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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients are described who were examined with the bone-seeking substance 99mTc-E.H.D.P. The abnormalities discovered were ascribed to metastatic calcification in the lungs. The patients suffered from three quite different conditions, but in each there was hypercalcaemia. One patient had chronic renal insufficiency with secondary hyperparathyroidism, in the other cases the cause of the hypercalcaemia could not be determined. In one patient, it was possible to confirm the diagnosis of pulmonary calcinosis histologically. Previously published cases indicate that it is possible to demonstrate lung calcification by using Tc-phosphate compounds, particularly 99mTc-E.H.D.P. This is important, since it is often not possible to demonstrate it radiologically. It further demonstrates that the accumulation of 99mTc-E.H.D.P. is dependent on active bone metabolism.
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PMID:[The diagnosis of pulmonary calcinosis by scintigraphy (author's transl)]. 13 Oct 61

Five groups of 4 weanling pigs were fed a diet with 1.2% calcium and 1.0% phosphorus for 8 weeks with vitamin D3 at 1, 5, 25, 125 and 625 times the recommended levels, respectively. Hypercalcemia and hypophosphatasemia developed rapidly and persisted in Group 5 and developed more slowly but steadily in Group 4. Increasing levels of vitamin D3 influenced progressively and negatively the activity of resorbing osteocytes with osteopetrosis in Groups 2 and 3 and with osteonecrosis in Group 5. Atrophy of osteoblasts further contributed to the osteopenia in Group 5. Cartilage growth activity was arrested in Group 5. The negative effect on the resorbing osteocytes, which finally lead to death of the cells, was ascribed directly to vitamin D3 toxicosis since hypoparathyroidism and hypercalcitonism, both resulting from hypercalcemia, are not known to induce osteonecrosis. Since hypercalemia was finally as severe in Group 4 as in Group 5 and since there was soft tissue calcinosis only in Group 5, the calcinosis was always considered dystrophic, an interpretation supported by the observation that degenerative histologic changes preceded soft tissue calcinosis.
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PMID:Bone pathology in hypervitaminosis D an experimental study in young pigs. 18 36

A review is given of the literature concerning the so-called plant induced calcinosis in animals (tabel I), i.e. diseases which in their patological-anatomical appearance show great similarities with vit. D-intoxication. The etiology of the diseases are discussed in view of the last 5--10 years rapid development of knowledge concerning vit. D3 metabolism. It is pointed out that the most recent results indicate that enzootic calcinosis is caused by a 1,25-dihydrocholecalciferol-glycoside, which is hydrolysed in the intestinal tract. By this reaction 1.25 (OH) 2 cholecalciferol--the biological active metabolite of vit. D3 -- is set free, and thus able to act directly on the intestinal absorption mechanism. By this reaction the point of calcium metabolism regulation is essentially by-passed and calcium and phosphate absorption proceeds essentially out of control, causing hypercalcaemia, hyperphosphataemia, hypersecretion of calcitonin and calcinosis.
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PMID:[Enzootic calcinosis and other plant induced calcinoses (author's transl)]. 19 May 89

A case of primary hyperparathyroidism and coincidental Cushing's syndrome of hypothalamic-hypophyseal origin is reported. The hyperparathyroidism was based on an adenoma of the parathyroid glands and produced a severe hypercalcaemia (4.5 mmol/l) and calcinosis of kidneys and lungs. The Cushing's syndrome was caused by a hyperplasiogenic ACTH cell-adenoma of the pituitary which had induced a regulative hyperplasia of the ACTH-dependent zones of the adrenal cortex. The ultrastructure of the zona fasciculata and reticularis showed a conspicuous activation of the steroid hormone-producing organelles. The two endocrine diseases added together in skeleton, heart, duodenum, and pancreas. As a sign of hyperparathyroidism the osteoclastic absorption of the bone was strongly increased, whereas the bone formation was reduced due to the hypercortisolism. The pancreas showed a severe acute recurrence of chronic pancreatitis which was induced by a parathyrotoxic crisis. This was the immediate cause of death.
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PMID:[Simultaneous occurrence of primary hyperparathyroidism and pituitary Cushing's syndrome (author's transl)]. 19 Dec 34

Two cases of childhood leukemia with hypercalcemia are reported. In the first case who died by acute granulocytic leukemia, autopsy showed a generalized calcinosis. The other case was an acute lymphocitic leukemia with hypercalcemia and destructive lessions of bones with pathologic fractures. Response to chemotherapy was good. Literature about mechanismes which can induce hypercalcemia in malignancy is reviewed.
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PMID:[Leukemia and hypercalcemia (author's transl)]. 29 Feb 88

Single administration of 0.25 microgram of sunthetic Ialpha-hydroxycholecalciferol (IalphaOHD3) into nephrectomized rats, maintained at D-avitaminous diet, improved the active transport of calcium ions against the concentration gradient in small intestine of these animals, whereas ergocalciferol was biologically inactive under the same conditions. Administration of IalphaOHD3 during 5 days at a dose 0.025 microgram normalized calcium content in blood serum of rats with D-avitaminosis, Increased doses of IalphaOHD3, administered into intact animals, caused transient hyperphosphatemia, hypercalcemia, calcinosis of internal tissues (kidney heart, aorta) as well as death of some animals. IalphaOHD3 exceeded 400-fold the hypercalcemic and calcinose effects of ergocalciferol. LD50 for IalphaOHD3 was equal to 100 microgram/kg, if it was administered during 5 days per os. Tissue calcinosis was developed after administration of a daily dose 10 microgram/kg, moderate hypercalcemia was caused by a daily dose 1 microgram/kg or 0.25 microgram per an animal; this amount is only 10-fold higher as compared with the physiologic requirement. Ergocalciferol caused hypercalcemia and metastatic calcification only at a dose 4000 microgram/kg. Clinical use of IalphaOHD3 at doses, exceeding the physiologic requirements, has to be prohibited due to high activity of the preparation and to toxicity of its increased doses.
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PMID:[Comparative study of the biological activity and toxic effect of 1alpha-hydroxycholecalciferol and ergocalciferol in rats]. 30 16

