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)

Following an intravenous loading injection of 75 U.S.P. Units of Para-Thor-Mone (Eli Lilly and Co), seven conscious, non-pregnant, non-lactating Merino ewes were infused with a maintenance dose of the hormone at a rate of 4-75 U.S.P. units/min for 2 hr. The classical hypercalcaemia and hypophosphataemia of the non-ruminant was observed, but the hypercalcaemi- was only small. Plasma potassium concentration decreases, while there were no changes in plasma sodium, chloride or mangesium. The classical phosphaturic effect of the hormone was not observed, only trace amounts of phosphate being exreted throughout the experiment. Urinary excretion of calcium and magnesium decreased, urine flow and urinary excretion of sodium, potassium, chloride, bicarbonate and urine pH increased. Glomerular filtration rate was unaffected, but renal plasma flow increased. The concentration and secretion rate of salivary phosphate increased markedly. Changes in the other important salivary electrolytes (sodium, potassium, chloride, bicarbonate and hydrogen ion) also occurred, but it was difficult to separate primary from secondary effects of the hormone. Saliva flow rate increased transiently following hormone injection, but the effect was not sustained by the maintenance infusion.
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PMID:The acute effects of intravenous infusion of parathyroid hormone on urine, plasma and saliva in the sheep. 23 58

A synthetic biologically active derivative of vitamin D (350 microgram of 1alpha-hydroxycholecalciferol [1alpha(OH)CC]) was injected into 2 nonlactating 7-year-old Israeli-Friesian cows. Plasma calcium values increased after 24 hours, peaked at 48 hours, and returned to base-line values 120 hours after injection. An injection of 350 microgram of 1alpha(OH)CC was given to 23 parturient-paresis-prone Israeli-Friesian cows from 7 days to 6 hours prepartum; 13 cows were injected once, 6 were injected twice, and 4 were injected 3 times, all at 48-hour intervals. Parturient-paresis-prone cows (n = 23) of the same breed were used as controls. Within 0 to 36 hours postpartum, plasma calcium concentrations were found to be higher in cows injected with 1alpha(OH)CC than in the control cows. The increase was highly significant (P less than 0.01) in cows injected at least twice. None of the cows injected with 1alpha(OH)CC, within 72 to 24 hours prior to calving developed parturient paresis; but 9 of 23 control cows developed parturient paresis. Prior to calving, none of the injected cows developed hypercalcemia and there was no local or systemic clinically detectable signs of toxiosis. When given at the right time prepartum, 1alpha(OH)CC is considered to be an improvement over previous methods of preventing bovine parturient paresis.
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PMID:Use of 1alpha-hydroxycholecalciferol in the prevention of bovine parturient paresis. 24 72

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 clinical course in two patients with acute renal failure and focal calcifications of skeletal muscle are reported. In the first case renal failure was due to a hypovolemia or shock combined with supercooling and alcoholic intoxication. In the second case a rhabdomyolytic crisis with myoglobinuria occurred. This patient was known to have a McArdle disease. Dialysis treatment was necessary in both cases in order to overcome the oligoanuric phase. Biopsy specimens from biceps muscle showed intense calcium deposits within the necrotic muscle fibres. In the beginning of oliguria remarkable hypocalcemia occurred followed by hypercalcemia. During the polyuric phase which was accompanied by hypercalcemia and hypercalcuria the calcium deposits disappeared completely. This could be demonstrated in our first case by a control biopsy.
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PMID:[Reversible calcification of skeletal muscles in acute renal failure (author's transl)]. 28 Jul 30

Simultaneous determinations of serum total calcium(TOCa), protein corrected total calcium (TOCac), ultrafiltrable calcium (UFCa) and ionised calcium (Ca++) were undertaken in 63 controls and in 76 patients with primary hyperparathyroidism. Raised levels of Ca++ were used as one criterion of the diagnosis which was confirmed by operation in all. For the purpose of estimating the relative value of TOCa and TOCac in the detection of mild hyperparathyroidism we selected all patients with TOCa values below 3.00 mmol/l (n = 46). As a group these patients turned out to be mildly hypoproteinaemic (p less than 0.01), probably because of high age and complicating conditions. Further subdivision of this group into frank hypercalcaemia, borderline hypercalcaemia and normocalcaemia was undertaken according to the respective 99% and 95% confidence limits of normal. Twenty-seven patients were classified as frankly hypercalcaemic by TOCa as well as by TOCac. The distribution of the remaining 19 patients within the three categories was 1:6:12 as judged from TOCa while TOCac gave a better distinction from normal, 9:4:6 (p less than 0.01). This compared well with the classification obtained by UFCa, 10:5:4. It is concluded that TOCac is definitely advantageous to TOCa in the detection of hypercalcaemia in mild primary hyperparathyroidism.
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PMID:Protein correction of serum calcium in mild primary hyperparathyroidism. 28 16

