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)

White Leghorn chick embryos were injected on the 15th day of incubation with 70 to 300 pmoles 1,25-(OH)2D3. All doses produced hypercalcemia; with the highest dose, the concentration of calcium in serum started to rise 4 h after the injection, reached a peak 20 h after, and was still high 48 h after. Twenty hours after the injection of the same dose, the concentration of inorganic phosphorus in the serum was significantly lower than in the corresponding controls. The tibias from 17-day-old chick embryos injected with 300 pmoles on day 15 were shorter, lighter, and had a lower ash content than those from controls. Histological signs of resorption appeared to be reduced with respect to controls, but no precise quantitation was conducted. The fact that hypercalcemia was not accompanied by hyperphosphatemia may suggest that the vitamin stimulates resorption of calcium from the shell, which is mainly formed by calcium carbonate rather than from the bone from which calcium and phosphate are usually resorbed together.
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PMID:Effects produced by the administration of high doses of 1,25-dihydroxycholecalciferol to the chick embryo. 57 6

Serum immunoreactive parathyroid hormone (S-iPTH) was measured together with serum and urinary calcium and phosphorus in 45 hyperthyroid patients in order to assess parathyroid fe of hyperthyroidism. The prevalence of hypercalcaemia was 51.1% using serum calcium values corrected for individual variations in serum albumin concentration compared to 15.6% using the uncorrected calcium values. S-iPTH was decreased and inversely correlated to serum calcium values. S-iPTH was decreased and inversely correlated to serum calcium (corrected). Subnormal levels of S-iPTH were found in 28.9% of the patients. The urinary excretion of calcium and phosphorus was increased and positively correlated to the degree of hyperthyroidism. The tubular reabsorption of calcium (TRCa%) was decreased, positively correlated to S-iPTH and inversely correlated to serum calcium. Increased mobilisation of bone mineral in hyperthyroidism is suggested mainly to be responsible for the elevated serarathyroid function.
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PMID:Decreased parathyroid function in hyperthyroidism: interrelationships between serum parathyroid hormone, calcium-phosphorus metabolism and thyroid function. 57 31

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
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PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

The present study is an investigation of the mechanism of hypercalcemia and hyperphosphatemia induced by the intravenous injection of lead acetate (Pb-Ac). A total of 118 male rats were injected with 30 mg/kg of Pb-Ac, or with 16.5 mg/kg of sodium acetate as the control. The levels of serum calcium, phosphorus and lead were then determined at various time periods after the injections. Serum calcium and phosphorus levels increased with time after Pb-Ac injection and the maximum values of calcium (17 mg%) were found after 1 h and of phosphorus (13.5 mg%) after 30 min. Both calcium and phosphorus levels reverted to the normal range after 12 h. The maximum net rates of increase of calcium and phosphorus were found immediately after Pb-Ac injection. At that time, deposition of lead at the calcifying sites of bone and incisor dentin was demonstrated by a histochemical examination. In other experiments the changes in the calcium and phosphorus contents in the medium after shaking bone powder in serum with Pb-Ac in an in vitro system were studied. It was confirmed that the calcium and phosphorus were displaced from the bone mineral, the extent of the displacement being correlated with the concentration of the Pb-Ac added to the medium, and that these displacements were very rapid reactions. These results suggest that hypercalcemia and hyperphosphatemia following Pb-Ac injection results from a direct action of lead on the bone mineral.
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PMID:Mechanism of induction of hypercalcemia and hyperphosphatemia by lead acetate in the rat. 59 44

We describe a boy who presented at 4 years of age with radiological hyperparathyroidism, osteosclerosis, and necrosis of the femoral heads. Plasma biochemistry was normal but the parathyroid hormone (PTH) level was very high. He was deaf and had an unusual facies but did not have the phenotype of Albright's hereditary osteodystrophy. Plasma and urine cyclic AMP reponses to bovine PTH were markedly subnormal. Vitamin D produced sustained hypercalcaemia and a fall in plasma phosphorus. After four hyperplastic parathyroid glands were removed he became hypocalcaemic and plasma phosphorus rose. After operation he remained unresponsive to exogenous PTH; We suggest that he had a form of pseudohypoparathyroidism without the phenotype of Albright's hereditary osteodystrophy and with some residual skeletal and renal responsiveness to PTH.
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PMID:Normocalcaemic pseudohypoparathyroidism with unusual phenotype. 64 42

