25 microgram/kg body-weight intravenously is usually sufficient to counteract a hypercalcaemic phase for at least 7-10 days, often much longer. There was a highly significant fall in serum-calcium levels from two days onwards after mithramycin injection. Toxic side-effects were minimal and restricted to transitory increase in transaminase levels, initially 5-6 times normal with a maximum on the third day and normalisation on the fifth day after mithramycin administration.
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PMID:[Treatment of hypercalcaemic syndrome in tumour patients, especially with mithramycin]. 14 99

Following an intravenous loading injection of 75 U.S.P. Units of Para-Thor-Mone (Eli Lilly and Co), seven conscious, non-pregnant, non-lactating Merino ewes were infused with a maintenance dose of the hormone at a rate of 4-75 U.S.P. units/min for 2 hr. The classical hypercalcaemia and hypophosphataemia of the non-ruminant was observed, but the hypercalcaemi- was only small. Plasma potassium concentration decreases, while there were no changes in plasma sodium, chloride or mangesium. The classical phosphaturic effect of the hormone was not observed, only trace amounts of phosphate being exreted throughout the experiment. Urinary excretion of calcium and magnesium decreased, urine flow and urinary excretion of sodium, potassium, chloride, bicarbonate and urine pH increased. Glomerular filtration rate was unaffected, but renal plasma flow increased. The concentration and secretion rate of salivary phosphate increased markedly. Changes in the other important salivary electrolytes (sodium, potassium, chloride, bicarbonate and hydrogen ion) also occurred, but it was difficult to separate primary from secondary effects of the hormone. Saliva flow rate increased transiently following hormone injection, but the effect was not sustained by the maintenance infusion.
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PMID:The acute effects of intravenous infusion of parathyroid hormone on urine, plasma and saliva in the sheep. 23 58

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

In intact eels in sea water (SW), ovine prolactin (PRL) treatment induces hypercalcemia, but its mechanism of action, which is discussed, remains to be defined. Corpuscles of Stannius (CSt) are modified simultaneously: two cell categories then become evident. The first cell type (type 1) predominates; it has an oval shape and large granules, it shows a nuclear and nucleolar hypertrophy and a mitotic activity, and appears greatly stimulated by PRL; it may elaborate a hypocalcemic factor (hypocalcin) which would compensate for the PRL-induced hypercalcemia. A similar effect, although slightly less intense, is detected in hypophysectomized-PRL treated eels in SW. A second cell type (type 2), is more elongated, smaller in size, and has an oval nucleus and fine granules. Scarcely less active in SW, it is significantly stimulated by PRL despite an increased blood sodium and potassium level. This experiment does not help to clarify its function.
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PMID:Prolactin, hypercalcemia and corpuscles of Stannius in seawater eels. 62 14

In two patients with extensive pulmonary tuberculosis who developed hypercalcaemia and hypokalaemia the hypercalcaemia appeared related to the use of small doses of vitamin D, which suggested patients with tuberculosis were hypersensitive to vitamin D. They were thus similar to patients with sarcoidosis, and it is interesting that the Kveim test result was positive in both cases. The hypercalcaemia was quickly suppressed with steroids. Hyperparathyroidism, thyrotoxicosis, Addison's disease, and multiple myeloma were excluded on clinical grounds and by the appropriate tests. The hypokalaemia was associated with increased renal excretion of potassium, and was probably due to distal tubular damage from hypercalcaemia.
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PMID:Hypercalcaemia and hypokalaemia in tuberculosis. 69 98

Hypokalemia is a potentially life-threatening biochemical abnormality in patients with hypercalcemia. We studied a large group of patients with hypercalcemia to determine the prevalence of hypokalemia. One hundred three patients with normal renal function and no history of taking potassium-depleting drugs comprise the substance of this study. Thirty three of 103 patients (32%) were hypokalemic. A higher prevalence (52.3%) was found in patients with hypercalcemia associated with malignant disease than in those with primary hyperparathyroidism (16.9%). In addition, the degree and frequency of hypokalemia were greatest at the higher serum calcium levels. The presence of hypokalemia must be considered when treating severe hypercalcemia; otherwise, vigorous use of diuretics may result in profound hypokalemia and tachyrhythmias.
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PMID:Hypokalemia with hypercalcemia. Prevalence and significance in treatment. 92 Oct 86

