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)

To determine the functional capabilities of the parathyroid glands, 17 EDTA infusions were given to 11 children (ages 1 month to 12 years) and to two mothers of four of the children. Serum ionized Ca fell from 4.1 mg/dl to 3.4 mg/dl. Excessive parathyroid hormone responses were elicited during seven of nine EDTA infusions in five children and in one adult with hypophosphatemic rickets, during the active phase of rickets. In four of five subjects with problems related to hypercalcemia, borderline low or undetectable PTH responses were elicited. Three relatively normal PTH responses were obtained, two in an infant after phosphate-induced hypocalcemic tetany was corrected, and one in a child with a malabsorption syndrome. The renal tubular reabsorption of phosphate was inversely related and the urinary cyclic AMP excretion was positively related to the PTH response. Thus EDTA infusions in infants and children might be useful in the identification of hyper-, normo-, or hypoparathyroid states and would be of value in defining the functional condition of the parathyroid glands in children with deranged Ca or P metabolism.
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PMID:Parathyroid function tests with EDTA infusions in infancy and childhood. 17 44

States of hypersecretion of PTH may occur primarily, or in response to other physiologic abnormalities. Primary hyperparathyroidism must be considered in the differential diagnosis of hypercalcemia, nephrolithiasis, metabolic bone disease, and pancreatitis and peptic-ulcer disease. The clinical manifestations of this disease have become more subtle with improved detection. The serum calcium level is almost always elevated, and when it it accompanied by relatively high serum PTH levels or increased urinary cAMP excretion, the diagnosis is usually secure. Findings of hypophosphatemia, decreased renal tubular reabsorption of phosphorus, hypercalciuria, and characteristic roentgenographic changes support the diagnosis of hyperparathyroidism, but are not prerequisites for that diagnosis. Most cases will come to operation, and experienced intraoperative assessment is necessary for the correct distinction between multiglandular disease and that involving only a single gland. We expect that a clearer understanding of the histopathologic features of these diseases, and improvement in the methods for measurement of PTH will be the main areas of advancement in the diagnosis of hyperparathyroidism in the next few years.
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PMID:Diagnosis of hyperparathyroidism. 19 30

In a patient with hypercalcaemia secondary to a renal-cell carcinoma, a concentration gradient of bioactivity was detected between the tumour effluent vein and the peripheral venous blood that was capable of stimulating adenylate cyclase in bone cells. Immuno-reactive PTH was undetectable in the tumour effluent and in the peripheral blood. It is concluded that a non-parathyroid humoral factor whose action involved cyclic AMP stimulation was responsible for the hypercalcaemia.
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PMID:Humoral hypercalcaemia in a patient with renal-cell carcinoma. 21 93

The occurence of hypercalcemia appears to be unusual in leukemia. The mechanisms are numerous: secretion of PTH of PTH like substance, prostaglandin E2 or vitamin D like sterols. The reported case is one of lymphoblastic acute leukemia and hypercalcemia associated with osteoclast activating factor secreted by leukemic cells. In this patient the serum levels calcium closely paralleled the course of acute leukemia.
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PMID:[Hypercalcemia and osteoclast activating factor (OAF) associated with acute lymphoblastic leukemia (author's transl)]. 22 85

Twelve children with chronic renal failure (CRF) and sixteen children receiving regular dialysis therapy (RDT) were treated with between 10,000 and 50,000 IU of vitamin D daily. This was associated with an increase in serum calcium levels and reduction in PTH levels. In the children with CRF, secondary hyperparathyroidism was improved with treatment but its development was not completely prevented nor was healing complete. In the patients receiving RDT, treatment with vitamin D improved the changes associated with secondary hyperparathyroidism in 50% of cases but these features sometimes reappeared despite continuing treatment. Hypercalcaemia or metastatic calcification was not seen. Subsequently, 1,25(OH)2D3 was administered to 14 children receiving RDT. This was associated with the return of serum calcium levels to normal, inhibition of PTH synthesis and an improvement in intestinal calcium absorption. Fibro-osteoclasia was cured and there was improvement in actual bone resorption. There was also improvement in osteoidosis in those children who showed disturbances of mineralisation. Calcification in the limbus area of the eyes may occur and hypercalcaemia was seen commonly. Treatment with 1,25(OH)2D3 should only be offered to children with severe renal bone disease. Neither vitamin D3 nor 1,25(OH)2D3 can guarantee complete recovery of osteodystrophy and of growth arrest in uraemic children.
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PMID:Renal bone disorders in children: therapy with vitamin D3 or 1,25-dihydroxycholecalciferol. 23 17

