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)

In four healthy controls and three patients with hypoparathyroidism serum-1,25-dihydroxycholecalciferol (1,25-D.H.C.C.) concentrations, after oral or intravenous administration, declined biphasically with a rapid-phase half-time of about 14 hours. Repeated oral doses of 1 mug 1,25-D.H.C.C. (2-4 nmol) produced serum concentrations well below the assayed normal range but were nevertheless effective in raising serum-calcium. It is suggested that orally administered 1,25-D.H.C.C. acts directly on the intestinal mucosal-cell nucleus to promote calcium absorption. 1,25-D.H.C.C. is more rapidly eliminated from the body than vitamin D, and it is predicted that any hypercalcaemia caused by 1,25-D.H.C.C. therapy should be of relatively short duration.
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PMID:Metabolic fate of administered 1,25-dihydroxycholecalciferol in controls and in patients with hypoparathyroidism. 5 55

Quantitative analysis of urinary cyclic AMP in phospho-calcic pathology. The authors describe a method measuring amounts of cyclic AMP. Normal daily elimination in urine was measured in a group of normal subjects. Elimination was found to be raised in two-thirds of the patients with primary hyperparathryroidism, normal in those with idiopathic hypercalcaemia and neoplastic hypercalcaemia, and subnormal in patients with hypoparathyroidism. The urinary excretion of cyclic AMP after perfusion of parathyroid hormone was very low in cases of pseudo-hypoparathyroidism compared with that in surgical hypoparathroid controls. The results are compared with data from the literature. The theoretical and diagnostic value of these quantitative analyses is discussed.
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PMID:[Determination of urinary cyclic AMP in phosphorus and calcium pathology]. 16 26

Pseudohypoparathyroidism (PHP) is a hereditary disorder with typical dysmorphic signs, oligophrenia and clinical and laboratory signs of hypoparathyroidism, which is resistant to parathyroid extract (PTE). Pseudopseudohypoparathyroidism (PPHP) is a genetically identical, partial form of PHP without hypoparathyroidism. Many hypotheses exist to explain the pathogenesis of these disorders: Albright and coworkers first demonstrated the PHP is caused by an inability of the renal tubules to respond to parathyroid hormone (PTH). Later hypotheses proposed a general defect in phosphorus transport, defects in the synthesis of PTH, the existence of antibodies to this hormone or hyperthyrocalcitonism. The possibility of measuring PTH in the peripheral serum by radioimmunoassay and improved knowledge of the role of cyclic adenosine monophosphate (cAMP) as a mediator of the action of PTH were necessary to explain the pathogenesis of PHP and PPHP. Three children suffering from PHP and two adults with PPHP were investigated as follows: measurements of PTH in the peripheral serum; assays of PTH levels during artificial hypercalcaemia; serial assays of calcium, phosphorus and PTH levels during vitamin D treatment; changes in the Ellsworth-Howard tests indicative of PTE resistance during vitamin D treatment and measurements of urinary cAMP excretion before and during vitamin D therapy. The following results were obtained: Secondary hyperparathyroidism in PHP, which could be suppressed by hypercalcaemia; normal levels of PTH in PPHP; normalization of serum calcium, phosphorus and PTE during treatment with vitamin D; abnormally low basal levels of cAMP in PHP, which could not be stimulated by PTE either before or during vitamin D treatment. The results of these investigations confirm Albright's hypothesis of endorgan resistance to PTH in PHP. This is caused by the inability of the PTH-sensitive adenylcyclase-system to mediate the action of PTH on its target cells. This is responsible for the distrubances in calcium and phosphorus metabolism and for secondary hyperparathyroidism. While this mediatorial defect seems to be total or almost total in PHP, a partial defect has to be assumed in PPHP.
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PMID:[Pseudohypoparathyroidism: investigations of the serum parathyroid hormone level, pte resistance and urinary camp excretion before and during vitamin d treatment (author's transl)]. 17 30

Five groups of 4 weanling pigs were fed a diet with 1.2% calcium and 1.0% phosphorus for 8 weeks with vitamin D3 at 1, 5, 25, 125 and 625 times the recommended levels, respectively. Hypercalcemia and hypophosphatasemia developed rapidly and persisted in Group 5 and developed more slowly but steadily in Group 4. Increasing levels of vitamin D3 influenced progressively and negatively the activity of resorbing osteocytes with osteopetrosis in Groups 2 and 3 and with osteonecrosis in Group 5. Atrophy of osteoblasts further contributed to the osteopenia in Group 5. Cartilage growth activity was arrested in Group 5. The negative effect on the resorbing osteocytes, which finally lead to death of the cells, was ascribed directly to vitamin D3 toxicosis since hypoparathyroidism and hypercalcitonism, both resulting from hypercalcemia, are not known to induce osteonecrosis. Since hypercalemia was finally as severe in Group 4 as in Group 5 and since there was soft tissue calcinosis only in Group 5, the calcinosis was always considered dystrophic, an interpretation supported by the observation that degenerative histologic changes preceded soft tissue calcinosis.
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PMID:Bone pathology in hypervitaminosis D an experimental study in young pigs. 18 36