14 patients receiving small doses of predisolone and 7 high doses were divided at random into three groups. Each group received for four weeks, 100 microgram of vitamin D2 or 25 hydroxyvitamin D3 or 5,6 trans-25 hydroxyvitamin D3. The 25 hydroxy and 5,6 trans-25 hydroxyvitamine D3 were able to increase intestinal calcium absorption. 25 Hydroxyvitamin D3 had an osteolytic action, increasing urine calcium and hydroxyproline and, once, in a patient slight hypercalcemia was observed. By constrast, 5,6 trans-25 hydroxyvitamin D3 decreased PTH and caused a significant decrease in urine hydroxyproline.
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PMID:[Effect of cortisone on calcium metabolism. Attempt at correction by 5,6 trans 25-hydroxycholecalciferol, 25-hydroxycholecalciferol and vitamin D2]. 30 29

Tests staged on normal and hypophysectomized rats demonstrated thyroxin to potentiate the general toxic effect of ergocalciferol, with final death of the animals. At the same time, the blood calcium content in animals receiving thyroxin decreases under the effect of the latter. Hydrocortisone, while producing no effect on the high calcium content in the blood of the animals receiving ergocalciferol, attenuates the general toxic action of the latter. These data point to the possibility of dissociating the general toxic action of ergocalciferol and its influence on the blood calcium level, which disproves the existing notion on the correlation between general toxic action of ergocalciferol and hypercalcemia produced by it. Thyroxin and hydrocortisone do not have any effect on the nature of the action exerted by high doses of vitamin A.
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PMID:[Effect of thyroid and adrenal hormones on the course of hypervitaminosis A and D]. 30 61

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

Single administration of 0.25 microgram of sunthetic Ialpha-hydroxycholecalciferol (IalphaOHD3) into nephrectomized rats, maintained at D-avitaminous diet, improved the active transport of calcium ions against the concentration gradient in small intestine of these animals, whereas ergocalciferol was biologically inactive under the same conditions. Administration of IalphaOHD3 during 5 days at a dose 0.025 microgram normalized calcium content in blood serum of rats with D-avitaminosis, Increased doses of IalphaOHD3, administered into intact animals, caused transient hyperphosphatemia, hypercalcemia, calcinosis of internal tissues (kidney heart, aorta) as well as death of some animals. IalphaOHD3 exceeded 400-fold the hypercalcemic and calcinose effects of ergocalciferol. LD50 for IalphaOHD3 was equal to 100 microgram/kg, if it was administered during 5 days per os. Tissue calcinosis was developed after administration of a daily dose 10 microgram/kg, moderate hypercalcemia was caused by a daily dose 1 microgram/kg or 0.25 microgram per an animal; this amount is only 10-fold higher as compared with the physiologic requirement. Ergocalciferol caused hypercalcemia and metastatic calcification only at a dose 4000 microgram/kg. Clinical use of IalphaOHD3 at doses, exceeding the physiologic requirements, has to be prohibited due to high activity of the preparation and to toxicity of its increased doses.
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PMID:[Comparative study of the biological activity and toxic effect of 1alpha-hydroxycholecalciferol and ergocalciferol in rats]. 30 16

The Authors analyse the variation of the calcium plasmatic concentration during extra corporeal circulation (E.C.C.). The Authors remind the importance of the calcium plasmatic concentration preserving a good cardiac output. They say that amount of calcium given assures a good plasmatic concentration and aid the cardiac output after E.C.C. The possible hypercalcemia after A.C.D. blood transfusion doesn't compromit the cardiovascular function.
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PMID:[Behavior of the blood calcium in operations during extracorporeal circulation]. 31 Dec 7


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