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)

Two patients are described in whom the preliminary clinical and laboratory investigations suggested a diagnosis of osteomalacia, from gluten-sensitive enteropathy in one and from anticonvulsant therapy in the other. However, when the primary disease was corrected by diet and extra vitamin D, respectively, both patients developed hypercalcaemia. A standard hydrocortisone test in the second patient failed to reduce the hypercalcaemia. In both patients parathyroid tumours were found at operation. It is suggested that both patients had tertiary hyperparathyroidism in which the normally tell-tale hypercalcaemia was at first masked by the other abnormalities, and that this masking may account for some cases reported as having normocalcaemic primary (or tertiary) hyperpatathyroidism. Interpretation of total plasma-calcium is likely to be unreliable unless the 25-hydroxyvitamin-D levels can be shown or assumed to be normal.
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PMID:Masked primary (or tertiary) hyperparathyroidism. 4 76

Ten uraemic patients on regular haemodialysis were treated with 1alpha-hydroxycholecalciferol (1alpha-H.C.C.) for 5 to 14 months. Five patients who had histological osteitis fibrosa with or without osteomalacia responded well, with resolution of musculoskeletal pain, return of raised serum-alkaline-phosphatase concentrations to normal, resolution of radiological subperiosteal erosions, and improvement in histological signs of osteitis fibrosa and osteomalacia. In these patients 1alpha-H.C.C. proved a safe and effective drug. Five other patients did not improve. Characteristically these patients started with moderately severe histological osteomalacia and minimal, if any, osteitis fibrosa. Proximal myopathy was a prominent symptom and serum-alkaline-phosphatase was normal in four of them. Treatment with 1alpha-H.C.C. resulted in early troublesome hypercalcaemia, and repeat bone histology 5--11 months later showed no improvement. It is suggested that in these patients lack of 1,25-dihydroxycholecalciferol may not have been wholly responsible for the observed osteomalacia, hence 1alpha-H.C.C. alone was ineffective. Phosphate depeltion may have been an important contributing factor.
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PMID:Variable response to long-term 1alpha-hydroxycholecalciferol in haemodialysis osteodystrophy. 5 5

A patient presented with the classic features of anticonvulsant-induced osteomalacia. Following discontinuance of diphenylhydantoin therapy and repletion with physiologic quantities of vitamin D, hypercalcemia and persistent biochemical hyperparathyroidism developed, and a parathyroid adenoma was removed. A history of nephrolithiasis and hypercalcemia preceding the institution of drug therapy allowed this patient's underlying parathyroid disease to be defined as primary hyperparathyroidism, which had been obscured by anticonvulsant therapy.
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PMID:Primary hyperparathyroidism presenting as anticonvulsant-induced osteomalacia. 19 3

About 30% of patients with clinical osteoporosis had histological signs of osteomalacia, in spite of normal serum 25-hydroxyvitamin D3 (25-OHD3). The excess osteoid disappeared during treatment with 1alpha-hydroxyvitamin D3 (1alpha-OHD3). These patients might have reduced ability to convert 25-OHD3 to 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3). The intestinal calcium absorption increased during treatment with 1alpha-OHD3, but this was accompanied by a rise in urinary calcium excretion. Photon absorptiometry of the forearm indicated increased bone mineral content during treatment with a daily dose of 2 microgram 1alpha-OHD3 and a supplement of 1 g of calcium. This therapeutic combination, however, caused frequent episodes of hypercalcaemia, so further studies are necessary to evaluate an appropriate dose of 1alpha-OHD3 with or without a calcium supplement.
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PMID:Treatment of senile osteoporosis with 1alpha-hydroxyvitamin D3. 34 43

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

Five biochemical variables, S-Ca, U-Ca, S-P, U-P and S-ALP, all involved in calcium metabolism, have been investigated in 86 epileptics on long-term medication. We found hypocalciuria in half of the epileptics and increased S-ALP in one third. In contrast to earlier reports there was no hypocalcemia, whereas hypercalcemia was found in 7 epileptics. We have previously reported a high frequency of fractures in these epileptics. An increased fracture rate was found in the 13 epileptics with both hypocalciuria and increased S-ALP, indicating osteomalacia.
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PMID:Biochemical variables related to calcium metabolism in epileptics. 44 79

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

A sensitive and simplified radioreceptor assay for 1, 25-dihydroxyvitamin D (1, 25-(OH)2D) in human plasma was described and applied to preliminary clinical studies. Tritium-labeled 1, 25-(OH)2D3 was produced by incubating chick kidney homogenate with tritium labeled 25-hydroxyvitamin D3 (25-OHD3). A cytosol receptor was obtained from rachitic chick intestine (Kd=5.3 X 10(-11) M). Lipids in 5 ml of heparinized human plasma were extracted with dichloromethane, and 1, 25-(OH)2D was isolated by a Sephadex LH-20 column followed by high pressure liquid column chromatography. Recovery of 1, 25-(OH)2D3 after the plasma extraction and chromatography ranged from 58 to 100%. The assay was sensitive to 5 pg/tube. Diluted plasma from a patient on a high dose of 1 alpha-OHD3 showed a dilution curve parallel to the standard curve. The cytosol receptor showed a cross reactivity to various vitamin D3 metabolites physiologically present in the circulation and it was thought to be essential to eliminate other vitamin D3 metabolites 1,25-(OH)2D from plasma samples by high pressure liquid chromatography. Plasma concentrations of 1, 25-(OH)2D were, in the case of most normal subjects, distributed from 7 to 33 pg/ml and the range of distribution became greater in relation to age, indicating that plasma values should be matched to age. Whereas markedly high values of 1, 25-(OH)2D in plasma were found in some cases of primary hyperparathyroidism with prominent bone resorption, relatively low values were seen in some patients with chronic renal failure, senile osteoporosis, osteomalacia and hypercalcemia due to bone metastasis.
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PMID:Competitive protein binding assay for 1,25-dihydroxy-vitamin D in human plasma. 74 68

Report on a patient with osteomalacia due to renal phosphate loss. At onset the patient was aged 43 years. No other tubular defects were detected except glycinuria. The patient was followed over a period of 12 years. 3 years after treatment with oral phosphate and vitamin D3 persistent hypercalcemia developed with highly elevated levels of parathyroid hormone. After removal of one enlarged parathyroid gland serum calcium normalized, but elevated parathyroid hormone levels still persist. The spontaneous occurrence of hypophosphatemic osteomalacia in an adult male and its connections with the development of hyperparathyroidism are discussed.
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PMID:[Sporadic adult hypophosphatemic vitamin D resistant osteomalacia (phosphate diabetes) and hyperparathyroidism]. 101 14

Five patients who had gross abnormalities of calcium and phosphorus metabolism due to long standing renal failure are described to illustrate the difficulties with the term "tertiary hyperparathyroidism". One patient who had unequivocal biochemical tertiary hyperparathyroidism was found histologically to have nodular hyperplasia of all four glands even though one gland weighed twice as much (12g) as the combined weight of the other three. Another patient was not hypercalcaemic but had all the other features of the condition including rapid onset of osteitis fibrosa, vascular calcification and a probable parathyroid adenoma, with hyperplasia of the three glands. The other three had hypercalcaemia only after a reduction in the plasma inorganic phosphorus due either to renal transplantation or aluminum hydroxide therapy. The bone histology of the five patients varied from severe osteomalacia to severe osteitis fibrosa. A consideration of the factors involved in causing hypercalcaemia in these patients and a review of the literature leads to the conclusion that the term tertiary hyperparathyroidism is often misleading and best avoided.
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PMID:What is tertiary hyperparathyroidism? 106 86


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