Two groups of weanling pigs, injected with 45Ca, were fed diets containing optimal calcium and phosphorus, and vitamin D3 at 1320 IU/kg feed in the control group, and 825,000 IU/kg feed in the test group. The groups were further subdivided with 2 pigs in each subgroup, with survival times of 1, 2, 3, 4, 7, and 14 days. Pigs fed the high level of vitamin D3 lost weight and anorexia, weakness, rough hair coat and labored breathing were observed. Hypercalcemia began at 12 hours and progressed rapidly after 2 days. Radioisotope sutdies interpreted in the light of histopathologic findings indicated that bone was the primary source of increased plasma calcium. Calcium was released at a rapid rate into blood from prelabeled bone which was undergoing necrosis; it was also removed from blood and deposited into bone at a slower rate due to decreased apposition. Histopathologic examination of bones from test pigs showed regressive changes in the osteocytes, chondrocytes and osteoblasts which bean within 1 day of treatment and resulted in evidence osteopenia within 7 days. Arrested osteocytic osteolysis led to the appearance of cementing lines and to chondroid core retention. Further regressive changes in the osteocytes resulted in osteocytic death and osteonecrosis with subsequent osteoclasia and osteopenia. Retardation and arrest of cartilage maturation as well as osteoblastic deficiency contributed to the osteopenia. The osteopenia was further evidenced by decreased specific gravity and ash content per unit volume of humerus. The initial negative effect on the osteocytes, chondrocytes and osteoblasts is attributed to a direct toxic effect of excessive dietary vitamin D3 since hypoparathyroidism and hypercalcitoninism, which occur secondarily to hypercalcemia, could not account for the rapid appearance of this effect, nor are they known to induce osteocytic death. The release of bone calcium and the resulting hypercalcemia in vitamin D3 toxicosis is therefore due to a direct toxic effect of the vitamin, or its metabolites, on the osteocyte resulting in osteonecrosis. It is not due to increased resorption as has been reported previously from both in vivo and in vitro investigations. Degeneration, with subsequent inflammation, but without calcification, was observed in the kidneys and in the lungs. Epithelial cells, basement membranes, and smooth muscle were affected. This conclusively demonstrates that degeneration is the primary soft tissue lesion in vitamin D3 toxicosis, and that the subsequent calcification is therefore dystrophic. Degenerative changes occurred in the parathyroid glands within 1 day of treatment resulting in necrosis, inflammation and atrophy within 4 days. Relative fibrosis was seen as the parenchyma receded. The parathyroid gland changes were considered a direct effect of vitamin D3 toxicity since they occurred with only mild hypercalcemia and since necrosis of parathyroid cells has not been demonstrated with hypercalcemia either in vivo or in vitro.
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PMID:Vitamin D toxicity. Initial site and mode of action. 66 94

The effect of oral administration of betamethasone (25 microgram kg-1 day-1) on the duodenal absorption of calcium has been studied in chicks using the ligated loop technique in vivo. The chicks were fed normal calcium, normal phosphorus (NCaNP), low calcium, normal phosphorus (LCaNP) or normal calcium, low phosphorus (NCaLP) diets. Daily oral administration of betamethasone for 2-3 weeks markedly reduced the absorption of calcium in chicks fed the NCaNP diet, but did not significantly affect the adaptation in absorption when the NCaLP or LCaNP diets were fed for the same period of time. In one group of chicks, betamethasone was administered daily for 10 days before the birds were transferred to the NCaLP or LCaNP diets. Adaptation was again unaffected by betamethasone treatment. Administration of betamethasone caused a marked retardation in growth-rate, hypercalcaemia and an increased percentage of ash in the tibiae.
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PMID:Effects of low calcium and low phosphorus diets on the duodenal absorption of calcium in betamethasone-treated chicks. 70 18

The authors studied the clinical characteristics of primary and post-operative hypoparathyroidism in 39 patients. Laboratory follow-up data were compared under two different treatment programs using either AT 10 or 25 Hydroxycholecalciferol (25 OHCC). Clinical analysis revealed the atypical characteristics of primary hypoparathyroidism. From a therapeutic standpoint, AT 10 and 25 OHCC were equally effective in provoking a return to normal plasma calcium levels, except in complex cases of vitamin D resistance. 25 OHCC proved much easier to manipulate than at 10 and offered a higher security with respect tothe risk of hypercalcemia. The biological activity of 25 OHCC seems to differ from that of AT 10, especially regarding phosphorus metabolism.
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PMID:[Hypoparathyroidism in adults (author's transl)]. 74 36

Hyperparathyroidism during pregnancy is clearly associated with an increased incidence of neonatal morbidity and mortality. Although it is impossible to define the precise incidence of this entity, we believe that its occurrence will be seen more frequently with the increasing numbers of female patients who have successfully received renal transplants and with the routine determination of serum chemistries in the nontransplanted pregnant patient. A review of case reports since 1962 of women known to be hyperparathyroid during pregnancy revealed 80 per cent of these pregnancies to be complicated by neonatal tetany, death, or abortion. This review substantiates Ludwig's earlier report [1], which noted a 50 per cent incidence of neonatal complications despite the advances of prenatal and postnatal medical care. There have been only eight reported cases in which parathyroid resection was performed during pregnancy. Successful operation dramatically reduced the incidence of neonatal complications. An adaptive normocalcemic hyperparathyroidism occurs routinely during pregnancy. However, in the hypercalcemic hyperparathyroid pregnancy, transplacental passage of calcium leads to a profound hypercalcemia in the fetus. Since the fetal parathyroid glands are functionally responsive, parathyroid suppression is thought to occur in utero due to high calcium levels. This can lead to neonatal tetany or perhaps permanent neonatal hypoparathyroidism. When a patient presents with significant hypercalcemic hyperparathyroidism during pregnancy, we suggest that an explorative parathyroid operation be performed during the second trimester of pregnancy. After delivery, the baby's course should be carefully monitored with frequent calcium determinations. Cow's milk or other formula feedings high in phosphate content should be avoided in favor of feedings with a calcium:phosphorus ratio similar to that of human milk.
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PMID:Hyperparathyroidism during pregnancy. 76 83

Parathormone levels were determined in 17 patients with functioning renal transplants. In 8 patients recently transplanted, very high serum levels of parathormone were found without obvious relation to the glomerular filtration rate. Hypophosphatemia was also present in these cases. In 9 other patients studied 2-7 years after transplantation the mean level of parathormone was lower than in the previous group but levels above normal were noted in half of the patients, some of which had perfect renal function and normal serum phosphorus. The response to induced hypercalcemia was used as a sensitive test to reveal abnormal responses even in cases which initially had normal peripheral levels of parathormone. From these results, tertiary hyperparathyroidism would appear to be rare although hyperfunctioning parathyroid glands can be demonstrated long after kidney transplantation, even when renal function is close to normal.
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PMID:Evolution of secondary hyperparathyroidism after renal transplantation. 77 58


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