Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal handling of phosphorus was studied in the following groups of parathyroidectomized rats with maleate-induced Fanconi syndrome: 1) 6 rats receiving intravenous parathyroid hormone, 2) 6 rats receiving intravenous dibutyryl cyclic AMP (DBcAMP), 3) 6 rats undergoing volume expansion with saline, 4) 12 rats receiving intravenous 25 (OH)vitamin D3, 5) 12 rats with acute hypercalcemia induced by intravenous CaCl2, 6) 6 rats with phosphate deprivation, and 7) 6 rats receiving intravenous calcitonin. Parathyroid hormone and calcitonin failed to increase the urinary excretion of both cAMP and phosphorus. Likewise, DBcAMP failed to increase the urinary excretion of phosphorus. Extracellular volume expansion and hypercalcemia (serum calcium 12.9 +/- 0.7 mg/100 ml) did not alter the tubular reabsorption of phosphorus. In phosphate-deprived animals, the fractional excretion 0.16 +/- 0.05 (mean +/- SE) was lower than that in the control animals (maleate-treated without phosphate depletion), 0.46 +/- 0.04 (P less than 0.001). 25 (OH)vitamin D3 decreased the fractional excretion of phosphorus from 0.39 +/- 0.03 in the control (maleate-treated not receiving 25 (OH)vitamin D3) to 0.23 +/- 0.02 (P less than 0.001) in the experimental animals. The present study demonstrated an antiphosphaturic effect of 25(OH)vitamin D3 in experimental Fanconi syndrome; the mechanism of this action is not well understood.
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PMID:Antiphosphaturic action of 25 (OH) vitamin D3 in experimental Fanconi syndrome. 21 76

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

Patients with steroid-induced, juvenile and senile osteoporosis were studied using balance techniques. The changes in calciun and phosphorus balance associated with glucocorticoid therapy were corrected with vitamin D and bendrofluazide given in combination. No hypercalcaemia occurred in osteoporotic patients who continued to receive glucocorticoids. Calcium and phosphorus balance was also improved in the osteoporotic subjects not receiving steroids, but these patients became hypercalcaemic during treatment. It is suggested that vitamin D, bendrofluazide and steroids antagonize the actions of one another on the renal tubule, gut and bone and in this way prevent the increased calciuria which occurs with glucocorticoid therapy. Since the increased calciuria and negative calcium balance induced by glucocorticoids is considered to be the result of excessive bone resorption, an adequate dose of bendrofluazide and vitamin D in combination might prevent the development of, or even reverse, steroid-induced osteoporosis.
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PMID:Possible prevention and treatment of steroid-induced osteoporosis. 30 43

Hypercalcemia after renal transplantation (post-T hypercalcemia) has been detected in 29 (16.7%) of 174 long-term survivors. The mean time of onset of hypercalcemia was 69 days after renal transplantation (range 3-210). In 18 patients the hypercalcemia was mild and resolved spontaneously (transient) from 2-65 months (mean 19) after onset. In 4 patients serum calcium normalized concurrently with rejection episodes. In 7 patients the hypercalcemia was more pronounced (permanent), being terminated by subtotal parathyroidectomy in 5 and persisting in 2 recipients. The hypercalcemia was asymptomatic except in one patient, who developed calculi in the graft and a fall in graft function, all of which disappeared after parathyroidectomy. At operation the parathyroid glands showed hyperplasia, except in one case with an adenoma in one of the hyperplastic glands. Serum phosphorus was markedly decreased, to the same extent in transiently and permanently hypercalcemic recipients. Serum parathyroid hormone (S-PTH) was increased in all of 5 patients with permanent and in 3 of 8 with transient post-T hypercalcemia. In normocalcemic and in transiently hypercalcemic recipients the mean S-PTH was identical, but significantly lower than in the permanently hypercalcemic recipients. S-PTH was suppressed to the same extent during an i.v. calcium infusion in patients with post-T hypercalcemia and with primary hyperparathyroidism.
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PMID:Hypercalcemia and parathyroid function after renal transplantation. 31 22

Excess of phosphorus (the ratio Ca : P = 1 : 2) in a diet of growing rats strengthened such manifestations of vitamin D insufficiency as hypercalcemia and inhibition of animal growth. The data obtained suggest that excess of phosphorus is apparently important for pathogenesis of rachitis and the optimal ratio Ca : P should not be ignored in child diet.
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PMID:[Experimental vitamin D deficiency with different dietary calcium-phosphorus ratios]. 42 76