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

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

Hypercalcemia after renal transplantation (post-T hypercalcemia) has been detected in 29 (16.7%) of 174 long-term survivors. The mean time of onset of hypercalcemia was 69 days after renal transplantation (range 3-210). In 18 patients the hypercalcemia was mild and resolved spontaneously (transient) from 2-65 months (mean 19) after onset. In 4 patients serum calcium normalized concurrently with rejection episodes. In 7 patients the hypercalcemia was more pronounced (permanent), being terminated by subtotal parathyroidectomy in 5 and persisting in 2 recipients. The hypercalcemia was asymptomatic except in one patient, who developed calculi in the graft and a fall in graft function, all of which disappeared after parathyroidectomy. At operation the parathyroid glands showed hyperplasia, except in one case with an adenoma in one of the hyperplastic glands. Serum phosphorus was markedly decreased, to the same extent in transiently and permanently hypercalcemic recipients. Serum parathyroid hormone (S-PTH) was increased in all of 5 patients with permanent and in 3 of 8 with transient post-T hypercalcemia. In normocalcemic and in transiently hypercalcemic recipients the mean S-PTH was identical, but significantly lower than in the permanently hypercalcemic recipients. S-PTH was suppressed to the same extent during an i.v. calcium infusion in patients with post-T hypercalcemia and with primary hyperparathyroidism.
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PMID:Hypercalcemia and parathyroid function after renal transplantation. 31 22

Hypercalcemia after renal transplantation (post-TH) was detected in 32 (17%) of 188 long-term survivors. The mean time from renal transplantation (RT) till onset of post-TH was 60 (3-210) days. In 19 patients the hypercalcemia was mild and transient, resolving spontaneously within 1-65 (mean 18) months. In 6 patients s-calcium normalized simultaneously with a rejection episode treated with increased prednisone doses. The hypercalcemia was more pronounced (permanent) in 7 patients, and terminated by subtotal parathyroidectomy in 5 and still persists in 2. The hypercalcemia was asymptomatic and did not affect the function of the graft except in one patient who developed calculi in the graft and a fall in graft function, all of which disappeared after subtotal parathyroidectomy. The frequency of aseptic bone necrosis and spontaneous fractures was the same in recipients with and without post-TH. Serum parathyroid hormone (s-PTH) was significantly higher in patients with permanent than in those with transient post-TH, who had the same slight elevation of s-PTH as the normocalcemic recipients. A permanent course of post-TH can be expected when both s-calcium and s-PTH are persistingly elevated.
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PMID:The clinical significance of hyperparathyroidism after renal transplantation. 35 92

The prevalence and duration of secondary hyperparathyroidism in 42 renal transplant recipients, and the sequelae of this condition, were studied. Immediately before transplantation, an elevated PTH-value was recorded in 76% of the patients, postoperatively there was a marked drop. Early after successful transplantation, 57% of the patients had hypercalcemia. At follow-up 3 years later, moderate hypercalcemia persisted in half of the patients but only 3 patients had significantly elevated PTH. The quality of renal graft function was not inferior in the hypercalcemic patients. Subperiosteal bone resorption and soft tissue calcifications were more common among the hypercalcemic patients. Our data suggest that secondary hyperparathyroidism can be managed conservatively in most renal transplant recipients. If progressive bone changes occur, surgical removal of parathyroid tissue should be considered.
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PMID:Secondary hyperparathyroidism and its sequelae in renal transplant recipients. Long term findings in a series of conservatively managed patients. 35 96


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