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)

A 66 year-old man with chronic renal failure developed hypercalcaemia during acetolyte medication. A technetium-99m phosphate bone scan at this time showed extraosseous isotope uptake in the stomach, which disappeared 2 weeks later after normalisation of the serum calcium level. This phenomenon can be interpreted as transient metatastic calcification during hypercalcaemia.
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PMID:[Transient extra-osseous increase of isotope activity in the bone scintigram in acetolyt-induced hypercalcemia]. 318 40

We evaluated musculoskeletal complaints related to arthropathy in 28 patients with end stage renal failure receiving maintenance dialysis. Twenty-three of 28 patients had arthritic complaints and 14 had an arthropathy. Six of 14 patients with arthropathy had a pattern resembling calcium pyrophosphate dihydrate deposition (CPPD) disease, 4 patients had moderately severe osteoarthritis, 3 had calcific periarthritis, and 1 patient had acute arthritis with intermittent pain and swelling. Factors which predispose to metabolic arthropathies were observed as follows: 29% elevated ferritin; 39% history of hyperparathyroidism; 68% elevated parathormone; 54% hyperphosphatemia; 36% hypercalcemia, 29% HLA haplotypes A3, B7, or B14; and 60% hyperaluminemia. The arthropathy group had more abnormalities per patient (mean 3.6) than the group without arthropathy (mean 2.7) (p less than 0.05). Our data suggest that (1) arthritic complaints occur frequently in patients receiving dialysis; (2) arthropathy accounted for 61% of the complaints; (3) 43% of patients with arthropathy had CPPD-type; (4) renal osteodystrophy caused 17% of arthritic complaints; and (5) in patients receiving dialysis, there is a high incidence of metabolic abnormalities that are known to be associated with arthropathy.
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PMID:Musculoskeletal symptoms related to arthropathy in patients receiving dialysis. 323 May 70

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

Intact parathormone (PTH 1-84) was measured with a new immunoradiometric method in serum from 83 children and adults with various abnormalities of calcium metabolism. The results were compared with those of an assay of midregional PTH fraction (44-68). Both measurements discriminated well between normal controls and patients with primary or secondary hyperparathyroidism. In patients in chronic renal failure intact PTH measurement was best for demonstrating parathyroid secretion. An important advantage of the new method is in the diagnosis of PTH hyposecretion in hypoparathyroidism and of tumour hypercalcaemia, which is not possible by mid-regional PTH determination. Intravenous injection of calcium (2 mg/kg over 5 min) and of synthetic PTH fragment (6 U/kg 1-38 hPTH over 2 min) caused a reduction in intact serum-PTH to about half the initial value after five minutes. Measuring intact PTH is thus a suitable method for determining both raised and decreased parathyroid secretion in disease and in the course of function tests. It is simple to perform, subject to only minor interference, and thus suitable also as a routine laboratory test.
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PMID:[Intact serum parathormone (PTH 1-84). A suitable parameter for the diagnosis of calcium metabolism disorders]. 334 39

During maintenance hemodialysis in patients with chronic renal failure, acute elevations of the plasma calcium are common, although of doubtful significance. Because the mechanisms for this hypercalcemia are unclear, calcium, magnesium, and inorganic phosphate mass transfer data was collected during routine hemodialysis. While the increase in the plasma calcium did not significantly correlate with the gain of calcium from the dialysate nor with the dialysate calcium concentration, there was a significant positive correlation between the degree of hypercalcemia and the loss of body phosphate (r = 0.66, P less than 0.05, n = 15). Hemodialysis without ultrafiltration and concomitant hemoconcentration depressed the dialysis hypercalcemia by 46% (P less than 0.001). However, continuous infusion of 33.5 mmol of phosphate during a 5-hour dialysis period, which reduced the plasma phosphate fall (1.53 +/- 0.16 to 0.87 +/- 0.08 mmol/L, P less than 0.01, in the control group; compared with 1.59 +/- 0.19 to 1.35 +/- 0.11 mmol/L, not significant [NS], in the phosphate infusion group) abolished the hypercalcemia (2.38 +/- 0.07 to 2.54 +/- 0.04 mmol/L, P less than 0.01, in the control group and 2.39 +/- 0.06 to 2.41 +/- 0.04 mmol/L, NS, in the phosphate infusion group). It is suggested that during routine hemodialysis, the loss of inorganic phosphate from the body is excessive, and that phosphate as well as calcium is released from the intracellular pool in response to the rapid fall in the plasma phosphate concentration. Such rapid, repetitive, and excessive losses of phosphate, particularly from bone, may be an important cause of renal osteodystrophy.
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PMID:Acute dialysis hypercalcemia and dialysis phosphate loss. 336 42

