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)

Eleven uremic children with osteodystrophy aged 3 to 17 years were studied during administration of 1,25-(OH)2D3 for periods up to 21 months. Nine children presented with pure hyperparathyroidism, one with osteomalacia and one with mixed bone disease. Bone biopsies were performed before initiation of therapy and after 6 to 21 months of treatment following double tetracycline labeling. Skeletal lesions were improved but not cured in 5 of 9 children with hyperparathyroidism. In three instances lesions remained unchanged and worsened in one. No significant change was observed in the child with osteomalacia. Moderate improvement was noted in the patient with mixed bone disease. The propensity to develop hypercalcemia was the major factor associated with treatment failure since it precluded administration of adequate amounts of medication. Therapy with 1,25-(OH)2D3 was associated with a spectacular improvement in growth velocity in two of six children under age twelve.
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PMID:Renal osteodystrophy in children treated with 1,25-dihydroxy-cholecalciferol [1,25-(OH)2D3]. Histologic bone studies. 654 59

Parathyroidectomy was carried out in 26 patients over a 14-year period. Excellent results were obtained in patients with severe hyperparathyroidism. Vascular calcification, hypercalcaemia and pruritus did not justify surgery unless associated with unequivocal hyperparathyroidism. 13 patients required intravenous calcium infusion for up to 2 weeks to control post-operative hypocalcaemia. Calcium requirements could be predicted from the pre-operative plasma alkaline phosphatase level. Following operation continued treatment with vitamin D was necessary to prevent hypocalcaemia. Hyperparathyroidism recurred in 1 patient after 8 years and 4 patients developed osteomalacia. Since parathyroid hormone may have toxic effects other than those on bone, maintenance of normal levels should be a long-term objective in the treatment of patients with chronic renal failure. Where large parathyroid glands are present, surgical reduction in gland mass is a logical prelude to long-term suppression of parathyroid hormone with vitamin D and phosphate-binding agents.
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PMID:Parathyroidectomy in chronic renal failure. 668 30

Bone biopsy specimens from the iliac crest were obtained during surgical operations from 45 patients with rheumatoid arthritis (RA) and 41 with osteoarthritis (OA). Control material was obtained from 20 cases of sudden death due to cardiovascular disease. By both conventional histology and image analysis techniques about a quarter of all patients showed some osteoporosis. This was equally common among the OA and RA patients. It was more common among those with transparent skin and those taking corticosteroids. The only case showing mild osteomalacia suffered from OA. No gross differences were apparent between the groups in relation to plasma biochemical studies, diet, or exposure to sunlight. These results are in striking contrast to the high incidence of osteomalacia in RA reported from the west of England; moreover they do not confirm reports of hypercalcaemia among rheumatoid subjects. We conclude that the differences regarding osteomalacia are due to selection of cases. We find no evidence that osteomalacia is specifically associated with RA.
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PMID:Incidence of metabolic bone disease in rheumatoid arthritis and osteoarthritis. 674 98

The state of vitamin D nutrition depends on synthesis in the skin under the influence of sunlight as well as on dietary intake. In European countries that do not fortify milk with vitamin D, reduced sun exposure is the major factor leading to a fall in body stores of vitamin D with age and to a high frequency of hypovitaminosis D in the elderly sick. In the US, because vitamin D is added to milk and the use of vitamin D supplements is more common, the dietary intake of vitamin D is relatively more important than in Europe, and the total vitamin D intake and body stores of vitamin D are generally higher. Nevertheless, body stores of vitamin D probably fall with age in the US as they do in Europe, and it is likely that some sick elderly persons in the US, especially among those confined to institutions, become vitamin D deficient. For several reasons, the vitamin D requirement increases with age, and a total supply of 15 to 20 micrograms/day (600 to 800 IU) from all sources is recommended. Special attention should be paid to persons most likely to need supplementation, such as the housebound, persons with malabsorption, and persons with interruption of the enterohepatic circulation. Osteomalacia, the bone disease produced by severe vitamin D deficiency, is less common in the US than in Europe, but subclinical vitamin D deficiency may contribute to the pathogenesis of hip fractures, both through increased liability to fall and through PTH-mediated bone loss. The extent to which vitamin D deficiency contributes to hip fractures in the US is unknown, and is an important area for future research. Excess intake of vitamin D or of its metabolites may result in hypercalcemia and extra-osseous calcification, particularly in arterial walls and in the kidney, leading to chronic renal failure. The dose of vitamin D that causes significant hypercalcemia is highly variable between individuals but is rarely less than 1000 micrograms/day. Smaller doses can cause hypercalciuria and nephrolithiasis and possibly impaired renal function. Vitamin D administration may raise plasma cholesterol but there is no convincing evidence that the risk of myocardial infarction is increased. The recommended total supply for the elderly of 20 micrograms/day is most unlikely to be harmful, except in patients with sarcoidosis or renal calculi.
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PMID:Vitamin D and bone health in the elderly. 676 68

