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

There are conflicting reports on the effect of insulin on plasma Ca concentration in rats. Low doses appear to decrease and higher doses to increase plasma Ca. Since birds are known to be very sensitive to parathyroid hormone and have resistance to the hypoglycemic effects of insulin, the effect of commercial and highly purified insulin on plasma Ca concentration was studied in 10-day-old chicks 60 min after the administration of the hormone. Both commerical bovine and purified porcine insulin provoked a dose-related elevation of plasma Ca. Although hypophosphatemia was observed with the highest dose of insulin used (0.4U), hypercalcemia was observed with 0.05 U insulin, a dose that did not modify plasma phosphate concentration. The slopes of the dose-response curves of insulin and parathyroid hormone were indistinguishable and different from that of 1 alpha-hydroxyvitamin D3. Neither propranolol nor deprivation of vitamin D altered the hypercalcemic response to insulin. Unexpectedly, propranolol (40 microgram/chick) provoked elevation of plasma Ca. It is concluded that insulin raises plasma Ca concentration in the chick by a mechanism(s) not yet elucidated.
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PMID:Hypercalcemic effect of insulin in the chick. 44 96

Dogs given excess vitamin D (500 or 1,000 micrograms/kg of body weight each day for 1 to 3 weeks were observed for clinical and pathologic changes of increased blood pressure and of characteristic nephropathy associated with vitamin D toxicosis or hypercalcemia. Serum calcium and serum urea nitrogen (UN) increased throughout the treatment period, but serum phosphorus remained within the normal range. Plasma renin activity increased markedly. Blood pressure showed only insignificnat changes (P = greater than 0.05). Gross and microscopic examination of the kidneys suggested vascular-oriented changes with an ischemic basis. Glomerular vascular poles showed hypertrophy and hyperplasia of juxtaglomerular cells. Ultrastructually, an increase in the number of secretory granules was noticed in these cells. A hypothesis regarding the mechanism of renal injury during vitamin D toxicosis is presented.
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PMID:Vitamin D intoxication and the pathogenesis of vitamin D nephropathy in the dog. 45 87

Hypercalcemia is most commonly seen in normal infants as the result of normal rapid bone growth. The most common causative diseases are malignant disease and hyperparathyroidism. A variety of pharmacologic agents, especially vitamin D and its metabolites and thiazide diuretics, can elevate serum calcium levels. Hypersensitivity to vitamin D appears to be a cause of hypercalcemia in infants and in patients with granulomatous disease, such as sarcoidosis. Ingestion of escessive amounts of calcium, especially with alkali, may also cause hypercalcemia, as may prolonged immobilization, particularly under conditions of rapid bone turnover.
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PMID:Causes of hypercalcemia. 48 79

Two cases of paraneoplastic hypercalcemia secondary to ovarian tumors are presented. Both cases were secondary to ectopic parathormone (PTH) production. Other mediators postulated to cause this syndrome are prostaglandins, vitamin D-like sterols, non-vitamin D sterols, vitamin A, cortisol, and "osteoclast-activating factor.' The key treatment modalities for acute hypercalcemia are hydration and diuresis with furosemide; phosphates, steroids, antiprostaglandins, and hemodialysis may also be of value. Calcitonin is theoretically the most attractive treatment modality, but the rapid development of resistance limits its use to acute management. Mithramycin is most effective for long-term palliation of hypercalcemia if tumor-directed therapy is unsuccessful. Review of the literature confirms the previously made observation that mesonephromas are disproportionaately represented in association with this syndrome.
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PMID:Paraneoplastic hypercalcemia in ovarian tumors. 49 33

When correction was made for hypoalbuminaemia, 23 of 50 ambulant patients with definite or classical rheumatoid arthritis were found to have hypercalcaemia. When these 23 patients were studied 6 months later, 7 had hypercalcaemia as defined by the correction factor for a low serum albumin level, and 6 of these patients had raised serum ionised calcium concentrations. Biochemical studies in the 23 patients indicated evidence of hyperparathyroidism, namely, hypophosphataemia, increased serum alkaline phosphatase, hyperchloraemia, and reduced tubular reabsorption of calcium. However, serum immunoreactive parathyroid hormone concentrations were normal. Only one patient had an abnormally low serum 25-hydroxy-vitamin D result: this patient had a high level of urinary D-glucaric acid and was receiving phenobarbitone for treatment of epilepsy. The biochemical features suggestive of parathyroid overactivity were particularly found in patients with raised serum calcium levels. The cause of hypercalcaemia in rheumatoid arthritis remains to be explained.
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PMID:Hypercalcaemia in rheumatoid arthritis: investigation of its causes and implications. 51 39

