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)

Mean plasma 1(alpha),25-dihydroxyvitamin D[1(alpha),25(OH)(2)D] was significantly increased and serum parathyroid hormone was suppressed in three patients with sarcoidosis and hypercalcemia. Prednisone lowered the mean plasma 1(alpha),25(OH)(2)D to normal range and corrected the hypercalcemia. To elucidate the mechanism for the increased sensitivity to vitamin D in this disorder, the effects of orally-administered vitamin D(2) were determined in seven normal subjects, four patients with sarcoidosis and normal calcium metabolism and three patients with sarcoidosis and a history of hypercalcemia who were normocalcemic when studied. Serum and urinary calcium, serum 25-hydroxyvitamin D (25-OHD), plasma 1(alpha),25(OH)(2)D and, in some studies, calcium balance were measured. Vitamin D(2), 250 mug a day for 12 d, produced little, if any, change in mean plasma 1(alpha),25(OH)(2)D and in urinary calcium in the normals and in the patients with normal calcium metabolism. In contrast, vitamin D(2) produced increases in plasma 1(alpha),25(OH)(2)D from concentrations which were within the normal range (20-55 pg/ml) to abnormal values and increased urinary calcium in two patients with abnormal calcium metabolism. In an abbreviated study in the third patient, vitamin D(2), 250 mug a day for 4 d, also increased plasma 1(alpha),25(OH)(2)D abnormally from a normal value. There was a highly significant correlation between plasma 1(alpha),25(OH)(2)D and urinary calcium. Serum 25-OHD and serum calcium remained within the normal range in all subjects and patients. These findings provide evidence that the defect in calcium metabolism in sarcoidosis probably results from impaired regulation of the production and(or) degradation of 1(alpha),25(OH)(2)D. Prednisone may act to correct the abnormal calcium metabolism by reducing circulating 1(alpha),25(OH)(2)D.
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PMID:Evidence that increased circulating 1 alpha, 25-dihydroxyvitamin D is the probable cause for abnormal calcium metabolism in sarcoidosis. 31 11

The prophylaxis and treatment of renal osteodystrophy are based on pathophysiological principles. Development of secondary hyperparathyroidism should be averted by early prevention of hyperphosphatemia through diet and phosphate ligants, and by normalization of the calcium balance through calcium supplements and vitamin D or its analogues. This treatment requires close clinical and laboratory control in order to avoid several hazards (hypercalcemia, hypophosphatemia, and refractory constipation). In cases with severe secondary hyperparathyroidism, subtotal parathyroidectomy is sometimes required. Nevertheless, in one such case this operation resulted in sudden hypoparathyroidism two years postoperatively.
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PMID:[Treatment of renal osteodystrophy: physiopathology and secondary effects]. 33 72

A case of transient hypercalcemia in a 53-year-old female, who received a necro-kidney transplant, has been examined. The hypercalcemia was caused by vitamin D intoxication on three separate occasions. Each period of even moderate hypercalcemia produced a rapid fall in renal function. The effect was reversible. These findings are discussed in the light of earlier reports on stable renal function in post-transplant hypercalcemia.
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PMID:Renal function in hypercalcemia after renal transplantation. 35 99

Four cases of wide-spread arterial calcifications and peripheral necroses developing after successful renal transplantation are presented. In two cases parathyroidectomy was performed to prevent progress of the peripheral ischemic ulcers. In one of these cases, this was followed by healing of the necroses. In the two other cases parathyroidectomy had been performed because of hypercalcemia in the post-transplantation period. Ischemic ulcers appeared in these patients during treatment with vitamin D and healed after withdrawal of this therapy. Prevention of uremic arterial disease might be obtained by early control of serum phosphate levels and by renal transplantation at an early stage of renal disease. Parathyroidectomy should be considered in the treatment of developing peripheral gangrene in uremic patients and renal transplant recipients. Also, there are obvious hazards connected with vitamin D therapy in these patients.
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PMID:Arterial disease with ischemic ulcerations in renal transplanted recipients. 35 7

FOR THE PURPOSES OF THIS REVIEW, THE VAST AND INCREASINGLY COMPLEX SUBJECT OF HYPERCALCEMIC DISORDERS CAN BE BROKEN DOWN INTO THE FOLLOWING CATEGORIES: (1) Physiochemical state of calcium in circulation. (2) Pathophysiological basis of hypercalcemia. (3) Causes of hypercalcemia encountered in clinical practice: causes indicated by experience at the University of California, Los Angeles; neoplasia; hyperparathyroidism; nonparathyroid endocrinopathies; pharmacological agents; possible increased sensitivity to vitamin D; miscellaneous causes. (4) Clinical manifestations and diagnostic considerations of hypercalcemic disorders. (5) The management of hypercalcemic disorders: general measures; measures for lowering serum calcium concentration; measures for correcting primary causes-the management of asymptomatic hyperparathyroidism.
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PMID:The pathophysiology and clinical aspects of hypercalcemic disorders. 36 22