We have prospectively investigated calcium and bone metabolism in 16 patients receiving total parenteral nutrition for periods ranging from 7 to 89 months. In 12 patients, bone biopsies at 6 to 73 months after the start of parenteral nutrition showed osteomalacia. Plasma 25-hydroxyvitamin D levels were normal in all patients. Seven persons developed hypercalcemia, and 10 had hypercalciuria with a negative calcium balance. Serum phosphorus was normal and plasma parathyroid hormone level, normal or decreased. Three patients with the severest form of the disease had vitamin D withdrawn from their solutions. Subsequently, urinary calcium decreased, and serum calcium became normal; two persons reverted to a positive calcium balance. Thus, patients receiving total parenteral nutrition may develop metabolic bone disease characterized by osteomalacia, hypercalcemia, hypercalciuria, and a negative calcium balance. This may be caused by both defective mineralization and increased bone resorption induced by vitamin D, its metabolites, or another unrecognized factor.
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PMID:Metabolic bone disease in patients receiving long-term total parenteral nutrition. 676 94

The majority of chronic hemodialysis patients have elevated serum iPTH levels and bone disease characterized by osteitis fibrosa. However, a small group of patients develop osteomalacic bone disease associated with normal or slightly elevated iPTH values and a tendency to hypercalcemia which occurs either spontaneously or after treatment with small doses of vitamin D sterols. To examine the causes of the relatively low iPTH levels, we evaluated the change in serum iPTH levels that occurred in response to acute hypocalcemia, produced by dialysis using a low calcium dialysate, in 11 patients with osteomalacia and 8 control hemodialysis patients. Dialysis against a dialysate free of calcium for 60 to 90 min led to a fall in serum calcium to 7.5 +/- 0.2 and 7.2 +/- 0.2 mg/dl in the osteomalacic and control patients, respectively. Serum iPTH rose in controls from 1380 +/- 287 to 1960 +/- 287 pg/ml (P less than 0.01), whereas in patients with osteomalacia it rose from 360 +/- 58 to 507 +/- 104 pg/ml (P less than 0.05), a value only slightly above normal for this PTH assay. These data suggest that the relatively low basal levels of serum iPTH do not arise as a consequence of physiologic suppression of parathyroid gland function. This reduction in parathyroid function could contribute to the pathogenesis of low turnover osteomalacia.
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PMID:Parathyroid gland responsiveness to acute hypocalcemia in dialysis osteomalacia. 687 68

