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

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.
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PMID:Mechanism of lithium-induced hypercalciuria in rats. 62 44

Hypercalcemia causes lethargy and coma in patients with head and neck cancer. It is important to realize that coma may be due to hypercalcemia and need not be a terminal event in the progress of the tumor. Also, the development of hypercalcemia in a previously normocalcemic patient requires investigation as to the cause of the hypercalcemia. I report two cases of comatose patients, hypercalcemic from bony metastases from tongue cancer, in whom treatment by furosemide and intravenous fluid diuresis, prednisone, sodium phosphate, and mithramycin produced worthwhile remissions. Hypercalcemia may be due to (1) bony metastases, (2) pseudohyperparathyroidism, (3) unrelated associated parathyroid tumors, or (4) a second primary tumor. Even with treatment, hypercalcemia is a bad prognostic sign in patients with head and neck cancer.
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PMID:Hypercalcemia and head and neck cancer. Bony metastases from tongue cancer. 69 40

Patients with asymptomatic or smoldering multiple myeloma should not be treated but should be observed closely for progression. For symptomatic myeloma, chemotherapy is indicated. Melphalan, the agent of choice, should be given with prednisone for 1 week of every 6 weeks, If melphalan brings no response, or response and then relapse, cyclophosphamide (Cytoxan) should be give intravenously every 4 weeks or orally every day. BCNU, CCNU, and doxorubicin (Adriamycin) have also shown activity in myeloma. Hypercalcemia occurs in one-third of patients and should be countered with hydration, corticosteroids, Neutra-Phos, or mithramycin. Long-term hemodialysis has achieved some success. The combination of sodium flouride and calcium carbonate produces new bone formation; it seems a useful adjunct in treatment for myelomatous bone disease. Radiation should be utilized only for severe, localized pain or for solitary lesions. Survival with multiple myeloma varies, mean durations being 2 to 3 years. Multivariate analysis indicates that serum creatinine and calcium levels are the most significant indicators regarding 2-year survival. We have found monoclonal proteinuria not significantly more frequent with renal insufficiency than with normal renal function, renal insufficiency not significantly more frequent with lambda than with kappa chains, and survival not significantly greater with IgG myeloma than with IgA.
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PMID:Management and prognosis of multiple myeloma. 79 81

Four patients having high-level quadriplegia developed elevated serum calcium concentrations (11 to 15.8 mg/100 ml) within three months of injury. All were young males (ages 15 to 19 years) and quadriplegic (C4-C7). Presenting symptoms were nausea, vomiting, polydipsia, polyuria and lethargy. In two patients severe muscle wasting and cachexia with clinical symptoms developed and persisted for several months. Laboratory studies in all patients showed negative calcium balance with hypercalciuria. Reduced renal function was seen in all patients but returned to normal with return of normal serum calcium. Alkaline phosphatase level was normal in three and elevated in one. Serum parathormone levels were normal. Roentgenograms revealed diffuse demineralization. Nephrocalcinosis and soft tissue calcifications developed in one patient. Primary treatment included reduced calcium intake, correction of dehydration, sodium infusion and remobilization. Corticosteroids, oral phosphates, furosemide and mithramycin were used with varying success to control prologned symptoms and severe hypercalcemia.
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PMID:Immobilization hypercalcemia in spinal cord injury. 83 59

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

The effects of acute hypercalcemia on hemodynamics and on water and sodium excretion were studied on the blood-perfused isolated dog kidney. This model advantageously eliminates various factors which modify medullary osmolality and intrarenal hemodynamics, as well as collecting duct permeability. Calcium ion directly inhibits sodium reabsorption in the proximal tubule and in the ascending limb of Henle's loop, leading to increased sodium excretion rate and to decreased free water generation. The vasoconstrictive action of calcium, leading to decreased glomerular filtration rate, may mitigate the strong natriuretic effect of this ion.
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PMID:Effects of hypercalcemia on water and sodium excretion by the isolated dog kidney. 94 13