Dogs given excess vitamin D (500 or 1,000 micrograms/kg of body weight each day for 1 to 3 weeks were observed for clinical and pathologic changes of increased blood pressure and of characteristic nephropathy associated with vitamin D toxicosis or hypercalcemia. Serum calcium and serum urea nitrogen (UN) increased throughout the treatment period, but serum phosphorus remained within the normal range. Plasma renin activity increased markedly. Blood pressure showed only insignificnat changes (P = greater than 0.05). Gross and microscopic examination of the kidneys suggested vascular-oriented changes with an ischemic basis. Glomerular vascular poles showed hypertrophy and hyperplasia of juxtaglomerular cells. Ultrastructually, an increase in the number of secretory granules was noticed in these cells. A hypothesis regarding the mechanism of renal injury during vitamin D toxicosis is presented.
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PMID:Vitamin D intoxication and the pathogenesis of vitamin D nephropathy in the dog. 45 87

We studied weanling rats fed 0.06% (group 1) and 0.10% (group II) magnesium (Mg) during phosphate depletion (PD) in order to evaluate the role of Mg in the bone, soft tissue, and serum changes of PD. The following results were obtained: 1) serum Mg remained stable in the face of a negative Mg balance; 2) the hypercalcemic and hypercalciuric response to PD was the same in both groups; 3) bone Mg content was decreased with PD in both groups and was associated with a significant decrease in bone calcium and phosphorus. We conclude that: 1) the hypomagnesemia of PD is dependent mainly on the dietary intake of Mg; 2) the hypercalcemia and hypercalciuria of PD are not caused by primary changes in Mg homeostasis; 3) low-dietary Mg during PD may cause a defect in soft tissue utilization of P in the growing rat.
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PMID:Influence of dietary magnesium in experimental phosphate depletion: bone and soft tissue mineral changes. 46 91

Malignant disease and primary hyperparathyroidism are the most common causes of hypercalcemia, but there are many minor causes. Mechanical or humoral factors, or both, may underlie the increase in bone resorption. Parathyroid hormone (PTH) is a major mediator of bone resorption, but many other humoral agents have the same effect, eg, prostaglandin, osteoclast-activating factor, and thyroid hormone. Serial determination of total calcium concentration is the most important laboratory test in hypercalcemia. Other useful tests include the determination of serum and urinary phosphorus concentration, chloride/phosphate ratio, urinary cyclic adenosine 3',5'-monophosphate (cAMP) level; carboxyl-terminal PTH assay; corticosteroid challenge; and appropriate radiologic studies. Nephrogenous cAMP and urinary prostaglandin determinations are research tools that hold great promise in the future. Differentiation between PTH- and non-PTH-mediated hypercalcemia determines subsequent steps in diagnosis and treatment.
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PMID:Differential diagnosis of hypercalcemia: a mechanistic approach. 48 78

A leiomyoma of the small bowel produced laboratory features of hyperparathyroidism which disappeared promptly after tumour resection. Hypercalcaemia, hypophosphatemia, hyperchloremia, elevated chloride/phosphorus ratio, increased urinary cyclic AMP, and blood levels of immunoreactive parathormone were present. Electron microscopy showed dense round granules in the tumour cells.
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PMID:[Leiomyoma of the small bowel with hypercalcaemia: presence of a substance with parathormone activity (author's transl)]. 53 84

In male Wistar rats, 1 alpha-HCC and 1 alpha, 25-DHCC induced diuretic effects in doses of 2.5 and 25 micrograms/kg p.o., while no such effects of 1 alpha-HCC were seen with a dose of 0.25 microgram/kg p.o. Effect of 1 alpha-HCC appeared later than that of 1 alpha, 25-DHCC, but at 24 hr, the difference disappeared. Similar results were obtained with urinary concentrations of calcium (increase) and phosphorus (decrease). Glomerular filtration rate (GFR) and tubular reabsorption of phosphate (TRP) were remarkably elevated by 1 alpha, 25-DHCC, and effects of 1 alpha-HCC were rather weak and apparently not dose dependent. In light of these results and the finding that there was no difference between the effects of 1 alpha-HCC and 1 alpha, 25-DHCC on serum calcium and phosphorus at 24 hr, the mechanism of action of these sterols on the renal function seems to differ. In male Beagle dogs, 0.25 microgram/kg/day p.o. of 1 alpha-HCC or 1 alpha, 25-DHCC induced a severe hypercalcemia and GFR was decreased in the 1 alpha, 25-DHCC treated group. A gradual recovery occurred with cessation of the administration. Thus decrease in GFR was considered to be due to calcification of the kidney.
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PMID:[Studies on biopharmacological actitivy of active vitamin D3 analogues (VII) Effect of 1 alpha-hydroxycholecalciferol on renal function in rats and Beagle dogs (author's transl]. 54 Aug 87


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