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 25-year-old white woman with sporadic hypophosphatemic rickets presented with a 7 year history of chronic mild hypercalcemia, osteitis fibrosa cystic and hypercalcemic nephropathy. Serum immunoreactive parathyroid hormone was elevated by greater than 100-fold and a 3.5 g parathyroid tumor was found at operation. Survey of the literature reveals that of 9 previous cases in which hypercalcemic hyperparathyroidism occurred in association with hypophosphatemic rickets, only two had classical x-linked familial hypophosphatemic rickets. It appears more than likely that this unusual combination of skeletal diseases represents the chance occurrence of primary hyperparathyroidism in patients with underlying x-linked familial hypophosphatemic rickets rather than a complication of phosphate therapy.
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PMID:Hypercalcemic hyperparathyroidism in hypophosphatemic rickets. 87 68

Hypercalcemia of multiple myeloma has been discussed widely in the medical literature. The role of calcitonin and phosphate in the treatment of hypercalcemia of multiple myeloma has not yet been studied to our knowledge, although experimental animal models have been pointing to the role of phosphate supplement to calcitonin treatment in multiple myeloma. A patient had multiple myeloma and hypercalcemia. The usual medical treatment for hypercalcemia failed; however, the treatment with combined orally administered phosphate and calcitonin was successful. The role of phosphate depletion in this setting is brought up as an important factor in the failure of calcitonin therapy.
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PMID:Combined calcitonin and oral phosphate treatment for hypercalcemia in multiple myeloma. 87 32

Sham-operated and parathyroidectomized (PTX) rats were divided into two pair-fed groups, one on a normal mineral intake (0.5% Ca, 0.3% P), the other on a regimen low in phosphorus (0.5% Ca, 0.03% P). P depletion led to a drop in plasma P and urine P, a rise in plasma Ca and a marked rise in urine Ca, a drop in serum magnesium and a rise in urine Mg. The changes were more pronounced in the PTX animals, but final values were the same in both groups. Parallel bone-seeking isotope (85Sr, 177Lu, 237Np) studies in nonablated animals revealed an increase in the urinary nuclide output and in the urine/tibia ratio in P-deficient animals. Normal and primary bone osteocytes decreased and enlarged osteocytes increased as a result of P deficiency; osteoclasts and osteoblasts also increased. Bone composition showed a drop in ash content and a rise in water, with a light decrease in both Ca and P, and a corresponding rise in hydroxyproline and nitrogen in the P-deficient animals. The results are interpreted to mean that P-deficiency in the young growing rat leads to an increase in bone resorption which occurs also in the absence of parathyroid hormone (PTH). The fact that final values were similar in the control and PTX P-deficient animals suggests that steady-state regulation can also occur without PTH. Because P-deficiency leads to rapid hypercalcemia and rapid marked hypercalciuria, there may exist a mechanism for phosphate regulation which would then supersede Ca homeostasis. The change in serum and urine Mg levels may reflect a decrease in tubular Ca and Mg reabsorption associated with P-deficiency.
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PMID:Phosphorus deficiency, parathyroid hormone and bone resorption in the growing rat. 95 82

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

The assay of parathyroid hormone has contributed greatly to our understanding of calcium metabolism in health and disease. The most important clinical application of the assay is in the differential diagnosis of hypercalcaemia, which is an increasing clinical problem. PTH assays are of little or no value in the absence of other biochemical data, especially accurate determinations of plasma calcium and phosphate.
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PMID:Assay of parathyroid hormone in human serum and its uses. 101 86

Osteodystrophy is almost universally present in chronic renal failure. Mild, but detectable, abnormalities--especially in parathyroid hormone (PTH) secretion--occur even when the glomerular filtration rate is greater than 30 cc/min. Osteomalacia is common in areas in which vitamin D intake and exposure to sunlight are minimal; when these factors are plentiful, osteitis fibrosa predominates. Osteoporosis is seen with increasing frequency in hemodialyzed patients. Nonosseous complications of secondary hyper-parathyroidism include hypercalcemia, metastatic calcification and pruritus. The most important factor in the medical therapy of osteodystrophy is control of serum phosphate levels. Next, a positive calcium balance must be provided either by giving vitamin D as dihyrdotachysterol, raising dialysate calcium or administering calcium orally. Parathyroidectomy is sometimes indicated, especially when the patients are transplant candidates and manifest hypercalcemia. Whether or not transplant is contemplated, patients with persistently high calcium-phosphate products, severe metastatic calcification or rapidly progressive osteodystrophy should be considered for parathyroidectomy. Newer, experimental vitamin D preparations, such as 1,25-dihydroxycholecalciferol or 1-alpha-hydroxycholecalciferol, should improve the managemet of patients with renal osteodystrophy and decrease the need for parathyroidectomies.
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PMID:Calcium metabolism in renal failure. 109 Jan 50