Urinary cyclic AMP (UcAMP) appropriate for the serum calcium concentration was determined in normal subjects during the base-line state and during alteration in their serum calcium concentrations by saline and calcium infusions. This was compared to the UcAMP in 76 patients with hypercalcemia and 5 patients with hypocalcemia. In 54 of 56 patients with primary hyperparathyroidism, the UcAMP was inappropriately high for their serum calcium concentration, the 2 exceptions having renal failure. In four patients with vitamin D intoxication, sarcoidosis, milkalkali syndrome, and thiazide-induced hypercalcemia and in five patients with hypocalcemia due to hypoparathyroidism, the UcAMP was appropriately low for their serum calcium concentration. In 16 patients with nonparathyroid neoplasms, 10 had UcAMP levels that were inappropriately high suggesting ectopic parathyroid hormone (PTH)-mediated hypercalcemia and 6 had UcAMP levels that were appropriately low suggesting that their hypercalcemia was due to osteolytic factors other than PTH. Correlations between UcAMP, serum calcium concentration, and carboxyl-terminal immunoreactive PTH suggest that random UcAMP is a sensitive accurate reflection of circulating biologically active PTH. If there is adequate renal function (serum creatinine concentration less than 2.0 mg/dl), a random UcAMP expressed as mumol/g creatinine and analyzed as a function of the serum calcium concentration completely separates patients with PTH and non-PTH-mediated hypercalcemia.
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PMID:Urinary cyclic AMP analyzed as a function of the serum calcium and parathyroid hormone in the idfferential diagnosis of hypercalcemia. 18 21

25-Hydroxyvitamin D (25-OHD) levels were measured in 39 patients with metabolic bone disease or hypoparathyroidism who had been treated with a constant high dose of vitamin D2 or D3 for at least 12 weeks. Plasma 25-OHD levels rose with increasing dosage, the relationship between dose and plasma level being approximately linear whether or not the dose was expressed on a weight-corrected basis. A therapeutic range of 25-OHD to be expected when patients with these conditions are treated with vitamin D has been established. There may be certain exceptions in which plasma 25-OHD levels within the range are associated with either an inadequate response to treatment or, conversely, the hypercalcaemia of vitamin D toxicity. There was no correlation between plasma calcium level and 25-OHD concentration in the group of patients studied. There was also no difference between the dose/25-OHD relationship of patients treated with vitamin D2 and that of patients receiving vitamin D3. Ten patients were started on treatment with large doses of vitamin D during the period of the study. The rate of rise of plasma 25-OHD was followed during treatment. The incremental rise in 25-OHD was calculated at the end of the first week of treatment in terms of dose per unit body weight. The rate of rise of plasma 25-OHD level was highly correlated with the dose used. Plasma 25-OHD levels after one weeks' treatment were only 15-20% of the expected steady-state level on the same dosage. The importance of a high priming dose when a rapid response is needed is thus emphasised.
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PMID:25-Hydroxyvitamin D levels in patients treated with high-dosage ergo- and cholecalciferol. 19 73

Nephrogenous cyclic AMP (NcAMP), total cyclic AMP excretion (UcAMP), and plasma immunoreactive parathyroid hormone (iPTH), determined with a multivalent antiserum, were prospectively measured in 55 control subjects, 57 patients with primary hyperparathyroidism (1 degrees HPT), and 10 patients with chronic hypoparathyroidism. In the group with 1 degrees HPT, NcAMP was elevated in 52 patients (91%), and similar elevations were noted in subgroups of 26 patients with mild (serum calcium </=10.7 mg/dl) or intermittent hypercalcemia, 19 patients with mild renal insufficiency (mean glomerular filtration rate, 64 ml/min), and 10 patients with moderate renal insufficiency (mean glomerular filtration rate, 43 ml/min). Plasma iPTH was increased in 41 patients (73%). The development of a parametric expression for UcAMP was found to be critically important in the clinical interpretation of results for total cAMP excretion. Because of renal impairment in a large number of patients, the absolute excretion rate of cAMP correlated poorly with the hyperparathyroid state. Expressed as a function of creatinine excretion, UcAMP was elevated in 81% of patients with 1 degrees HPT, but the nonparametric nature of the expression led to a number of interpretive difficulties. The expression of cAMP excretion as a function of glomerular filtration rate was developed on the basis of the unique features of cAMP clearance in man, and this expression, which provided elevated values in 51 (89%) of the patients with 1 degrees HPT, avoided entirely the inadequacies of alternative expressions. Results for NcAMP and UcAMP in nonazotemic and azotemic patients with hypoparathyroidism confirmed the validity of the measurements and the expressions employed.
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PMID:Nephrogenous cyclic adenosine monophosphate as a parathyroid function test. 19 23

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

The prophylaxis and treatment of renal osteodystrophy are based on pathophysiological principles. Development of secondary hyperparathyroidism should be averted by early prevention of hyperphosphatemia through diet and phosphate ligants, and by normalization of the calcium balance through calcium supplements and vitamin D or its analogues. This treatment requires close clinical and laboratory control in order to avoid several hazards (hypercalcemia, hypophosphatemia, and refractory constipation). In cases with severe secondary hyperparathyroidism, subtotal parathyroidectomy is sometimes required. Nevertheless, in one such case this operation resulted in sudden hypoparathyroidism two years postoperatively.
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PMID:[Treatment of renal osteodystrophy: physiopathology and secondary effects]. 33 72

Current concepts concerning the mechanisms, diagnosis and means of treatment of a number of the major causes of hypercalcemia and hypocalcemia are reviewed. In particular, the role of abnormalities in metabolism of vitamin D including (1) excessive hepatic production of 25-hydroxyvitamin D (vitamin D intoxication), (2) increased production of 1 alpha, 25-dihydroxyvitamin D (hyperparathyroidism and sarcoidosis), (3) impaired production of 1 alpha, 25-dihydroxyvitamin D (hypoparathyroidism, renal failure, vitamin-D-dependent rickets type I, pseudohypoparathyroidism) and (4) resistance to 1 alpha, 25-dihydroxyvitamin D; the use of vitamin D and its metabolites therapeutically is discussed.
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PMID:Hypercalcemic and hypocalcemic disorders: diagnosis and treatment. 44 May 8


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