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)

Radionuclide imaging with Tc-99m diphosphonates is not an effective method for detecting or ruling out most osteoporotic diseases including senile osteoporosis or accelerated postmenopausal osteoporosis, and the slow loss of bone tissue generally remains undetected by this modality. Nonetheless, it frequently surpasses or supplements radiographic findings in evaluating the focal complications of metabolic bone disease, including fractures, microfractures, stress fractures, vertebral compressions, Milkman-Looser zones, aseptic necrosis, and acute infarction. In contrast to its secondary role in osteoporosis, bone imaging is of prime importance in investigating hypercalcemia, because the major cause of this abnormality is skeletal metastatic malignancy. In defective bone mineralization due to hyperparathyroidism or osteomalacia, a general increase in diphosphonate skeletal uptake is detected more frequently than radiographic abnormalities. However, normal skeletal images do not rule out metabolic bone disease. Biochemical testing is more reliable in detecting primary hyperparathyroidism. On the other hand, in renal osteodystrophy, biochemical abnormalities are variable and bone imaging is helpful in assessing the severity of skeletal involvement, but not its etiology. Many methods of quantitating the kinetics of Tc-99m diphosphonates have been explored, such as plasma clearance, bone-to-soft-tissue ratios, 24-hour total body retention and 24-hour urinary excretion. None of these have been widely accepted. The value of bone imaging is established in other systemic diseases, most notably in Paget's disease, hypertrophic pulmonary osteoarthropathy, sickle cell disease, fibrous dysplasia, and sympathetic dystrophy.
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PMID:Radionuclide imaging in metabolic and systemic skeletal diseases. 331 47

Hypercalcemia is associated with a few primary malignant neoplasms and with a variety of tumors that have spread by metastases. Hyperparathyroidism is a diagnosis that is usually not considered in these patients. At our institution, 18 patients with malignant tumors presented over a 6-year period with hypercalcemia caused by hyperparathyroidism. There were five men and 13 women with a mean age of 48 years (range 24-87 years). Primary tumors in these patients included colon carcinoma (four cases), breast carcinoma (four cases), lymphoma (four cases), thyroid carcinoma (four cases), Paget's disease (one case), and lung carcinoma (one case). Metastases of the primary tumor occurred in seven patients, and in 11 patients the tumor was not metastatic or recurrent. Serum levels of calcium, phosphate, and chloride averaged 11.8 mg/dl, and 100 mEq/liter, respectively. C-terminal parathyroid hormone (PTH) levels ranged from 300 to 1,900 pg/ml with an average of 1,150 pg/ml (normal 50-340 pg/ml). At operation, a single parathyroid adenoma was discovered in 15 patients, and four-gland hyperplasia was noted in three patients. In all cases, serum levels of calcium returned to normal after operation. We conclude that patients with malignant tumors and concomitant hypercalcemia should be evaluated for the possibility of hyperparathyroidism. In cases of primary hyperparathyroidism, elevated C-terminal PTH level should be diagnostic. If hyperparathyroidism is determined to be the cause of hypercalcemia, neck exploration and parathyroidectomy are indicated.
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PMID:Malignancy and concomitant primary hyperparathyroidism. 333 14

The changes of parathyroid hormone (PTH) and of vitamin D metabolites after intravenous administration of the bisphosphonate APD were studied in ten patients with Paget's disease of bone and in ten patients with tumour-induced hypercalcaemia. After APD all patients with Paget's disease became hypocalcaemic and showed an increase in both N-PTH and C-PTH values. Patients with malignancies had a nearly six-fold greater decrease in serum calcium but rises in N-PTH and C-PTH were observed only in those who developed hypocalcaemia. Overall, a clear rise in PTH was found when serum calcium fell below 2.20 mmol/l. Basal 25-hydroxy- and 24,25-dihydroxyvitamin D concentrations were similar in the two groups and showed no change after APD treatment. Circulating 1,25-dihydroxyvitamin D, however, increased in all patients with Paget's disease and in six of the hypercalcaemic patients. It is concluded that the main regulator of PTH secretion is the concentration of calcium per se rather than the magnitude or the rate of its change. The production of 24,25-dihydroxyvitamin D is not affected by wide variations in serum calcium while that of 1,25-dihydroxyvitamin D is sensitive to these changes.
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PMID:Effects of decreasing serum calcium on circulating parathyroid hormone and vitamin D metabolites in normocalcaemic and hypercalcaemic patients treated with APD. 350 18

A 32 year old man presented on two separate occasions with severe hypercalcaemia. Both episodes followed the fracture of a single pagetic bone but were not associated with immobilization. To our knowledge this patient, the youngest described with hypercalcaemia secondary to Paget's disease of bone is also the only reported case of recurrent hypercalcaemia in this condition.
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PMID:Recurrent hypercalcaemia in a young man with mono-ostotic Paget's disease. 377 81

