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 51-year-old man has had absorptive hypercalciuria and corticosteroid-responsive hypercalcemia for at least 12 years. There has been no clinical or laboratory proof of primary hyperparathyroidism, hypervitaminosis D, or other known causes of hypercalcemia and absorptive hypercalciuria. Hypercalciuria as well as the elevated serum level of calcium and 1 alpha, 25(OH)2D fell to normal during treatment with corticosteroids. The disturbed calcium metabolism in this patient is characteristic of that observed in sarcoidosis, but extensive studies have failed to uncover evidence of this condition.
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PMID:Corticosteroid-responsive hypercalcemia with elevated serum 1-alpha, 25 dihydroxyvitamin D. 743 65

Powdered Cestrum diurnum leaves, mixed with two diets differing in calcium and phosphorus contents, produced nephrocalcinosis in young chicks regardless of serum calcium elevation. The calcific deposits, found in both proximal and distal portions of cortical tubules, began either in the cytoplasm or in lysosomal bodies as a unilaminar spheroid structure containing apatite crystals. The ultrastructural characteristics of intraluminal concretions suggested that they were formed intracellularly but later were extruded into the lumen. The extent of calcific deposits increased with duration and with hypercalcemia. Although Cestrum contains an analog of 1,25-dihydroxycholecalciferol, neither mitochondria nor basal lamina contained calcific deposits described in nephrocalcinosis secondary to hypervitaminosis D.
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PMID:The ultrastructure of nephrocalcinosis induced in chicks by Cestrum diurnum leaves. 746 73

Hypercalcemia may be a manifestation of a variety of disorders including hyperparathyroidism, hypervitaminosis D, sarcoidosis, multiple myeloma, hyperthyroidism, acute osteoporosis, metastatic bone disease, and a number of primary malignancies. Hypercalcemia may be seen in as many as 1.5% of all patients with malignant disease, with or without bony metastases. The neoplasms most commonly associated with hypercalcemia include carcinoma of the lung (all cell types), breast cancer, squamous cell carcinomas, hematologic malignancies, and renal cell carcinoma. Observation of a number of instances of hypercalcemia attendant on urologic malignancies prompts the brief report of 4 characteristic cases with documentation of response to therapy. Management of severe and debilitating hypercalcemia is emphasized. Urologists should be aware of new agents available for such treatment.
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PMID:Hypercalcemia and urologic malignancies. 781 68

We present two cases of hemodialysis patients developing vitamin A toxicity related to excessive consumption of nutritional supplements containing large quantities of vitamin A. In one patient, severe hypercalcemia was the lone presenting sign; in the other, hypercalcemia was associated with unusual neurologic manifestations. We will discuss the reason why hemodialysis patients are at special risk for the development of hypervitaminosis A and review the mechanism leading to the associated hypercalcemia.
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PMID:Hypervitaminosis A in two hemodialysis patients. 784 65

The converging epidemics of tuberculosis and acquired immunodeficiency syndrome (AIDS) in the RSA and their expected catastrophic interaction afford an ideal opportunity for well-planned and essential research by clinicians, molecular biologists, epidemiologists and other health workers. The enigmatic relationship between tuberculosis, vitamin D and calcium is a field of study which should be considered urgently. An optimal vitamin D status not only assures sound calcium-phosphorus homeostasis, but is also essential for maximal immune competency. Hypovitaminosis D probably predisposes towards vulnerability to tuberculosis due to deficient monocyte-macrophage function. In contrast, hypervitaminosis D can correct this deficiency, but would do so at the cost of both B- and T-lymphocyte efficiency. One example of such a state is the endogenous over-production of activated vitamin D by gamma-interferon-activated monocytes, tissue macrophages and granulomatous tissue in tuberculosis. This would not only cause the coincidental hypercalcaemia, but may also complicate the effective co-ordination of monocyte-lymphocyte interaction and consequently compromise an appropriate immune response. It can reasonably be expected that the raised plasma interferon levels in the AIDS patient may trigger similar vitamin D-related pathophysiological processes. It is proposed that the ideal situation for enhanced vulnerability to tuberculosis in the AIDS patient will have been created if the known destructive effects of the human immunodeficiency virus on CD4-positive lymphocytes act synergistically with the vitamin D-mediated complications listed above.
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PMID:[The relationship between tuberculosis, vitamin D, potassium and AIDS. A message for South Africa?]. 804 2

Humoral hypercalcemia refers to the elevated blood calcium levels caused by neoplasms which release a bone resorptive substance into the circulation. Previously reported infants with malignant and benign solid tumors causing humoral hypercalcemia have presented with large abdominal masses. The case we describe, a hypercalcemic infant due to an occult parathyroid hormone-related protein-containing metanephric adenoma of the kidney, shows that radionuclide bone scanning can be a useful test to identify humoral hypercalcemia. Humoral hypercalcemia stemming from a soft tissue neoplasm should be ruled out, even in the absence of clinical signs of a tumor, if bone scans show generalized uptake in the absence of hypervitaminosis D or radiological signs of bone lesions, and serum parathyroid hormone is low.
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PMID:Humoral hypercalcemia due to an occult renal adenoma. 920 87