An unusual finding of systemic calcinosis in a patient with a nonparathyroid malignant neoplasm stimulated us to do a sclinicopathologic review of similar cases at our institution in the past seven years. Of 3,268 autopsies performed from 1968 to 1975, a total of 17 cases of calcinosis were found, 11 with solid tumors and 6 with hematopoietic neoplasms. Calcinosis was most prominent in the lung, kidney, heart, and stomach and was rarely discovered prior to death. Eighty-two percent of the patients had hypercalcemia and 53% had associated bony metastatic disease. Corticosteroid or phosphate treatment for the hypercalcemia may have contributed to the tissue deposition of calcium. Significant hepatic, renal, metabolic, and pulmonary dysfunctions were also associated with this disorder. Thirty-six percent of the patients had hypercalcemia without skeletal involvement; tumor-produced parathormone-like substances may be responsible for these calcium abnormalities. Calcinosis was a significant complication of neoplastic disease in these patients and contributed to morbidity and mortality.
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PMID:Calcinosis in nonparathyroid malignant disease: an unusual case report and clinicopathologic review of 17 cases. 62 63

The effect of ingestion of dried leaves of Cestrum diurnum, a plant shown to contain a 1,25-dihydroxycholecalciferol-like principle, was tested in normal pigs fed 1.2% calcium and 1.0% phosphorus for 10 weeks from weaning and in hyperparathyroid pigs fed 0.8% calcium and 1.6% phosphorus for the same periods of time. Addition of 3% Cestrum diurnum leaf meal rapidly resulted in decreased feed consumption and weight gain, hypercalcemia and hypophosphatasemia. In normal pigs, plasma calcium rose to 16 mg/100 ml within one week and remained high for the 4 week experimental period. In hyperparathyroid pigs with hypocalcemia, plasma calcium rose to 12.75 mg/100 ml within one week and later approached 15 mg/100 ml. Ingestion of Cestrum diurnum retarded cell differentiation of growth cartilages. Arrested osteocytic osteolysis was observed within one week with osteopetrosis of epiphyses and metaphyses. The negative effect on the resorbing osteocytes then caused osteonecrosis which, in combination with lack of bone formation because of atrophy of osteoblasts, resulted in osteopenia within 4 weeks. Dystrophic calcinosis occurred within 2 weeks and was widespread after 4 weeks in lungs, kidneys, heart and vessels. Atrophy of parathyroid cells was severe after one week. Hyperparathyroid pigs responded with skeletal lesions, dystrophic calcinosis and parathyroid atrophy more rapidly and severely than normal pigs. The biochemical and anatomical changes in Cestrum diurnum ingestion are closely similar to those in vitamin D3 intoxication in pigs. Whereas pigs can tolerate large amounts of vitamin D3 because of feed-back control of 1 alpha-hydroxylation in the kidney, this control point is by-passed in Cestrum diurnum ingestion and intoxication occurs promptly.
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PMID:Cestrum diurnum intoxication in normal and hyperparathyroid pigs. 87 Feb 84

Development of experimental chronic renal insufficiency in rats was accompanied by an increase in concentration of residual nitrogen and phosphorus in blood and also by a decrease in intestinal absorption of Ca2+, however, no hypocalcemia was observed and the alkaline phosphatase activity was unaltered in blood serum. At the same time the renal insufficiency caused in some animals metastatic calcification of aorta and kidney, which was manifested by increased calcium concentration in these tissues. Administration of dihydrotachysterol increased the active transport of Ca2+ in rat intestine at the later steps of the impairment and led to development of moderate hypercalcemia and particularly to an increase in the degree of calcinosis of aorta and kidney. Administration of thyrocalcitonine did not prevent the hypercalcemia and calcinosis of internal tissues.
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PMID:[Changes in phosphorus-calcium metabolism in experimental renal insufficiency and after administration of dihydrotachysterol and thyrocalcitonin]. 103 Aug 98

A 67-year-old male was admitted for detailed investigation of an abnormal chest roentgenogram showing a tumor shadow about 3 cm in diameter in the left S1+2. The shadow was surrounded by minute granular and striate shadows. Small cell carcinoma of the lung was diagnosed and chemotherapy was commenced, but without effect. Hypercalcemia and superior vena caval syndrome followed. Autopsy indicated highly specific calcinosis present in the left upper lobe peripheral to the primary disease. This calcinosis was observed subepithelially in bronchi and bronchioles, in the tunica intima of the veins, and in the alveolar septa. It could not be detected in the tumor or arterial or lymphatic systems. The calcinosis had been present prior to the development of hypercalcemia, and the density of the calcinosis was greatest close to the tumor, gradually decreasing with increased distance from the tumor. The calcinosis appeared to have been caused by some substance, and to have been accelerated by venous congestion, resulting in its unique distribution.
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PMID:[A case of lung cancer with specific calcification]. 131 36


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