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)

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

Fifteen patients, 13 women and 2 men (mean age 60 years) with osteoporosis of different types have been under treatment with 1 alpha-hydroxyvitamin D3 and calcium. The responses were observed clinically and by the use of roentgen morphometry, photon absorptiometry and by blood and urine chemical analyses. The treatment had beneficial clinical effect in all but 3 patients. The intestinal calcium absorption rate increased significantly. Slight hypercalcemia and a significant hypercalciuria occurred during treatment. Serum and urine phosphate levels, alkaline phosphatase and parathyroid hormone values were within normal ranges. The bone mineral content increased significantly during treatment. 1 alpha-hydroxyvitamin D3 and calcium was well tolerated by the patients. Three patients had coincidental acute attacks of spinal pain and 2 had further vertebral crush fractures. A period of time longer than one year is necessary to further evaluate the effects of 1 alpha-hydroxyvitamin D3 therapy on the clinical course of severe osteoporosis.
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PMID:Interim report on treatment of osteoporotic patients with 1 alpha-hydroxyvitamin D3 and calcium. 70 36

Hypercalcemia occurs in approximately one of every five patients with thyrotoxicosis, and one of seven patients with hypercalcemia and thyrotoxicosis will have hyperparathyroidism as the cause of the serum calcium elevation. While there are no clinical features which permit easy identification of patients with hyperparathyroidism and thyrotoxicosis, determination of serum parathyroid hormone levels may help. Parathyroid hormone levels may be normal or suppressed if hypercalcemia is due to hyperthyroidism alone, and an elevated parathyroid hormone level suggest coexisting hyperparathyroidism.
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PMID:Hypercalcemia in thyrotoxicosis. 71 46

The results of morphologic studies performed in 18 patients who had total parathyroidectomy and autotransplantation of parathyroid tissue into the forearm muscle are presented. All patients had long-standing renal disease with azotemia, hyperphosphatemia and high levels of parathyroid hormone. The histologic findings after total parathyroidectomy, before gland transplantation, are important for selection of parathyroid tissue for surgery. Diffuse hyperplasia with the development of multiple nodules of the parathyroids can possibly be adverse for the transplant. In one case, nine month after autotransplantation we found a tumor in the forearm, measuring 2.0 X 3.0 X 2.2 cm in diameter. Morphologic findings in this case before implantation showed diffuse hyperplasia with adenomatous nodules but no signs of carcinoma. The grafted parathyroid tissue after excision was seen with blood vessel invasion in the normal skeletal muscle. In the case of primary renal disease with secondary parathyroid hyperplasia, the light microscopic examination revealed an autonomous tumorlike adenomatous formation in the autografted parathyroid tissue, with graft-dependent hypercalcemia. The invasive growth with some signs of neoplasia following autotransplantation raises the question of the development of certain neoplasia.
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PMID:[Morphological aspects of parathyroid gland transplantation. Contribution on the clinical relevance of induced, invasive tissue growth]. 72 Jan 63

Calcium enters the pancreatic juice from two sources, one fraction associated with enzyme protein and another small fraction presumably by diffusion. The calcium concentration in pancreatic juice is lower than in plasma. It decreases with high flow rates and increases asymptotically to plasma concentration with low rates. In chronic pancreatitis calcium concentration is raised in the secretin-stimulated juice. After pancreozymin in moderate chronic pancreatitis it is low but in severe stages of the disease it is high signalling total dissociation from the entrance of enzyme protein, which is very low in these cases. Hypercalcemia stimulates enzyme secretion in the pancreas, hypocalcemia inhibits it. Calcium is essential for intracellular processes associated with secretion, the exact place in the sequence of "stimulus-secretion-coupling" still being unknown. Calcitonin as one of the hormones which regulates calcium homeostasis, inhibits secretion of enzymes but not of fluid and bicarbonate. The action of the parathyroid hormone on the exocrine pancreas is unknown. In primary hyperparathyroidism with chronic hypercalcemia acute and chronic pancreatitis occur 10 to 20 times more frequently than in the general population. In acute pancreatitis of whatever origin hypocalcemia is atypical feature of the disease indicating bad prognosis. The mechanism of its development is still unclear. In chronic pancreatitis the forming of calcified stones in the ducts is typical in cases associated with alcoholism, with protein malnutrition and with primary hyperparathyroidism. But it occurs also in cases with unknown etiology signalling a more general pathophysiological phenomenon. The calcium salts form a precipitate on protein plugs in the juice, which have been observed even in early stages of the disease in the small and larger ducts of the gland.
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PMID:The role of calcium in pancreatic secretion and disease. 77 77