1,25-Dihydroxyvitamin D3 [1,25(OH)2D3] treatment in vitamin D-deficient (-D) rats results in a dose-dependent decrease in phosphorylation of a 91-kDa protein (PP-D91) in particulate fractions of the kidney. This recently reported 1,25(OH)2D3 effect was examined in detail herein. In contrast to the pattern expected of a rapid signal transduction event, time course (4 h-7 days) experiments demonstrated that PP-D91 phosphorylation was not decreased until 3-5 days 1,25(OH)2D3 treatment, resulting in a 61 +/- 3% (P < 0.01, n = 3) decrease in PP-D91 phosphorylation by 7 days. These effects paralleled increases in plasma calcium from 9.3 +/- 0.6 to 13.9 +/- 0.7 mg/dl after 0 vs 7 days 1,25(OH)2D3 treatment, respectively. Subcellular fractionation demonstrated that the renal PP-D91 was predominantly localized and 1,25(OH)2D3-regulated in crude mitochondrial and microsomal fractions. Further, PP-D91 was present and 1,25(OH)2D3-regulated in enriched preparations of both proximal and distal renal tubule segments. Tissue distribution studies demonstrated that the PP-D91 was predominantly present and 1,25(OH)2D3 regulated in the kidney, although low levels of a vitamin D-independent phosphorylated band of similar size were observed in the lung and heart. In contrast to 1,25(OH)2D3, estradiol-17B treatment (1 mg/day x 7 day) significantly (P < 0.01) increased PP-D91 phosphorylation in kidney of both -D and +D rats (increased 118.5 +/- 10.6 and 81.9 +/- 6.3%, respectively). Phosphoamino acid analysis after PP-D91 phosphorylation, isolation, and proteolysis indicated that these hormones alter 32P incorporation into phosphoserine residues. In conclusion, the 1,25(OH)2D3 effect to reduce PP-D91 phosphorylation in particulate fractions of the rat kidney is a protracted, tissue-specific effect which parallels elevated plasma calcium levels in this model. Moreover, renal PP-D91 phosphorylation is differentially regulated by 1,25(OH)2D3 vs E2 treatment and occurs on phosphoserine residues. The parallel between decreased PP-D91 phosphorylation and 1,25(OH)2D3-induced hypercalcemia may suggest a role for PP-D91 in the renal response to hypervitaminosis D.
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PMID:Altered phosphorylation of a 91-kDa protein in particulate fractions of rat kidney after protracted 1,25-dihydroxyvitamin D3 or estrogen treatment. 943 34

Vitamin D is required for the normal development of teeth and bones. When there is excess vitamin D, systemic and dental changes may occur. This is a case report of a girl who experienced hypercalcemia secondary to excess vitamin D derived from the consumption of milk that was incorrectly fortified. The changes in the permanent dentition to date are enamel hypoplasia and focal pulp calcification. These changes correspond to the timing of the toxemia caused by hypervitaminosis D.
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PMID:Dental changes in hypervitaminosis D. 957 50

Twin 17-day-old crossbred male lambs were examined to determine the cause of weakness and failure to thrive. Hypercalcemia attributable to hypervitaminosis D was diagnosed. The milk replacer or an accidental overdose of an injectable vitamin D product was suspected to be the source, although a definite cause was not confirmed. Lambs responded favorably to palliative treatment (administration of saline [0.9% NaCl] solution to induce calcium diuresis) and changing the diet to another milk replacer.
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PMID:Hypercalcemia and hypervitaminosis D in two lambs. 1075 74

In calcium homeostasis, vitamin D3 is a potent serum calcium-raising agent which in vivo regulates both calcitonin (CT) and parathyroid hormone (PTH) gene expression. Serum calcium is the major secretagogue for CT, a hormone product whose biosynthesis is the main biological activity of thyroid C-cells. Taking advantage of this regulatory mechanism, long-term vitamin D3-induced hypercalcemia has been extensively used as a model to produce hyperactivation, hyperplasia and even proliferative lesions of C-cells, supposedly to reduce the sustained high calcium serum concentrations. We have recently demonstrated that CT serum levels did not rise after long-term hypervitaminosis D3. Moreover, C-cells did not have a proliferative response, rather a decrease in CT-producing C-cell number was observed. In order to confirm the inhibitory effect of vitamin D3 on C-cells, Wistar rats were administered vitamin D3 chronically (25,000 IU/d) with or without calcium chloride (CaCl2). Under these long-term vitamin D3-hypercalcemic conditions, calcium, active metabolites of vitamin D3, CT and PTH serum concentrations were determined by RIA; CT and PTH mRNA levels were analysed by Northern blot and in situ hybridization; and, finally, the ultrastructure of calciotrophic hormone-producing cells was analysed by electron microscopy. Our results show, that, in rats, long term administration of vitamin D3 results in a decrease in hormone biosynthetic activities of both PTH and CT-producing cells, albeit at different magnitudes. Based upon these results, we conclude that hypervitaminosis D3-based methods do not stimulate C-cell activity and can not be used to induce proliferative lesions of calcitonin-producing cells.
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PMID:Decrease in calcitonin and parathyroid hormone mRNA levels and hormone secretion under long-term hypervitaminosis D3 in rats. 1133 96


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