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

Plasma calcium was measured routinely as a part of profile screening of patients admitted to a geriatric department. Pathological hypercalcaemia was found in 1.33% of those screened, the cause being bone metastases (29%), hyperparathyroidism (21%), bronchial carcinoma without bone metastasis (18.5%), lymphosarcoma without bone metastasis (8%) and multiple myeloma (2.5%). There remained a further group of patients with hypercalcaemia and renal failure (21%) in whom diagnosis was often obscure. Where renal function was normal, discriminant analysis showed that the four main diagnostic groups were biochemically distinguishable. Discriminant analysis thus seems likely to be of practical value in the differential diagnosis of hypercalcaemia in elderly patients with normal renal function, but requires prospective validation.
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PMID:Hypercalcaemia in elderly hospital in-patients: value of discriminant analysis in differential diagnosis. 57 68

All patients with hyperparathyroidism seen in a large referral military hospital within a twenty month period underwent neck exploration by one of us (HN). Three patients were found to have an unsuspected solid thyroid nodule measuring 0.5 to 1.5 cm. All were widely excised by thyroid lobectomy and isthmectomy and found to be follicular or papillary carcinoma of the thyroid. These three patients join thirty-one previously reported clinical cases documenting an association between parathyroid adenoma and nonmedullary carcinoma of the thyroid. Because of the high potential for malignancy in this clinical setting, we urge careful examination and palpation of the thyroid gland during neck exploration for hypercalcemia in order to detect and cure "early" malignancies of the thyroid.
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PMID:Unsuspected nonmedullary carcinoma of the thyroid in patients with hyperparathyroidism. 59 48

Between 1972 and 1976 15 patients with chronic renal failure of different aetiology and varying severity were observed who developed 23 hypercalcaemic phases during treatment with calcium-containing drugs. 12 instances of hypercalcaemia occurred during conservative treated during conservative treatment (serum creatinine 177-1061 mumol/l, equivalent to 20-120 mg/l) and 11 during chronic haemodialysis (serum creatinine 707-1061 mumol/l, equivalent to 80-120 mg/l). In 15 cases hypercalcaemia was caused by a hexacalciumhexasodium-heptacitratehydrate complex (Acetolyt), in 6 cases by the combined use of this drug with calcium ion-exchange resins on a calciumpolystyrolsulfonate base, and in two cases by the use of calcium tablets and calciumpolystyrolsulfonate, respectively. The daily doses of these drugs were in the usual therapeutic range in most cases. Deterioration of renal function was observed in two cases and coma in a further two cases. In 5 cases gastric ulcers were demonstrated. Three patients died. In no patient was there evidence of florid hyperparathyroidism. Treatment with calcium-containing drugs in patients with renal failure should only be carried out under regular control of calcium concentrations.
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PMID:[Hypercalcaemic crises in patients with chronic renal failure caused by ion-exchange resins, antacidotics and other calcium-containing drugs (author's transl)]. 59 99

Patients with severe symptomatic renal osteodystrophy were treated with either 1,25(OH)2D3 or 1 alpha(OH)D3. In 39 instances, there was either reversal of symptoms and/or a marked fall in plasma alkaline phosphatase. Bone biopsies showed improvement of either osteomalacia or osteitis fibrosa, and serum iPTH often fell. In thirteen patients, no improvement occurred. In seven patients, bone biopsy disclosed osteomalacia, and serum iPTH was normal or only slightly elevated. Thus, there was a defect in mineralisation. apparently unrelated to the lack of 1,25(OH)2D3 and in the absence of evidence of phosphate depletion. The other 'treatment failure' group showed osteitis fibrosa on biopsy and iPTH levels were markedly elevated. They are presumed to have marked secondary hyperparathyroidism. These 'treatment failure' groups had higher pre-treatment levels of serum Ca and Mg than in those showing a favourable response; also, hypercalcaemia developed rapidly during 1,25(OH)2D3 treatment. Thus, 1,25(OH)2D3 is efficacious in treating symptomatic osteodystrophy in many uraemic patients, and in other patients, it may help identify bone disease of other, as yet unknown, pathogenesis.
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PMID:Use of 1,25(OH)2-vitamin D3 to separate 'types' on renal osteodystrophy. 60 Sep 61