Parathyroid hormone (PTH) was given intravenously to anesthesized adult dogs. Blood flows were measured with electromagnetic probes in different vascular areas concomitant with analysis of glycerol, free fatty acid, calcium, glucose, sodium, potassium, albumin, carbon-dioxid and creatinine. PTH consistently caused an immediate increment in blood flow in the celiac vasculature and a following, less pronounced increase in the renal artery. These changes were effectuated by a vasodilatation. The degree and duration of the flow increments were dose dependent; The celiac artery was more sensitive to the effect of PTH than the renal artery. In celiac artery maximal increase above basal flow was 58 +/- 27% (Mean +/- S.D.), in renal artery 25 +/- 12%. A significant lipolytic action of PTH was consistently notable within minutes after the administration of PTH. The other parameters analysed in blood remained unchanged sixty to ninety minutes after the PTH injections. Then a hypercalcemic effect of PTH appeared. A lipolytic action of PTH could be demonstrated with PTH doses which did not induce hypercalcemia.
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PMID:Circulatory and lipolytic effects of parathyroid hormone. An experimental study in dogs. 92 52

Electrolyte-induced situations which are dangerous to life usually result from disturbances of the extracellular volume (ECV), osmolarity, the potassium level or the acid-base equilibrium. In recent years (thanks to the wide spread use of hormone therapy for mammary carcinoma) severe hypercalcemia has increased in importance as a life-threatening complication, while hypocalcemia, at least in adults, should only very seldom lead to unexpected emergencies. As long as serious clinical symptoms do not suggest an emergency, assessment of the threat to the patient as a result of the existing electrolyte disturbance often causes some difficulty. Besides the extent of the deviation from normal, the rate of development of the disturbance determines the resulting danger: chronic hypo-osmolarity, and especially hyperosmolarity are occasionally tolerated without symptoms while acute disturbances of the same or a less extent lead to severe central nervous symptoms. A similar state of affairs is also true of the emergency situations arising from disturbances of the acid-base equilibrium, among which the respiratory disorders are particularly important clinically. In the case of threatening disorders of the potassium metabolism, the accompanying circumstances (digitalis, simultaneous disorders and treatment of the acid-base equilibrium) often determine the clinical significance and danger to the patient. Clinical symptoms, anticipation ("expecting the unexpected"), prevention and treatment of emergency situations of fluid volume, osmolarity, potassium and acid-base equilibrium are the subjects of this paper.
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PMID:[Emergency stiuations connected with electrolyte disorders. Special aspects]. 99 9

1. Hypo- and hypercalcemia can be explained as derangements of the calcium homeostasis. Hypocalcemic tetany usually alarming the patient tremendously is, at least in adults, rarely life-threatening. Hypercalcemia leads in 30% of the cases to clinical symptoms which may inadvertedly pass into a state of hypercalcemic crisis. This latter requires an often difficult emergency treatment. 2. Hypocalcemic tetany may be reversed by administering calcium i.v. or, in severe cases, by a calcium infusion. Only rarely are magnesium supplements necessary to let the tetany disappear. Vitamin D or dihydrotachysterol (DHT) do not correct hypocalcemia immediately, since their effects may be delayed up to 15-25 days. In order to normalize the serum calcium permanently, vitamin D or DHT treatment should be instituted as rarely as possible. 3. Initially, hypercalcemic crisis is best treated by forced intravenous fluid administration with normal saline (and furosemide) in combination with high doses of prednisone. Fluid-, sodium- and potassium balances ought to be checked during this type of treatment. A first evaluation of the effectiveness of these measures is recommended after 24 hours: treatment is continued in patients who respond favorably, while subjects who do not show a significant decrease of the serum calcium may either be given a phosphate infusion or mithramycine as a bolus. Calcitonin appears to be useful only to start treatment before institution of a phosphate infusion.
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PMID:[Hypo and hypercalcemia as an emergency]. 110 94


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