1. Hypercalcemia was induced in S. murinus by alternate day intramuscular injections of vitamin D (25 000 IU) and by providing them 1% CaCl2 solution (prepared in tap water) for drinking. 2. After such a treatment the serum calcium values recorded a rise as compared to those of the control specimens. 3. The histological picture of the thyroid of the treated specimens reveals increased number of calcitonin cells. This observation is supported by the occurrence of mitotic figures among them. 4. Perpetual calcium challenge results in degranulation of the secretory material (calcitonin) among these cells (at 26th and 30th day of treatment). 5. It also results in degenerative changes in certain number of C cells. 6. The blood capillaries around these cells get dilated and secretory granules of C cells tend to gather at the periphery of cytoplasm and towards vascular pole. 7. The parathyroid shows atrophic changes.
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PMID:Studies of calcitonin cells and parathyroid gland of house shrew, Suncus murinus in response to experimental hypercalcemia. 53 67

In rats with experimental ischemic myopathy, there was a significant correlation (r = 0.778, p less than 0.001) between muscle uptake of technetium-99m (99mTc) diphosphonate and tissue calcium concentration. In addition, the accumulation of both calcium and 99mTc-diphosphonate in acutely injured muscles was further increased in rats with vitamin D-induced hypercalcemia. Histologic studies demonstrated staining of damaged muscle fibers with alizarin red, indicating the presence of microcrystalline or ultramicrocrystalline calcium salts. Staining of muscle fibers was most intense in the outer marginal zones of individual microscopic infarcts. Our results suggest that the uptake of 99mTc-diphosphonate in acutely damaged skeletal muscle is directly related to the deposition of calcium salts within the injured muscle fibers.
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PMID:Localization of technetium-99m diphosphonate in acutely injured muscle. Relationship to muscle calcium deposition. 55 59

Case report of a female neonate with hypocalcemia and spasms. The cause was parathyroid insufficiency due to hyperparathroidism of the mother. The hypocalcemia was treated with a massive dose of Vitamin D; this led to a sharp rise of 25-OH-vitamin D levels in serum. The mother had kidney stones. There was hypercalcemia and a raised parathormone level. Diagnosis was confirmed by surgery. An adenoma weighing 7 g was removed.
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PMID:[Neonatal hypocalcemia in hyperparathyroidism of the mother (author's transl)]. 55 75

Reversible hypertension occurred in a patient during episodes of hypercalcemia caused by hyperparathyroidism, vitamin D toxicity, and an infusion of calcium during an 11-year period of observation. It is suggested that normal renal function may be required for the hypertension of hyperparathyroidism to be reversible and that the hypertension may be directly related to the hypercalcemia in some patients. Early surgery is suggested for otherwise asymptomatic, mildly hypercalcemia hyperparathyroidism that is accompanied by hypertension.
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PMID:Reversible hypertension. Caused by the hypercalcemia of hyperparathyroidism, vitamin D toxicity, and calcium infusion. 57 60

The high circulating concentrations of immunoassayable parathyroid hormone observed in chronic renal failure are due to a number of factors. These include altered metabolism of the hormone and also end-organ unresponsiveness which may, indirectly, cause increased secretion of parathyroid hormone. The response of the overactive parathyroid glands to changes in plasma calcium and magnesium is variable and caution is needed in evaluating the suppressibility of parathyroid hormone secretion in acute studies. 1alpha-Hydroxylated derivatives of vitamin D can effectively suppress parathyroid gland overactivity. This effect may not necessarily be medicated through hypercalcaemia and vitamin D metabolites may act directly on the parathyroid glands.
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PMID:Hyperparathyroidism in chronic renal failure. 60 26


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