Porcine calcitonin in a slow-release gelatin vehicle was given by intramuscular injection to 10 patients-four with primary hyperparathyroidism, four with Paget's disease, and two with carcinoma of the breast and hypercalcaemia. All cases showed a fall in serum calcium with an immediate rise in urine calcium. All except three patients with primary hyperparathyroidism showed a fall in serum phosphorus, but an immediate rise in urine phosphorus occurred in all cases. Urine hydroxyproline output fell in three patients with severe Paget's disease. Urine sodium rose in all cases, but the effects on potassium, magnesium, water, and pH were not appreciably different from results obtained in four control subjects who were given the gelatin vehicle alone.The data suggest that calcitonin caused a decrease in the tubular resorption of calcium and phosphorus. The hypocalcaemic effect appeared to be due to a decrease in bone resorption in the patients with Paget's disease but in the remaining cases could be accounted for in part or entirely by the rise in urine calcium.
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PMID:Renal effects of calcitonin. 546 Aug 39

A new radioimmunoassay for human parathyroid hormone (PTH) in serum, which can measure the hormone present in 94% of the normal sera tested, is described. It is based on the ability of human PTH to compete with (131)I-labeled bovine PTH for binding to an antiserum directed against porcine PTH. This antiserum distinguishes between human PTH extracted from parathyroid adenomata and that present in hyperparathyroid sera. Evidence is given to suggest that this is due to immunochemical changes in the hormone extracted from adenomata and not to immunochemical heterogeneity of the hormone present in serum. Physiologic data supporting the validity and specificity of the assay are presented. Induced episodes of hypercalcemia and hypocalcemia resulted in appropriate responses in serum immunoreactive PTH (IPTH) in normal subjects and in patients with Paget's disease of bone. In normals, there was a progressive increase in serum IPTH in the late afternoon and evening, suggesting a diurnal secretory rhythm. A negative correlation was found between the serum calcium and serum IPTH over the normal range of serum calcium values; a positive correlation was found between these variables in patients with primary hyperparathyroidism. There was apparent overlap between serum IPTH values in normal subjects and patients with primary hyperparathyroidism, but formal discriminate analysis of values for serum calcium and IPTH demonstrated separation of these two groups, without overlap.
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PMID:Radioimmunoassay of human parathyroid hormone in serum. 554 77

(Asu) E-CT is a deaminodicarba-analog of the synthetic eel-calcitonin (E-CT) that shows specific activity and the potency reasonably high in comparison with that of the most potent natural hormone. The structure of its molecule indicates that the disulphide bond in calcitonins is not essential for the biological activity but only for the maintenance of the specific conformation by forming an intramolecular bridge. The instability of calcitonins should mainly be attributed to the presence of the disulfide bond and (Asu)E-CT proved to be more stable "in vitro" than native calcitonins. The more prolonged hypocalcemic effect of E-CT and its aminosuberic analog (Asu)E-CT has been accounted for to a greater stability of and persistence at the receptor site. (Asu) E-CT has been largely studied in Japan on experimental animals and successfully used in the treatment of hypercalcemia in man. On the contrary investigations on human administration of this analog are very scarce. The present paper reports studies carried out in normal subjects and Paget's disease patients to investigate the effects of (Asu)E-CT in man in comparison with the effects of synthetic human calcitonin (H-CT) and synthetic salmon calcitonin (S-CT). Two different experimental procedures have been used: 1) rapid intravenous injection of (Asu)E-CT (80 MRC. U.) or respectively of H-CT and S-CT (100 MRC. U.) in 15 subjects (7 normals and 8 with Paget's disease); 2) slow 7 days continuous subcutaneous infusion of similar daily amounts of (Asu)E-CT, H-CT and S-CT administered by a microjet pump device in 21 subjects (7 normals and 14 with Paget's disease). The intravenous administration of (Asu)E-CT induced a rapid and persistent decrease in total plasma calcium, ionized calcium and plasma phosphate that was more evident in Paget's disease patients than in normal subjects. No clearly cut differences have been observed with the hypocalcemic and hypophosphatemic effect of H-CT and S-CT administered intravenously; nevertheless the hypocalcemic effect proved to be more persistent in Paget's disease patients treated with (Asu)E-CT. After intravenous infusion of (Asu)E-CT the plasma level of cAMP rose more evidently in pagetic than in normal subjects but the rise was lower than in H-CT and S-CT treated subjects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Asu(1,7)E-CT, an analog of eel calcitonin. A comparative study in man with reference to other synthetic calcitonins]. 608 15