New information has elucidated many of the biochemical pathways in the formation, release and metabolism of parathyroid hormone (PTH). The hormone is biosynthesized in the parathyroid cells from two distinct precursors, or prohormones, that are modified by specific enzymic cleavages during the synthesis and intracellular transport of the hormonal polypeptide. Release of the hormone from the gland inversely depends on the extracellular calcium concentration, but is regulated over a much narrower range of calcium concentration than was realized previously. This new information points to a pattern of regulation that is more appropriate for homeostasis than was the pattern indicated by earlier studies. The persistence of a basal level of PTH secretion, despite sustained hypercalcaemia, suggests a possible mechanism for the abnormal secretion seen in states of hyperparathyroidism. The discovery of a calium-dependent degradative pathway for PTH in the parathyroid cell indicates that changes in the turnover of PTH may be one means by which calcium regulates the amount of hormone available for secretion. Of the multiple immunoreactive forms of PTH present in the circulation of man and animals, the predominant form in blood appears to be a large biologically-inactive fragment consisting of the middle and carboxy two-thirds of the hormone sequence. At times, smaller biologically-active fragments of PTH may also appear in blood. Most circulating fragments of PTH probably arise from peripheral cleavage of the intact, secreted hormone in kidney and liver, but some forms of the hormone, including prohormones, may also be secreted from the parathyroid gland. The heterogeneity of circulating PTH and the concomitant uncertainties regarding its precise character have introduced difficulties in the interpretation of immunoassay measurements. A further delineation of the pathways and regulation of PTH biosynthesis, secretion and metabolism should lead to the development of more-specific immuno-assays and result in improved diagnosis and management of patients with disorders of the parathyroid glands.
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PMID:New concepts in the formation, regulation of release, and metabolism of parathyroid hormone. 78 74

Sixty-eight patients were observed for a period of up to seven years after transplantation. Serum parathyroid hormone levels were measured in 41 patients; 17 patients had persistent hypercalcemia for a period of from one to seven years. Serum parathyroid hormone levels were elevated in seven of these 17 patients. Serum parathyroid hormone was elevated in 11 of the other 24 patients with normocalcemia. The function of the kidney was not affected either by the state of hypercalcemia or persistent hyperparathyroidism. Aseptic necrosis was significantly present in those of the hypercalcemic group. It is suggested that persistent hypercalcemia is an important precipitating, if not the main, cause of an aseptic necrotic condition of the bones.
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PMID:The high incidence of persistent secondary hyperparathyroidism after renal homotransplantation. 78 41

76 kidney transplant recipients who were up to 4 years post transplant, were studied to assess the incidence of secondary hyperparathyroidism. All patients had good renal function with a mean serum creatinine of 1.4 mg/100 ml. Secondary hyperparathyroidism, as evidenced by increased serum parathyroid hormone levels, was present in 53 of the 76 patients (66%) and radiologic bone disease in 26 of the 76 patients (34%), while hypercalcemia (serum calcium greater than 11.0 mg/100 ml) occurred in only 6 patients (8.5%). The incidence of secondary hyperparathyroidism decreased slightly with time following transplantation, but the degree of secondary hyperparathyroidism as indicated by the levels of serum parathyroid hormone at various times following renal transplantation was essentially similar. The causes for the persistence of this condition are not totally known, but it was found that its incidence was related to the duration of dialysis prior to transplantation.
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PMID:Secondary hyperparathyroidism in human kidney transplant recipients. 78 18

The first case of primary hyperparathyroidism associated with renal cell carcinoma, nasopharynx carcinoma and thyroid carcinoma is reported. Selective venous sampling with radioimmunoassays for parathyroid hormone was helpful in the differentiation of primary hyperparathyroidism from hypercalcemia associated with malignancy.
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PMID:Primary hyperparathyroidism with triple cancers consisting of renal cell carcinoma, nasopharynx carcinoma and thyroid carcinoma. 83 5


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