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

Severe hypercalcemia with decreased renal function, hypertension, and renal calcifications developed in a 14-year-old boy who required prolonged immobilization for multiple fractures. Parathyroid hormone was not detectable in the serum. Urinary calcium excretion was high. Initially, mobilization was impossible and the patient was treated with a high fluid intake, low calcium intake, acidification of the urine, furosemide, and a passive exercise program. Renal function improved and renal calcifications resolved but hypercalcemia did not resolve. After mobilization the serum calcium concentration became normal rapidly. This treatment regimen is suggested for use in patients with immobilization hypercalcemia when mobilization is impossible.
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PMID:Severe immobilization hypercalcemia, renal insufficiency, and calcification. 44 Jul 90

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

Parathyroid hormone (PTH), creatinine, calcium and phosphate blood levels were repeatedly measured in 5 patients with acute renal failure. 1 patient developed hypercalcemia during the recovery phase of the illness. PTH was elevated in all cases before starting hemodialysis treatment and returned to normal when renal function recovered. Calcium and PTH were inversely correlated in 3 patients including the patient with transient hypercalcemia. These data show that parathyroid function in acute renal failure is closely related to changes in renal function and the hypercalcemia, when occurring, is not necessarily due to parathyroid hyperactivity.
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PMID:Parathyroid hormone and calcium blood levels in acute renal failure. With special reference to one patient developing transient hypercalcemia. 63 17

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

Parathyroid hormone (PTH) secretion rate was measured in 16 anesthetized calves by using a technique involving radioimmunoassay of parathyroid venous blood which was collected during timed intervals and measured volumetrically. The calves ranged in age from 2-14 weeks. Plasma calcium concentration was altered by infusion of solutions of CaCl2 or disodium ethylenediamine tetracetate (Na2 EDTA) into the jugular vein. When plasma calcium concentrations exceeded 10.5 mg/100 ml, a basal, non-suppressible secretion rate of 0.3 ng/kg/min was maintained despite the induction of hypercalcemia. Slight changes in secretion rate were observed in response to changes of plasma calcium in the range between 9 and 10.5 mg/100 ml. Below 9 mg/100 ml, a small decrease in plasma calcium concentration evoked a pronounced increase in secretion rate. A maximal secretion rate of about 5.5 ng/kg/min was attained at a plasma calcium concentration of approximately 7.5 mg/100 ml and it was not increased by more severe hypocalcemia. These observations confirm the sigmoidal relationship between PTH secretion rate and plasma calcium concentration which was previously suggested by measurement of PTH concentration in peripheral plasma of hypocalcemic, parturient cows.
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PMID:Sigmoidal relationship between parathyroid hormone secretion rate and plasma calcium concentration in calves. 74 6

Tthe findings of 150 patients with proven primary hyperparathyroidism are reported. The purpose of the analysis was to find differences between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups. Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck. The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The success of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There is still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are responsible for the different action on bone and kidney is discussed. In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in ov er 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcemia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.
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PMID:[Primary hyperparathyroidism. An analysis of 152 patients with special references to acute life threatening complications (acute hyperparathyroidism)]. 79 28

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

Parathyroid hormone (PTH), a major regulator of mineral ion metabolism, and PTH-related peptide (PTHrP), which causes hypercalcemia in some cancer patients, stimulate multiple signals (cAMP, inositol phosphates, and calcium) probably by activating common receptors in bone and kidney. Using expression cloning, we have isolated a cDNA clone encoding rat bone PTH/PTHrP receptor from rat osteosarcoma (ROS 17/2.8) cells. The rat bone PTH/PTHrP receptor is 78% identical to the opossum kidney receptor; this identity indicates striking conservation of this receptor across distant mammalian species. Additionally, the rat bone PTH/PTHrP receptor has significant homology to the secretin and calcitonin receptors but not to any other G protein-linked receptor. When expressed in COS cells, a single cDNA clone, expressing either rat bone or opossum kidney PTH/PTHrP receptor, mediates PTH and PTHrP stimulation of both adenylate cyclase and phospholipase C. These properties could explain the diversity of PTH action without the need to postulate other receptor subtypes.
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PMID:Expression cloning of a common receptor for parathyroid hormone and parathyroid hormone-related peptide from rat osteoblast-like cells: a single receptor stimulates intracellular accumulation of both cAMP and inositol trisphosphates and increases intracellular free calcium. 131 66

Parathyroid hormone-like peptide (PLP) is produced by a number of tumors commonly associated with hypercalcemia as well as by nontumorous tissue, including some endocrine organs. We applied immunohistochemistry using the avidin-biotin-peroxidase technique to localize PLP in formalin-fixed, paraffin-embedded tissues of two human pancreatic carcinomas associated with hypercalcemia and normal blood parathyroid hormone levels. One tumor was endocrine and one was exocrine in differentiation. There was no evidence of bone metastasis in either case. We documented normalization of serum calcium level after removal of the pancreatic endocrine tumor. These observations support the suggestion that PLP production by pancreatic carcinoma may play a role in the development of hypercalcemia. However, the presence of PLP in tumors not associated with hypercalcemia indicates that other factors in addition to PLP are necessary for the manifestation of hypercalcemia. Hypercalcemia associated with exocrine pancreatic tumor has rarely been reported. Our exocrine pancreatic tumor appears to be the first reported case in which immunohistochemistry localized PLP. Since PLP has been localized to cells of exocrine ducts and ductules of normal pancreas, our results provide insight into the cell of origin of this tumor type.
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PMID:Parathyroid hormone-like peptide in pancreatic endocrine carcinoma and adenocarcinoma associated with hypercalcemia. 132 59


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