30 patients with disorders of calcium metabolism were treated with dichloromethylene diphosphonate (C1(2)MDP, or clodronate disodium), an inhibitor of bone resorption. 13 patients with Paget's disease of bone were given C1(2)MDP by mouth (1.6 g/day). Serum-alkaline-phosphatase and urinary hydroxyproline fell to normal or near-normal within 3-7 months, and there was a clinical improvement in all but 1 patient. C1(2)MDP (0.8-3.2 g/day) also reduced plasma-calcium and urinary calcium in 17 patients with hypercalcaemia due to primary hyperparathyroidism or secondary to malignant disease. C1(2)MDP seems to be an effective oral drug for inhibiting excessive bone resorption in man.
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PMID:Effect of dichloromethylene diphosphonate in Paget's disease of bone and in hypercalcaemia due to primary hyperparathyroidism or malignant disease. 610 89

(Asu1,7) E-CT (carbocalcitonin-elcatonin) is the aminoasuberic analogue of eel calcitonin differing from the natural hormone in that an ethylene bridge replaces the disulphide bridge in position 1-7. This modification preserves the conformation of natural calcitonin but enhances the physical, chemical and biological stability of the molecule. This in its turn facilitates maximum purification of the product as well as enhancing its resistance to degradation both in vitro and in vivo. The specific activity of carbocalcitonin is equivalent to 5000 U.MRC/mg and it possesses all the pharmacological and clinical properties of natural calcitonins. It has the same hypocalcemic potency of eel or salmon calcitonin, superior to the human and porcine types. Carbocalcitonin has the typical pharmacological effects of the natural hormone on the kidneys, bone and gastrointestinal tract, the target organs of calcitonins. When injected into the cerebral ventricle of laboratory animals it was found to have an analgesic effect. In clinical terms (Asu1,7) E-CT gave good results when used in the treatment of hypercalcaemia and senile osteoporosis. Carbocalcitonin was also employed in conditions characterised by a high bone metabolism turnover such as Paget's disease, Sudeck's atrophy and immobilisation osteoporosis. Experiments to date have shown carbocalcitonin to be extremely interesting in terms of tolerability with very few side effects being noted. This may well be attributable to the greater stability conferred by the absence of the S-S bridge.
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PMID:[Profile of a new calcitonin: carbocalcitonin-(Asu1,7) E-CT]. 620 66

Dichloromethylene diphosphonate (Cl2MDP) a potent inhibitor of osteoclast-mediated bone resorption, lowers serum calcium in hypercalcemia associated wit malignancies and with primary hyperparathyroidism, and reduces excess calcium mobilization from bone in multiple myeloma and in Paget's disease. We have evaluated the effectiveness of intravenously administered Cl2MDP in five patients with parathyroid carcinoma, a disorder characterized by severe hypercalcemia, very high parathyroid hormone (PTH) levels, and marked osteoclast-mediated bone resorption. All patients had biopsy-proved metastatic parathyroid carcinoma and hypercalcemia which persisted after multiple surgical procedures and other attempts at management. During a three-day observation period, each patients continued to demonstrate stable or progressive hypercalcemia despite infusion with saline solution and furosemide. Cl2MDP was administered over 2 hours at 2.5 mg/kg on day 1 and 5 mg/kg on days 2 through 7. Response was noted in all five patients; there was a gradual decline in the average serum calcium from 16.0 +/- 1.1 mg/dl (SEM) to 11.1 +/- 0.9 mg/dl by the eighth day (p less than 0.01). There were concomitant reductions in urinary calcium excretion, from 798 +/- 153 mg/g creatinine to 350 +/- 96 mg/g creatinine (p less than 0.05) and in the urinary hydroxyproline excretion, from 155 +/- 38 mg/g creatinine to 94 +/- 29 mg/g creatinine (p less than 0.02). Serum PTH levels remained markedly elevated (460 +/- 141 micrograms eq/ml to 493 +/- 169 micrograms eq/ml). In three patients, all indices returned to pretreatment levels by 10 days after the last infusion. In two of these patients there was a response to retreatment with Cl2MDP with a fall in calcium from 16.9 +/- 0.5 mg/dl to 12.4 +/- 1.5 mg/dl. There was no response in one patient. No adverse reactions to Cl2MDP were observed. The decrease in serum calcium and concomitant declines in urinary calcium and hydroxyproline suggest that Cl2MDP can effectively inhibit the excessive bone resorption associated with parathyroid carcinoma.
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PMID:Therapy of hypercalcemia due to parathyroid carcinoma with intravenous dichloromethylene diphosphonate. 621 78


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