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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Hypercalcemia is a not infrequent complication of cancer that every physician should be aware of. It is a significant factor in the morbidity and mortality of cancer patients. Almost invariably hypercalcemia is associated with accelerated resorption of bone, which is thought to be mediated by humoral or metabolic factors. Three such factors, parathyroid hormone, E2 prostaglandins and osteoclast activating factor, have been strongly implicated in the pathogenesis of hypercalcemia in cancer patients. Other mechanisms for the hypercalcemia may exist. Accurate diagnosis of the disorder is important in therapy, and current research into the various mechanisms for hypercalcemia in cancer patients may well lead to new modes of therapy that are more specific and perhaps less toxic.
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PMID:Hypercalcemia and cancer: an update. 36 55

Our results with radioimmunoassay studies for parathyroid hormone performed during the last 6 years are compared retrospectively to results of the laboratory tests customarily secured when hyperparathyroidism is suspected. The results obtained in patients with known primary hyperparathyroidism and in patients with unconfirmed but presumptive hyperparathyroidism are compared to the results obtained from a group of normal controls. Despite the fact that certain discrepant results were noted in the earlier assay techniques the over-all results and, in particular, those of more recent years have been highly sensitive and reproducible corroboratives of the existence of primary hyperparathyroidism. About two-thirds of the patients with primary hyperparathyroidism will present to the urologist. All patients with calcium-containing stones should have at least 3 determinations of the serum calcium in screening for primary hyperparathyroidism. The radioimmunoassay for parathyroid hormone provides the most reliable confirmation. The patient with calculous disease, elevation of the immunoreactive parathyroid hormone level and hypercalcemia is virtually certain to have primary hyperparathyroidism.
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PMID:Experience with the radioimmunoassay for parathyroid hormone in the diagnosis of primary hyperparathyroidism. 36 90

Six long-term hemodialysis patients with progressive skeletal deterioration during long-term pharmacologic vitamin D2 therapy were treated for six to 12 months with oral 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) to determine its therapeutic effectiveness in vitamin D2-unresponsive osteodystrophy. On bone biopsy, three of the patients had severe osteomalacia and three showed predominant osteitis fibrosa. Previous therapies, including phosphate binders and dialysis schedules, were maintained. The three patients with osteomalacia and the two with osteitis fibrosa showed clinical deterioration. There was no significant change in serum calcium, phosphate, alkaline phosphatase, bone densitometry, immunoreactive parathyroid hormone levels or bone histology. Roentgenograms showed multiple new fractures of ribs and femoral necks in the patients with osteomalacia and increased bone resorption in two of three patients with osteitis fibrosa. 1,25-(OH)2D3 dosage had to be decreased in all patients because of hypercalcemia with a mean tolerated dose of 0.22 microgram/day. In these patients, 1,25-(OH)2D3 was not effective therapy for progressive osteodystrophy unresponsive to pharmacologic vitamin D2.
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PMID:Experience with 1,25-dihydroxycholecalciferol therapy in undergoing hemodialysis patients with progressive vitamin D2-treated osteodystrophy. 38 92

A group of seven children with different malignant processes presenting with hypercalcemia was studied. Bone destruction, diffuse metabolic abnormalities, abnormal acid-base homeostasis and recurrent hypercalcemia characterized these patients. A different mechanism leading to the production of hypercalcemia and/or bone destruction by cancer cells is considered. The results of this report suggest that parathyroid hormone production (P.T.H.) by the parathyroid glands is normal and that ectopic secretion of PTH or PTH-like material is negligible in these cases.
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PMID:Hypercalcemia complicating childhood malignancies: a report of seven cases with some pathophysiological considerations. 38 12

A woman with metastatic carcinoma of the breast developed hypercalcemia 39 months after mastectomy. The hypercalcemia remitted after treatment but recurred 12 months later, accompanied by elevated levels of serum immunoreactive parathyroid hormone (PTH). A urea/HC1 extract of hepatic metastases contained immunoreactive PTH, material which stimulated the resorption of fetal rat bone in tissue culture, and material which stimulated chick renal adenylate cyclase activity. These findings strongly suggest that this breast cancer produced a PTH-like substance.
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PMID:Carcinoma of the breast associated with hypercalcemia and the presence of parathyroid hormone-like substances in the tumor. 42 76

An assessment of free and total calcium measurements was made in 691 patients with suspected hypercalcemia or disorders often associated with hypercalcemia. In 18.9% of the 1049 specimens analyzed from nine different patient groups, a different impression of hypercalcemia was obtained depending on whether the free or total calcium was considered. Analysis of the ratio of free to total calcium indicated that there are two main factors which influence the distribution of calcium in the serum of hypercalcemic patients: the concentrations of albumin and parathyroid hormone. A lowered albumin concentration accounted for the altered distribution of calcium in patients with malignancies and partially accounted for the altered distribution in patients postrenal transplantation. In patients with confirmed primary hyperparathyroidism a higher ratio of free to total calcium was found, which could not be explained by alterations in protein, albumin, pH, or CO2 content but was related to parathyroid hormone concentration. Free calcium appears to be a slightly better indicator of elevated calcium states than total calcium. Measurements of free calcium should be particularly useful in patients with altered albumin concentration, with multiple myeloma in whom a calcium-binding protein could be present, after renal transplantation, and with suspected hyperparathyroidism and normal or slightly elevated total calcium values.
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PMID:Relationship of free and total calcium in hypercalcemic conditions. 42 92

Two patients with hypercalcemia and hyperthyroidism had elevated levels of parathyroid hormone (PTH). When the patients were made euthyroid with appropriate medical therapy, both the levels of PTH and calcium returned to normal. Since thyroid hormone can increase tissue responsiveness to catecholamines, and since catecholamines can stimulate PTH secretion, we postulate that the elevated levels of PTH were secondary to thyrotoxicosis. In patients with coexisting hyperthyroidism and hyperparathyroidism, primary hyperparathyroidism should only be diagnosed when the patient is eumetabolic.
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PMID:Thyrotoxicosis, hypercalcemia, and secondary hyperparathyroidism. 44 69

There are conflicting reports on the effect of insulin on plasma Ca concentration in rats. Low doses appear to decrease and higher doses to increase plasma Ca. Since birds are known to be very sensitive to parathyroid hormone and have resistance to the hypoglycemic effects of insulin, the effect of commercial and highly purified insulin on plasma Ca concentration was studied in 10-day-old chicks 60 min after the administration of the hormone. Both commerical bovine and purified porcine insulin provoked a dose-related elevation of plasma Ca. Although hypophosphatemia was observed with the highest dose of insulin used (0.4U), hypercalcemia was observed with 0.05 U insulin, a dose that did not modify plasma phosphate concentration. The slopes of the dose-response curves of insulin and parathyroid hormone were indistinguishable and different from that of 1 alpha-hydroxyvitamin D3. Neither propranolol nor deprivation of vitamin D altered the hypercalcemic response to insulin. Unexpectedly, propranolol (40 microgram/chick) provoked elevation of plasma Ca. It is concluded that insulin raises plasma Ca concentration in the chick by a mechanism(s) not yet elucidated.
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PMID:Hypercalcemic effect of insulin in the chick. 44 96


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