This study reports the development of a specific and sensitive radioimmunoassay and a simple and accurate radial immunodiffusion (RID) assay for the human serum-binding protein for vitamin D and its metabolites (DBP). These immunoassays employed a monospecific antiserum that was prepared in rabbits against human DBP. The radioimmunoassay effectively measured DBP in amounts of 1-10 ng, whereas the RID assay measured DBP accurately in amounts of 0.2-0.8 mug. The results obtained with the two immunoassays on the same samples of serum agreed well with each other. Using the RID assay, the mean (+/- SD) serum DBP concentration observed in 35 normal persons was 422 +/- 27 micrograms/ml. Generally similar levels were observed in 66 hyperlipidemic subjects. In molar terms, the mean DBP concentration (approximately 8 microgramsM) was of the order of 50 times the usual serum level of 25-hydroxyvitamin D (25-OH-D) plus vitamin D. Thus, most of plasma DBP circulates as apo-DBP, not containing a bound molecule of 25-OH-D or of vitamin D. DBP and 25-OH-D concentrations were measured in a limited number of patients with hypercalcemia, mild hypocalcemia, and markedly elevated serum 25-OH-D levels due to oral vitamin D supplementation. It was found that major changes can occur in the serum levels of 25-OH-D and of calcium with very little or no associated changes occurring in the serum concentration of DBP, The results suggest that neither serum 25-OH-D nor serum calcium plays an important role in the regulation of the metabolism of DBP. Data were obtained that confirmed and extended an earlier report on the identity of the group-specific component (Gc) protein in plasma with the plasma vitamin D-binding protein. On immunodiffusion against whole serum, the line formed with the anti-DBP antiserum showed a complete reaction-of-identity with the line formed with commercial antiserum against Gc protein. Furthermore, serum that had been depleted of DBP by treatment with Sepharose containing covalently coupled antibodies against DBP was found to be depleted also of immunoreactivity against anti-GC protein antiserum. In addition, the properties of the purified DBP preparation agreed closely with those previously reported by others for Gc protein. Finally, a comparative immunology study showed that sera from several different mammalian orders showed some immunoreactivity against the antihuman DBP antiserum. Thus, proteins immunologically similar to human DBP are present in sera from a number of mammalian species and orders.
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PMID:Immunological and immunoassay studies of the binding protein for vitamin D and its metabolites in human serum. 40 85

Excess of phosphorus (the ratio Ca : P = 1 : 2) in a diet of growing rats strengthened such manifestations of vitamin D insufficiency as hypercalcemia and inhibition of animal growth. The data obtained suggest that excess of phosphorus is apparently important for pathogenesis of rachitis and the optimal ratio Ca : P should not be ignored in child diet.
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PMID:[Experimental vitamin D deficiency with different dietary calcium-phosphorus ratios]. 42 76

We ascertained the incidence of hypercalcemia in 79 consecutive patients with active pulmonary tuberculosis and a control group of 79 patients with chronic obstructive pulmonary disease. Twenty-two patients developed hypercalcemia (serum calcium greater than 10.5 mg/dl) within 4 to 16 weeks after initiation of chemotherapy for tuberculosis. The duration of hypercalcemia ranged from 1 to 7 months, and remission occurred spontaneously in all patients. The mean daily vitamin D supplement was greater in hypercalcemic patients than in the normocalcemic group. There was a positive correlation between daily vitamin D supplement and degree and duration of hypercalcemia. Mean serum calcium in patients with tuberculosis was higher than in patients with chronic obstructive pulmonary disease supplemented with the same dose of vitamin D. Hypercalcemia appears to be related to the activity of pulmonary tuberculosis and the intake of vitamin D; the exact mechanism, however, remains unknown.
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PMID:Hypercalcemia in active pulmonary tuberculosis. 42

Current concepts concerning the mechanisms, diagnosis and means of treatment of a number of the major causes of hypercalcemia and hypocalcemia are reviewed. In particular, the role of abnormalities in metabolism of vitamin D including (1) excessive hepatic production of 25-hydroxyvitamin D (vitamin D intoxication), (2) increased production of 1 alpha, 25-dihydroxyvitamin D (hyperparathyroidism and sarcoidosis), (3) impaired production of 1 alpha, 25-dihydroxyvitamin D (hypoparathyroidism, renal failure, vitamin-D-dependent rickets type I, pseudohypoparathyroidism) and (4) resistance to 1 alpha, 25-dihydroxyvitamin D; the use of vitamin D and its metabolites therapeutically is discussed.
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PMID:Hypercalcemic and hypocalcemic disorders: diagnosis and treatment. 44 May 8

Fifteen cases of hypervitaminosis D in childhood are reviewed. In all of them, vitamin D was given following medical prescription. In four occasions, excessive dosage of vitamine D impaired the evolution of a previous nephropathy. The clinical, analytical, radiological and histological findings as well as the therapeutical aspects are commented. Hypercalcemia, hypercalciuria, polyuria with hypostenuria, renal failure, bone lesions and nephrocalcinosis are the most prominent features of the picture. Occasionally, arterial hypertension and glycosuria were found. Prednisone, thyrocalcitonine and phosphates were used as therapeutical means. In spite of nephrocalcinosis and renal failure generally present at diagnosis, the clinical course was rather good.
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PMID:[Hypervitaminosis D. Review of fifteen cases]. 44 41


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