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

The treatment of rapidly progressive skeletal demineralisation in myelomatosis has been studied with the help of metabolic calcium balance in two patients; In one, osteoporosis accelerated during treatment with melphalan and prednisolone, although he remained normocalcaemic throughout, suggesting that osteoporosis was aggravated by corticosteroid therapy. In the other patient, who was initially hypercalcaemic, conventional treatment produced clinical remission before eventual relapse with more hypercalcaemia and skeletal dissolution. Both patients were then treated with mithramycin alone, and, although neither obtained haematological remission, bone pain was relieved, hypercalciuria and hypercalcaemia were abolished, and calcium balances proved that mithramycin was effective in restoring calcium equilibrium. The results indicate that mithramycin may abolish excessive bone resorption in myelomatosis and that severe bone dissolution may occur in the absence of hypercalcaemia. Regular determination of 24-hour urinary calcium excretion as well as of plasma-calcium is important in monitoring process. Mithramycin should be considered in the early treatment not only of hypercalcaemia but also of severe hypercalciuria, if these complications do not rapidly remit during the first course of conventional myeloma therapy, with or without steroids. Finally, these results add to evidence that a humoral factor may be responsible for osteoclast stimulation in myelomatosis.
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PMID:Treatment of osteolytic myelomatosis with mithramycin. 4 84

Anorexia, constipation, vomiting and somnolence in a 39-year-old woman were at first misinterpreted as being of psychological and autonomic nervous system origin. Further clinical and biochemical tests revealed hyperthyroidism associated with hypercalcaemia and hypercalciuria. Thyrostatic treatment for 12 days caused regression of the hypercalcaemia and, after subtotal resection, serum calcium levels and urinary calcium excretion returned to normal for good. The hypercalcaemia syndrome must therefore be assumed to have been the direct result of the hyperthyroidism.
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PMID:[Hyperthyroidism with hypercalcaemia (author's transl)]. 5 61

A test was developed to diagnose various forms of hypercalciuria. A two-hour urine sample after an overnight fast and a four-hour urine sample after 1 g of calcium by mouth were tested for calcium, cyclic AMP and creatinine. The 24 patients with absorptive hypercalciuria had normocalcemia and normal fasting urinary calcium (less than 0.11 mg per milligram of urinary creatnine). Urinary calcium was high (greater than or equal to 0.2 mg per milligram of creatinine) after a calcium load. Of the 28 patients with primary hyperparathyroidism (resorptive hypercalciuria), 25 had hypercalcemia and 21 had high fasting urinary calcium. Urinary cyclic AMP, elevated in 30 per cent of fasting patients, was high (greater than 4.60 mu moles per gram of creatinine) in 82 per cent of cases after calcium load. Six patients with renal hypercalciuria had normocalcemia, high fasting urinary calcium, and high (greater than 6.86 mu moles per gram of creatinine) or high-normal fasting urinary cyclic AMP was normal. This simple test should facilitate the differentiation of various causes of hypercalciuria.
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PMID:A simple test for the diagnosis of absorptive, resorptive and renal hypercalciurias. 16 60

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

The effect of the light-darkness cycle on the efficiency of the ultimobranchial and parathyroid glands in altering duodenal calcium transport and plasma and urinary concentrations of calcium was examined in the adult male frog (Rana pipiens). Frogs were unfed, but were allowed access to 0.05 M-CaCl2 in the surrounding medium after ultimobranchialectomy or parathyroidectomy. Calcium transport, as assayed by the everted gut-sac technique, was increased in ultimobranchialectomized frogs at sunrise, concomitant with acute hypercalcaemia and hypercalciuria. An opposite but chronic response was observed in parathyroidectomized frogs with intact ultimobranchial glands. The maximum response observed at sunrise occurred when the concentration of calcium in the plasma of control frogs was decreasing; the minimum response, which occurred 6 h after sunrise, was coincident with a diurnal peak in the concentration of calcium. Vitamin D3 (500 microgram/frog) enhanced calcium transport in ultimobranchialectomized frogs, which resulted in chronic hypercalcaemia and hypercalciuria. The results suggest that diurnal variations in the plasma concentration of calcium do not initiate ultimobranchial activity, but are a response to endocrine control synchronized with the transition from darkness to light.
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PMID:Diurnal variations in the influence of the ultimobranchial glands on calcium homeostasis in the frog (Rana pipiens). 21 89

