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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 When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished.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

The influence of hypercalcemia on renal function was studied retrospectively in 13 patients suffering from primary hyperparathyroidism, sarcoidosis, vitamin D intoxication, malignant lymphoma or chronic lymphatic leucemia. Different kinds of treatment, depending upon the primary disease, often induced a rapid fall in the serum calcium concentration. The serum creatinine concentration always fell simultaneously. The serum phosphate concentration fell in all but two patients. Changes in serum calcium and serum creatinine correlated significantly (p less than 0.001), as did changes in serum calcium and serum phosphate concentrations (p less than 0.05). Serum calcium/serum creatinine and serum calcium/serum phosphate ratios were significantly higher in patients with primary hyperparathyroidism than in patients with hypercalcemia of non-hyperparathyroid origin (p less than 0.01, p less than 0.001). This suggests a different effect of calcium on the glomerular filtration rate in hyperparathyroid and non-hyperparathyroid patients, the latter group being more sensitive to the influence of hypercalcemia. Possible explanations for this difference, such as a protective effect of PTH on the glomerular filtration, are discussed.
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PMID:Reversible renal failure caused by hypercalcemia. A retrospective study. 64 44

We studied the effects of vitamin D metabolites on parathyroid hormone (PTH) secretion. Test materials were injected into the cranial thyroid artery of the dog, and immunoreactive PTH was measured frequently in serum samples from the inferior thyroid vein and the femoral vein. This model for the study of secretion had previously been validated with the use of known modulators on PTH secretion. In control experiments, injection of 100% ethanol, the vehicle in which cholecalciferol (D(3)) metabolites were suspended, resulted in no change in PTH secretion. Likewise, native vitamin D(3), in doses ranging from 250 to 1,250 ng had no effect on PTH secretion. 25-Hydroxycholecalciferol, 25-(OH)D(3), in doses of 125-240 ng, caused complete suppression of PTH secretion. When 24,25-dihydroxycholecalciferol, 24,25-(OH)(2)D(3), was injected in doses of 50-250 ng, suppression of PTH secretion was again complete; in doses of 5 ng, injection of this metabolite resulted in significant but incomplete suppression of secretion. In doses of 50-250 ng, 1,25-(OH)(2)D(3) strongly stimulated PTH secretion, but in a dose of 5 ng this metabolite had no effects. Injection of equal doses of 1,25-(OH)(2)D(3) and 24,25-(OH)(2)D(3) resulted in significant suppression of PTH secretion. Hypocalcemia-induced stimulation of PTH secretion was suppressed by 24,25-(OH)(2)D(3) while hypercalcemia-induced suppression of PTH secretion was stimulated by 1,25-(OH)(2)D(3). In all experiments showing suppression of PTH secretion, peripheral PTH decreased. Arguments are presented for considering the suppressive effects of D(3) metabolites as physiologic modulators. However, this stimulating effect of 1,25-(OH)(2)D(3) occurred only in pharmacologic doses and hence probably has no physiologic relevance.
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PMID:Inhibition of parathyroid hormone secretion by 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol in the dog. 65 99

We measured the concentrations of serum calcium and 25-hydroxy-vitamin D in a patient with hypervitaminosis D during 3 months of therapy directed toward correcting the hypercalcemia. Serum calcium could not be maintained at normal concentration without specific therapy until 9 weeks after vitamin D was discontinued. Concentration of 25-hydroxy-vitamin D at the time was 285 ng/ml, approximately half of the value measured three weeks after withdrawal of vitamin D. Serial measurements of the concentration of 25-hydroxy-vitamin D seem to be a useful means of assessing the degree of intoxication in patients with hypervitaminosis D.
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PMID:25-hydroxy-vitamin D levels in a patient with hypervitaminosis D. 67 43

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

Six patients with chronic renal failure on regular dialysis treatment were given low doses (0.5--1.0 microgram/day) of 1alpha-hydroxyvitamin D3, monitoring the serum calcium, inorganic phosphate, immunoreactive parathyroid hormone concentration (IPTH) and alkaline phosphatase activity. The serum calcium rose in all patients after 7 days' treatment, in some subjects to hypercalcemic range; this effect persisted 6--14 days after withdrawal of 1alpha-hydroxyvitamin D3. The elevated serum IPTH rose in the first days of treatment, but later decreased to normal values. It is suggested that active vitamin D metabolites are necessary for normal response of parathyroid glands to variation in serum calcium. Low-dose 1alpha-hydroxyvitamin D3 treatment appears to be a promising method of correcting hypocalcemia and secondary hyperparathyroidism in chronic renal failure. Careful control of serum calcium is necessary, as hypercalcemia may occur even after minute doses of 1alpha-hydroxyvitamin D3.
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PMID:Effects of 1alpha-hydroxyvitamin D3 on serum calcium and immunoreactive parathyroid hormone in patients with chronic renal insufficiency. 70 Sep 46