Four patients with mild, asymptomatic chronic renal failure became severely hypercalcaemic while taking over-the-counter antacids with daily calcium loads of only 4-8 g. Renal impairment carries an increased liability to this syndrome. Persistent elevation of serum parathyroid hormone levels led to parathyroid exploration in two of the cases, and normal glands were found. In retrospect the hormone levels were appropriate to the degree of renal impairment. Over-the-counter antacid preparations should carry dosage warnings to avoid the possibility of hypercalcaemia.
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PMID:Milk alkali syndrome following over-the-counter antacid self-medication. 345 93

Between 1978 and 1984, 19 patients at Royal Perth Hospital (RPH) underwent parathyroidectomy for secondary (renal) hyperparathyroidism. This represented 6.0% of the overall dialysis population treated at RPH during this period of time. The mean duration of pre-operative dialysis for these 19 patients was 48 months, compared with a mean duration of 30 months for the overall dialysis population. The principal indications for parathyroidectomy were symptomatic hyperparathyroid bone disease (10), hypercalcaemia (six), progressive lower limb ischaemia (two) and painful peri-articular calcification (one). The complications of chronic renal failure that were most consistently improved by parathyroidectomy were the clinical, radiological and biochemical manifestations of hyperparathyroid bone disease and hypercalcaemia. Features such as pruritus, soft tissue calcification, vessel wall calcification and peripheral ischaemia responded less predictably. Hyperparathyroid bone disease and hypercalcaemia remain the principal indications for parathyroidectomy in chronic renal failure. Profound postoperative hypocalcaemia was the major early postoperative management problem (seven patients) and was closely linked with the severity of pre-operative hyperparathyroid bone disease. It was also seen more frequently in those patients undergoing total parathyroidectomy with immediate autotransplantation of parathyroid tissue (TP-A), than in those in whom residual parathyroid tissue was left in situ (subtotal parathyroidectomy or STP). Recurrent hyperparathyroidism (four patients) was the major late postoperative complication, but was more frequently the result of a supernumerary or previously overlooked fourth parathyroid gland (three), than due to hyperplasia of residual parathyroid tissue (one). STP and TP-A were equally effective in controlling or reversing renal hyperparathyroidism, but the former was associated with a lower incidence of postoperative management problems and should be the preferred operation in this group of patients.
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PMID:Parathyroidectomy in chronic renal failure. 345 32