Mineral retention was measured during 39 metabolic balance studies in 34 patients with nutritional osteomalacia or late rickets; they were divided into 5 treatment groups consisting of oral vitamin D, artificial ultra-violet irradiation, 25-hydroxycholecalciferol (calcifediol), 1 alpha-hydroxycholecalciferol (alfacalcidol) and 1 alpha, 25-hydroxycholecalciferol (calcitriol). With the 1 alpha-hydroxylated derivatives, initial dosage of 2 to 6 micrograms daily was required to achieve optimal healing rates by comparison with other responses. Mineral retention was markedly enhanced by supplementation with microcrystalline hydroxyapatite compound (MCHC); untreated X-linked hypophosphataemic rickets healed in 7 weeks on 10 micrograms alfacalcidol daily and 6 grams MCHC daily without developing hypercalcaemia. By contrast, adult-presenting hypophosphataemic osteomalacia developed early hypercalcaemia on the same treatment; additional phosphate supplementation, without changing other treatment, abolished hypercalcaemia and improved calcium retention. A long-term crossover trial of the vitamins D in 6 patients with hypoparathyroidism suggested that relative potencies were as follows (assigning to vitamin D an arbitrary potency of l): vitamin D2 (or D3) l: dihydrotachysterol (DHT) 3: calcifediol 10: alfacalcidol 750: calcitriol 1500. The two-fold superiority of calcitriol over alfacalcidol was evident. Calcifediol and vitamin D controlled plasma calcium at comparable levels of circulating 25-hydroxyvitamin D (25-OH-D), elevated 25-OH-D persisting at least 1 to 2 years after discontinuing long-term (greater than 4 years) vitamin D. In 2 patients with myositis ossificans progressiva treated with 10 to 20 micrograms calcitriol daily, hypercalcaemia was minimized by a low-calcium diet supplemented with cellulose phosphate, suggesting that bone resorption did not play a major role in vitamin D intoxication. Net mineral loss was documented in a young male patient but not in a menopausal female, suggesting that calcitriol treatment was not likely to produce post-menopausal osteoporosis.
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PMID:Calcitriol dosage in osteomalacia, hypoparathyroidism and attempted treatment of myositis ossificans progressiva. 689 16

We describe a sporadic, vitamin-D-resistant osteomalacic syndrome in 19 patients undergoing hemodialysis. The syndrome was found in less than 1.5% of patients from referring dialysis centers. All 19 patients had multiple fractures, severe myopathy, and many developed spontaneous hypercalcemia. Severe osteomalacia without evidence of secondary hyperparathyroidism distinguished this syndrome from other forms of renal osteodystrophy. Bone aluminum, measured in six patients, was greatly elevated. Therapy with calcitriol (1 alpha, 25-dihydroxycholecalciferol) lad to clinical improvement in seven patients with reduced pain and myopathy, decreased serum alkaline phosphatase, or both, but no improvement in bone histology. Patients who did not respond clinically to calcitriol developed marked hypercalcemia. The cause of this severe osteomalacia, which occurs despite normal or slightly elevated levels of serum calcium and phosphorus and fails to mineralize with calcitriol, is unclear.
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PMID:Vitamin-D-resistant osteomalacia in hemodialysis patients lacking secondary hyperparathyroidism. 689 20

25OHD, 1,25,-(OH))2D, and 24,25-(OH)2D were assayed in the serum of 16 patients with the infantile, childhood, or adult form of hypophosphatasia. Except for diminished 1,25-(OH)2D and elevated 24,25-(OH)2D levels in 2 infants (which could be attributed to nonparathyroid hormone-mediated hypercalcemia), the mean circulating level of each vitamin D metabolite was normal in the 3 patient groups. Abnormalities in vitamin D metabolism do not appear to contribute to the pathogenesis of this rare hereditary form of rickets or osteomalacia, which occurs despite normal circulating calcium, inorganic phosphate, and vitamin D metabolite levels.
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PMID:Circulating vitamin D metabolite levels in hypophosphatasia. 697 89

A double-blind comparative study of 1 alpha-OHD3 and placebo was performed on 37 patients with osteoporotic hip fracture without clinical osteomalacia. 1 alpha-OHD3, in a dose of 1 microgram/day together with 2.5 g CaCO3, did not heal osteoporosis as judged from determinations of bone mineral density and histomorphometric analyses during four months of treatment. However, 1 alpha-OHD3 seemed to have an effect on fracture healing as concluded from the posttreatment alkaline phosphatase level. Hypercalcemia was common, occurring in six out of 19 patients treated with 1 alpha-OHD3. It is concluded that treatment of osteoporosis with 1 alpha-OHD3 and calcium is ineffective and potentially dangerous because it frequently causes hypercalcemia.
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PMID:Treatment of osteoporosis with 1-alpha-hydroxycholecalciferol and calcium. 698 71


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