The surgical management of primary hyperparathyroidism with severe bone disease (and tertiary hyperparathyroidism) has frequently been complicated by severe and prolonged post-operative hypocalcaemia. In seven such cases a short-pre-operative course of 1alpha-hydroxyvitamin D3 has been found to abolish these adverse features virtually completely and even to diminish pre-operative symptoms where present. Exacerbation of hypercalcaemia has not occurred and this regimen is thus recommended as a routine measure.
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PMID:1alpha-hydroxyvitamin D3 in primary hyperparathyroidism. 60 19

Neonatal hyperparathyroidism usually presents as a "failure to thrive" syndrome. It may be transmitted as an autosomal dominant trait and may involve more than one offspring. We report on two brothers with neonatal primary hyperparathyroidism. One underwent a total parathyroidectomy and has lived for 14 years. Hyperparathyroidism was found in their father, suggesting autosomal dominant inheritance. The disease is fatal unless recognized early and treated. The characteristic pathological change is chief cell hyperplasia of the parathyroid glands. Near-total parathyroidectomy is the minimal operation required to control the hypercalcemia. Permanent hypoparathyroidism may be the sequel of appropriate surgical management. Treatment of the totally parathyroidectomized infant, however, is possible and can result in normal growth and development.
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PMID:Hereditary neonatal hyperparathyroidism. 61 57

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. 63 70

Hypercalcemic crisis is a rare but often fatal complication of hyperparathyroidism (HPT). The reported mortality of 60% has been related to delay in diagnosis and appropriate treatment. During a 16-year period (1961 to 1977), 29 patients with severe symptomatic hypercalcemia caused by primary HPT were treated at the Surgical Service at the University of Michigan Hospital. This group represents 6% of the patients with primary HPT treated during this period. All but one patient had an exploration of the neck when the serum calcium level had been decreased to 12 mg/100 ml by intravenous hydration with saline, furosemide diuresis, and mithramycin when a hypocalcemic agent was required. One comatose patient died of irreversible shock. All of the 28 patients who had parathyroidectomies survived the early postoperative period. One patient died three weeks later of a myocardial infarction. This study demonstrates that emergent nonoperative care of parathyroid crisis, followed promptly by parathyroidectomy, can be successful in nearly all cases.
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PMID:Management of severe hypercalcemia caused by primary hyperparathyroidism. 63 7

We describe a boy who presented at 4 years of age with radiological hyperparathyroidism, osteosclerosis, and necrosis of the femoral heads. Plasma biochemistry was normal but the parathyroid hormone (PTH) level was very high. He was deaf and had an unusual facies but did not have the phenotype of Albright's hereditary osteodystrophy. Plasma and urine cyclic AMP reponses to bovine PTH were markedly subnormal. Vitamin D produced sustained hypercalcaemia and a fall in plasma phosphorus. After four hyperplastic parathyroid glands were removed he became hypocalcaemic and plasma phosphorus rose. After operation he remained unresponsive to exogenous PTH; We suggest that he had a form of pseudohypoparathyroidism without the phenotype of Albright's hereditary osteodystrophy and with some residual skeletal and renal responsiveness to PTH.
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PMID:Normocalcaemic pseudohypoparathyroidism with unusual phenotype. 64 42

Various hormones have been implicated in the genesis of hypercalcemia in patients with malignancy. Ectopic secretion of PTH by tumor has been documented in only a few patients; rather, elevated levels of circulating iPTH have been presumed to reflect tumor production of hormone in most patients. Small fragments of PTH, as well as polypeptides larger than native PTH, have been described; their biological roles are unclear. The pattern of immunoreactivity, however, has been used to differentiate patients with ectopic hyperparathyroidism from patients with concomitant primary hyperparathyroidism. Vitamin D-like sterols produced by breast cancer seldom reach plasma levels necessary for physiological effects. Members of the prostaglandin family have been proposed to induce hypercalcemia through osteoclast activation or alteration of the immune system and also to affect the frequency of bone metastases. At present, no direct evidence is available to prove a direct role for these effects and prostaglandins are most useful as possible indicators of disease activity.
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PMID:Mechanisms of hypercalcemia in malignancy. 65 92


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