Treatment of secondary hyperparathyroidism and the osteodystrophy of predialysis chronic renal failure (CRF) with 1,25(OH)2D3 has been advocated by several authors, but also opposed by others for alleged renal toxicity. However, current concepts of the pathogenesis of the early occurrence of secondary hyperparathyroidism in predialysis CRF point to deficiency of 1,25(OH)2D3 as a primary factor. The aim of this study was to evaluate if administration of 1,25(OH)2D3 (0.25 microgram daily) in a dose which would not induce hypercalcemia, would improve humoral and bone histomorphometric parameters in predialysis CRF. 15 patients with predialysis CRF (mean age 51.2 +/- 16.9 years, range 13-73 years), serum creatinine 4.93 +/- 1.7 mg/dl, were treated with the vitamin D metabolite for an average of 16.2 +/- 11.3 months, at the end of which a transiliac bone biopsy for histomorphometry was performed. In addition, 23 patients comparable for age, serum creatinine and causes of renal failure, served as controls. Treatment did not induce hypercalcemia nor adversely modify the rate of decline of renal function. Alkaline phosphatase fell significantly while immunoreactive parathyroid hormone (iPTH) and osteocalcin showed a moderate, not significant, decrease. Compared to the control patients, the bone histomorphometric parameters active resorption surface and active osteoblastic surface were significantly lower and almost normalized by treatment. In conclusion, the study provides conclusive evidence of the absence of toxicity of the metabolite at the low doses employed, together with good therapeutic response on bone histology. Treatment at this dosage could be made in the early stages of predialysis CRF without need of close and continuous monitoring of serum biochemical parameters.
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PMID:Treatment of secondary hyperparathyroidism of predialysis chronic renal failure with low doses of 1,25(OH)2D3: humoral and histomorphometric results. 349 62

The response of circulating 1,25-dihydroxyvitamin D [1,25-(OH)2D] to challenge with vitamin D treatment both before and after 7-10 days of prednisone therapy (25 mg/day) was investigated in five anephric subjects, six patients with chronic renal failure (CRF), two patients with vitamin D intoxication and four patients with hypoparathyroidism. In anephric subjects serum 25-hydroxyvitamin D [25-(OH)D] rose from 58 +/- 48 (SD) to 377 +/- 221 (SD) nmol/l after administration of 150 micrograms of 25-(OH)D3 for 1 month. Serum 1,25-(OH)2D, which was barely detectable in only two out of five patients under basal conditions, rose to 30 +/- 21 pmol/l after 2 weeks of therapy with 25-(OH)D3, but fell to 10 +/- 5 pmol/l during prednisone treatment. In CRF patients circulating 1,25-(OH)2D rose from 37 +/- 24 to 58 +/- 24 pmol/l during 25-(OH)D3 therapy, but fell to 41 +/- 31 pmol/l during prednisone treatment. In two patients with rheumatoid arthritis, hypercalcaemia due to vitamin D intoxication was associated with raised levels of 1,25-(OH)2D (288 and 317 pmol/l). Administration of prednisone resulted in suppression of 1,25-(OH)2D levels (132 and 96 pmol/l respectively) and reduction of serum calcium to within the normal range. In the hypoparathyroid patients prednisone therapy did not affect circulating 25-(OH)D levels but serum 1,25-(OH)2D fell from 192 +/- 42 to 117 +/- 23 pmol/l and serum calcium from 2.41 +/- 0.21 to 2.20 +/- 0.05 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Extrarenal synthesis of 1,25-dihydroxyvitamin D: sensitivity to glucocorticoid treatment. 349 10

Parathyroid cells were obtained by collagenase digestion of 2 g of human parathyroid tissue obtained at surgery from a patient with end stage renal failure and hypercalcemia. Cells were placed into monolayer culture in supplemented Waymouth's MB752/1. Secretion of parathyroid hormone (PTH) from monolayer cultures was inhibited for 3 weeks by 2.5 mM compared to 0.5 mM calcium. The inhibition was 50% on day 3 of culture, and decreased to 19% by day 21. When cultures were incubated with [3H]leucine, radioactive PTH and COOH-terminal PTH fragments were secreted. Sequence analyses were performed on material in radioactive and immunoreactive peaks following gel filtration and high performance liquid chromatography of media. The results indicated that cleavage of PTH or fragments thereof occurred at the 23-24, 27-28, and 33-34 peptide bonds. NH2-terminal fragments of PTH were not detected in media.
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PMID:Structural analysis of parathormone fragments elaborated by cells cultured from a hyperplastic human parathyroid gland. 350 16


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