Three indices of circulating parathyroid hormone (PTH) activity were compared between two groups: the first a group of 23 patients from three large kindreds with autosomal dominant hypercalcemia without hypercalciuria [familial hypocalciuric hypercalcemia (FHH)] and the second a group of 64 patients with typical primary hyperparathyroidism (1HPT) manifesting comparable hypercalcemia. The group with 1HPT differed from normal with respect to plasma PTH 1HPT concentration (normal, less 0.2 ng/ml), urinary cAMP excretion per 100 ml glomerular filtrate (U cAMP/GF) (normal, 2.3 x/divided by 0.6 nmol/100 ml glomerular filtrate; mean, x/divided 1 SD), and renal tubular maximum of phosphate transport corrected for glomerular filtration rate (TMP/GFR; normal, 3.4 +/- 0.4 mg/dl; mean, +/- 1 SD). The group with 1HPT also diverged significantly from the group with FHH for all three indices: for PTH, 0.37 x/divided by .48 vs. 0.25 x/divided .46 (P less than 0.05); for UcAMP/GF, 4.3 x/divided by .53 vs. 2.6 x/divided .60 (P less than 0.0005); and for TMP/GFR, 2.0 +/- 0.6 vs. 2.6 +/- 0.7 (P less than 0.01). The between-group differences for all three indices were also significant after adjustment for their variation with serum calcium. However, only the difference in TMP/GFR remained significant after adjustment for covariance attributable to serum calcium concentration, age, and creatinine clearance. The group with FHH differed from normal for TMP/GFR but not for UcAMP/GF. However, analysis of changes in UcAMP/GF and serum calcium concentration around the time of parathyroidectomy in three patients with FHH suggested that the parathyroid glands contributed to the abnormalities of mineral homeostasis in at least one. It was concluded that higher serum concentrations of PTH do not account for the lower renal clearance of calcium and magnesium in FHH calcium concentration, the group with FHH showed indices suggesting lower circulating PTH activity than the group with 1HPT.
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PMID:Circulating parathyroid hormone activity: familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism. 23 92

Using a whole body radiation detector, we have measured the total body retention of 47-Ca 7 days after oral administration of the isotope to patients with various disorders of calcium metabolism. The percent retention of 47-Ca given with 90 mg of unlabeled (carrier) calcium varied with the calcium metabolic status as follows: normals (n equals 14), 33-43 percent (mean 38); primary hyperparathyroidism (n equals 28), 32-74 percent (mean 52); idiopathic hypercalciuria (n equals 9), 34-49 percent (mean 42); and hypercalcemia of other etiology (n equals 3), 23-26 percent (mean 25). Almost half (13/28) of those with hyperparathyroidism showed a retention above 55 percent, distinguishing them from subjects with idiopathic hypercalciuria. Retention of 47-Ca correlated poorly with clinical measures of severity of hyperparathyroidism. When isotope was diluted with a smaller amount of carrier calcium (20 mg), retention was increaseed in normals (n equals 5) to 46-54 percent (mean 50) and in hyperparathyroidism (n equals 5) to 64-87 percent (mean 73). After surgical cure of hyperparathyroidism retention of isotope returned toward normal in 5 of 7 subjects. Whole body retention of orally administered 47-Ca may prove useful in detecting hyperparathyroidism in subjects with mild hypercalcemia or hypercalciuria.
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PMID:Total body retention of orally administered 47-calcium in primary hyperparathyroidism. 23 21

Catecholamines induce bone resorption and hypercalcaemia by the beta-adrenergic effect in bone and hypercalciuria by the alpha adrenergic effect in kidney. The interplay between the alpha-adrenergic hypercalciuria and beta-adrenergic hypercalcaemia explains why in some, but not all, phaeochromocytomas hypercalcaemia occurs. The hypothesis predicts hypercalciuria in both phaeochromocytoma and neuroblastoma. In hyperthyroidism, negative calcium balance and hypercalcaemia cannot be attributed to the direct effect of thyroid hormones on the bone but can be explained by augmentation of the catecholamine effects on bone and kidney by thyroid hormones. The hypothesis offers a solution for an apparent paradox in hyperthyroidism of increased urinary cAMP while nephrogenous cAMP is decreased. It also explains why propranolol corrects hypercalcaemia without influencing renal calcium loss.
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PMID:Catecholamines cause the hypercalciuria and hypercalcaemia in phaeochromocytoma and in hyperthyroidism. 33 Oct 32

In the literature there is a paucity of references on urolithiasis in children with spinal cord injury. In this paper 28 cases of urolithiasis in 97 children with spinal cord injury are analysed. An attempt is made to evaluate the role of hypercalcemia, hypercalciuria and urinary tract infection in the genesis of these calculi.
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PMID:Urolithiasis in children with spinal cord injury. 43 66

Fifteen cases of hypervitaminosis D in childhood are reviewed. In all of them, vitamin D was given following medical prescription. In four occasions, excessive dosage of vitamine D impaired the evolution of a previous nephropathy. The clinical, analytical, radiological and histological findings as well as the therapeutical aspects are commented. Hypercalcemia, hypercalciuria, polyuria with hypostenuria, renal failure, bone lesions and nephrocalcinosis are the most prominent features of the picture. Occasionally, arterial hypertension and glycosuria were found. Prednisone, thyrocalcitonine and phosphates were used as therapeutical means. In spite of nephrocalcinosis and renal failure generally present at diagnosis, the clinical course was rather good.
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PMID:[Hypervitaminosis D. Review of fifteen cases]. 44 41


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