The pathogenesis of hypercalcemia and mode of action of glucocorticoid therapy was examined in a patient with lymphosarcoma cell leukemia. Circulating neoplastic cells were cultured in vitro and secreted a bone-resorbing factor. The bone-resorbing factor was partially purified with the use of a bioassay for bone resorption, and was found to be chromatographically and pharmacologically similar to osteoclast activiating factor (OAF), which is produced by normal mitogen-activated peripheral blood lymphocytes. Other factors which stimulate bone resorption, such as parathyroid hormone, prostaglandins and the vitamin D metabolites, were excluded by criteria which included dose-response curves, radioimmunoassays, extraction in organic solvents and failure of glucocorticoids to inhibit bone-resorbing activity. The patient's hypercalcemia responded rapidly to prednisone therapy. The effects of the bone-resorbing factor secreted by the neoplastic cells on bone cultures to which cortisol was added were examined. Cortisol inhibited bone resorption directly at low doses (10(-8) M), which suggests that prednisone may have lowered the serum calcium in this patient by direct inhibition of bone resorption.
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PMID:Pathogenesis of hypercalcemia in lymphosarcoma cell leukemia. Role of an osteoclast activating factor-like substance and a mechanism of action for glucocorticoid therapy. 70 20

During a period of 4-7 days, synthetic 1 alpha-hydroxyvitamin D3 (1alpha-OH-D3) was given to osteoporotic patients with hip fractures in 3 different dose levels, viz. 1 microgram, 2 microgram, and 4 microgram, in combination with calcium. The increase in serum calcium level was more prominent during treatment with 2 microgram and 4 microgram doses of 1 alpha-OH-D3 and was also dependent on the duration of treatment. The level of serum phosphate was only slightly elevated. The urinary calcium excretion increased, while the urine phosphate and hydroxyproline excretion decreased. The intestinal absorption of calcium increased in rate during treatment with 1 alpha-OH-D3. On discontinuation of treatment, values did not normalize within 6 days. The administration of small doses of 1 alpha-OH-D3 did not seem to expose osteoporotic patients to the risks of hypercalcemia. The efficiency of vitamin D metabolites in the treatment of osteoporosis requires further investigation.
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PMID:Short-term effects of varying doses of 1 alpha-hydroxyvitamin D3 on blood and urine chemistry and calcium absorption of osteoporotic patients. 70 35

Hypercalcemia occurred in 4 dogs with renal failure. Primary causes of hypercalcemia previously described in the dog (primary hyperparathyroidism, pseudohyperparathyroidism, vitamin D toxicosis) were not identified. Increased concentrations of circulating immunoreactive parathormone were found in 2 dogs, and thyroparathyroidectomy of 1 dog resulted in decreased serum concentrations of that hormone as well as of calcium. The latter observations indicated that hypercalcemia was related to increased parathormone activity, but the possibility of other homeostatic imbalances was not excluded. It was concluded that renal failure should be considered as a primary cause of hypercalcemia, along with other causes previously identified.
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PMID:Hypercalcemia secondary to chronic renal failure in the dog: a report of four cases. 72 83

On the basis of 100 cases of hypercalcemia, the authors attempt to elucidate the criteria of the etiologic diagnosis. Kidney lithiasis or nephrocalcinosis suggested a primary hyperparathyroidism (HPT I) or an intoxication due to vitamin D. X rays of the skeleton and quantitative histological exams of the bone were not useful in the diagnosis of HPT I. The level of parathormone in the plasma is the best parameter to be used in distinguishing HPT I from other diseases. In the absence of renal insufficiency or severe intestinal disorders, a phospharemia below 2.6 mg/100 ml, a chloremia above 103 m EG/l and bicarbonates below 25 m Eg/l indicate an HPT I or a paraneoplasic. A phosphoremia above 3.2 mg/100 ml runs counter to this diagnosis. The chloremia/phosphoremia ratio is not more helpful than the phosphoremia alone.
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PMID:[Etiologic diagnosis of hypercalcemia. A study of 100 cases]. 72 66


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