1. Hypo- and hypercalcemia can be explained as derangements of the calcium homeostasis. Hypocalcemic tetany usually alarming the patient tremendously is, at least in adults, rarely life-threatening. Hypercalcemia leads in 30% of the cases to clinical symptoms which may inadvertedly pass into a state of hypercalcemic crisis. This latter requires an often difficult emergency treatment. 2. Hypocalcemic tetany may be reversed by administering calcium i.v. or, in severe cases, by a calcium infusion. Only rarely are magnesium supplements necessary to let the tetany disappear. Vitamin D or dihydrotachysterol (DHT) do not correct hypocalcemia immediately, since their effects may be delayed up to 15-25 days. In order to normalize the serum calcium permanently, vitamin D or DHT treatment should be instituted as rarely as possible. 3. Initially, hypercalcemic crisis is best treated by forced intravenous fluid administration with normal saline (and furosemide) in combination with high doses of prednisone. Fluid-, sodium- and potassium balances ought to be checked during this type of treatment. A first evaluation of the effectiveness of these measures is recommended after 24 hours: treatment is continued in patients who respond favorably, while subjects who do not show a significant decrease of the serum calcium may either be given a phosphate infusion or mithramycine as a bolus. Calcitonin appears to be useful only to start treatment before institution of a phosphate infusion.
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PMID:[Hypo and hypercalcemia as an emergency]. 110 94

Rats fed abnormally composed isocaloric diets during 21 days (low magnesium, atherogenous, high in proteins or carbohydrates) develop a mean increase in total number of pancreatic A cells, a significant increase of A/B ratio (atherogenous), and hyperglucagonemia in most of the groups under study. Histologic examination reveals calcification most marked in animals under low magnesium and atherogenous diets. They are only scarce following high protein diet; a normal or carbohydrate rich diet nullifies this phenomenon. Independent of the morphologic and functional state of the islets, supplementation by argining and histidine of normal chow is followed by a certain degree of renal calcification. Lowered urinary magnesium and calcium and elevated urinary sodium and phosphate together with a tendency toward hypercalcemia point to stimulation of parathyroids during malnutrition. Absolute or relative hyperglucagonemia must be considered the main causstive factor.
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PMID:[Pancreatic islets, plasma glucagon and renal calcification in rats fed various diets. Results of a pilot study (author's transl)]. 110 41

Using rats previously labeled with 45Ca, the effects of a severely phosphate deficient diet on calcium mobilization from bone into serum were examined in both intact and thyroparathyroidectomized (TPTX) RATS. With the TPTX animals, increased calcium mobilization from bone was evident 12 hr after the rats had been placed on the low phosphorus diet. At that time period, both TPTX and intact rats had become severely hypophosphatemic. However, in intact rats, calcium mobilization was not observed until 48 hr had elapsed. Both intact and TPTX hypophosphatemic rats developed hypercalcemia. To determine if inhibition of calcium deposition into bone contributed to this change, the course of 45Ca movement from blood into bone was followed in an experiment where rats received a single injection of the isotope at the time the low phosphorus diet was given. The animals on the low phosphorus diet showed a significantly lower bone specific activity and a higher serum specific activity compared to the control group, indicating calcium deposition into bone was inhibited. We conclude that the acute response to hypophosphatemia, resulting from the low phosphorus dietary regimen, was an increase in bone resorption and an inhibition of bone mineralization. The increase in bone resorption occurred more rapidly in TPTX rats than in the intact animals.
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PMID:Acute inhibition of mineralization and stimulation of bone resorption mediated by hypophosphatemia. 111 57

The growth hormone response to acute hypercalcemia was studied in 9 normal subjects. Growth hormone, calcium, glucose, phosphate and magnesium levels were determined at 30-min intervals during 4-h infusions. Infusions, performed in random order in the subjects, consisted of either normal saline at 3 ml/min for / h or 15 mg calcium/kg (calcium gluconate at 3 ml/min for 3 h followed by normal saline for the fourth hour. Significant hypercalcemia (P less than 0.05) was achieved within 60 min and maintained throughout the infusion. No change in calcium concentrations occurred during normal saline infusions, and phosphate, glucose and magnesium were unchanges in all studies. Growth hormone levels were significantly higher (P less than 0.05) at 60 min and all subsequent determinations during calcium infusion when compared to normal saline infusions. In 6 of the subjects, standard l-dopa provocative testing with an oral dose of 500 mg was preformed during normal saline and calcium infusions identical to those described above. Peak growth hormone responses did not differ significantly following l-dopa during saline or calcium infusion. These results suggest that an acute increase in circulating calcium promotes greater basal growth hormone secretion without a synergistic increase in hypothalamic mediated growth hormone release by l-dopa.
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PMID:The effect of acute hypercalcemia on growth hormone release in man. 112 88


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