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

Rats fed abnormally composed isocaloric diets during 21 days (low magnesium, atherogenous, high in proteins or carbohydrates) develop a mean increase in total number of pancreatic A cells, a significant increase of A/B ratio (atherogenous), and hyperglucagonemia in most of the groups under study. Histologic examination reveals calcification most marked in animals under low magnesium and atherogenous diets. They are only scarce following high protein diet; a normal or carbohydrate rich diet nullifies this phenomenon. Independent of the morphologic and functional state of the islets, supplementation by argining and histidine of normal chow is followed by a certain degree of renal calcification. Lowered urinary magnesium and calcium and elevated urinary sodium and phosphate together with a tendency toward hypercalcemia point to stimulation of parathyroids during malnutrition. Absolute or relative hyperglucagonemia must be considered the main causstive factor.
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PMID:[Pancreatic islets, plasma glucagon and renal calcification in rats fed various diets. Results of a pilot study (author's transl)]. 110 41

A 52 year old man with a long history of marked hypertension, peptic ulcer disease, nephrocalcinosis and intermittent hypercalcemia was referred to be evaluated for primary aldosteronism suspected on the basis of low plasma renin activity, hypokalemia and blood pressure responsive to spironolactone. Aldosterone excretion, however, was extremely low. Alkaluria, high urinary sodium excretion and hypercalciuria were observed. The patient admitted to chronic ingestion of large amounts of baking soda. Upon cessation of alkali abuse, his blood pressure fell dramatically; orthostatic hypotension, concomitant azotemia, hemoconcentration, hyperkalemia and weight loss occurred. Despite dramatic elevation in plasma renin activity, urinary aldosterone excretion remained low during this period. Adrenal glucocorticoid secretion was intact. All abnormalities of sodium, potassium and aldosterone subsequently returned to normal. A 10 day challenge with oral sodium bicarbonate was associated with a rise in blood pressure, but serum calcium remained normal. The patient remains normotensive 15 months after discontinuing alkali abuse.
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PMID:Hypertension corrected by discontinuing chronic sodium bicarbonate ingestion. Subsequent transient hypoaldosteronism. 111 72

The development of nephrocalcinosis in the rat following intraperitoneal injections of various concentrations of neutral sodium phosphate (pH 7-4) was studied using histology, histochemistry, electron microscopy and quantitative techniques. Daily injections of 0-5 M phosphate consistently produced nephrocalcinosis after 6 days or more. Calcium deposits were at first confined to the basement membranes of proximal tubules; but a longer course of injections, up to 10 days, resulted in additional basement membrane calcification in the outer cortes, and outer medulla, together with intra-luminal casts, often calcified, in the outer medulla and papilla. Calcification was not found in other organs such as liver, lung, heart or aorta. Results from quantitative estimations of total kidney calcium and phosphorus suggested that it was the calcium content which was important to the initiation of nephrocalcinosis. Ultrastructural changes, suggestive of degeneration or alteration in function, were found in mitochondria of proximal tubules in experimental animals before the onset of histologically evident nephrocalcinosis. Later changes, especially to the basal part of proximal tubular cells and their basal laminae, were thought to be consequent upon the mitochondrial changes. It is suggested that the initial renal damage was caused both directly, by a toxic effect of the phosphate load on the kidney and, indirectly, by stimulation of the parathyroid glands as a result of the hypocalcaemia and hyperphosphataemia which followed an injection of phosphate. Daily doses of 1 M phosphate for 3 days produced a type of nephrocalcinosis which was more typical of that reported by previous investigators, who used high doses of phosphate. Twice daily injections of 0-25 M phosphate for 6 days did not induce nephrocalcinosis, whereas 0-375 M phosphate given twice daily for 6 days produced only minimal calcium deposits compared with animals given 0-5 M phosphate once daily for the same period. This may have important clinical implications, since phosphate has been used to control hypercalcaemia of various etiologies.
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PMID:The development of nephrocalcinosis in the rat following injections of neutral sodium phosphate. 113 87


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