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

The urine-concentrating mechanism was studied in chronic hypokalemia (seven dogs given a low K(+), high NaCl diet plus injections of deoxycorticosterone acetate [DOCA]) and chronic hypercalcemia (seven dogs given vitamin D). In the potassium-depleted dogs, muscle, serum, and urine K(+) fell markedly, but glomerular filtration rate (GFR) and body weight varied little. Maximum urine osmolality fell in all dogs (mean decrease = 45%); however, solute-free water reabsorption (T(CH2O)) at high rates of solute excretion remained normal in three of four dogs. Free water excretion (C(H2O)) increased normally or supranormally as a function of increasing Na(+) delivery to Henle's loop in six dogs so tested. Hypercalcemia of several weeks duration caused a decrease in both GFR (mean 36%) as well as in maximum urine osmolality (mean 57%). Maximum T(CH2O) was not invariably depressed; in fact, when the values were adjusted for the reduced number of functioning nephrons (T(CH2O)/C(In)), four of seven studies were normal. C(H20)/C(In) increased normally (or supranormally) with increasing fractional Na delivery to Henle's loop in four of five dogs.I conclude that the lowered maximum urine osmolality in these hypokalemic and hypercalcemic dogs was not related to abnormal water reabsorption from the collecting ducts. Although not specifically measured in this study, it is very likely that solute accumulation in the renal medulla was reduced. This probably was not caused by abnormal delivery of sodium to, nor reabsorption of sodium from Henle's loop. It is likely that a more subtle defect exists in the countercurrent mechanisms for establishing a steep concentration gradient in the renal medulla. In the few hypercalcemic dogs in whom GFR was very low, I believe that injury to, and blockage of medullary tubules could account for most of the reduction in maximum U(Osm). Although not specifically ruled out, there is no evidence here to suggest that high serum Ca(+) or low serum K(+) per se causes a defect in sodium and water reabsorption in the mammalian nephron.
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PMID:Urine concentration and dilution in hypokalemic and hypercalcemic dogs. 543 74

Porcine calcitonin in a slow-release gelatin vehicle was given by intramuscular injection to 10 patients-four with primary hyperparathyroidism, four with Paget's disease, and two with carcinoma of the breast and hypercalcaemia. All cases showed a fall in serum calcium with an immediate rise in urine calcium. All except three patients with primary hyperparathyroidism showed a fall in serum phosphorus, but an immediate rise in urine phosphorus occurred in all cases. Urine hydroxyproline output fell in three patients with severe Paget's disease. Urine sodium rose in all cases, but the effects on potassium, magnesium, water, and pH were not appreciably different from results obtained in four control subjects who were given the gelatin vehicle alone.The data suggest that calcitonin caused a decrease in the tubular resorption of calcium and phosphorus. The hypocalcaemic effect appeared to be due to a decrease in bone resorption in the patients with Paget's disease but in the remaining cases could be accounted for in part or entirely by the rise in urine calcium.
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PMID:Renal effects of calcitonin. 546 Aug 39

Two elderly patients suffering from manic-depressive psychosis/depressive reaction had concurrently hypercalcaemia from vitamin D intoxication. They developed hypernatraemia with severe potassium and water depletion. Hypercalcaemia was pronounced, but both patients recovered quickly and their depressive symptoms resolved following water and potassium repletion and corticosteroid therapy.
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PMID:Vitamin D intoxication, with hypernatraemia, potassium and water depletion, and mental depression. 572 27

Urine specimens were collected from 26 normal subjects, 10 patients with proven primary hyperparathyroidism, and eight patients with hypercalcaemia due to other causes. After overnight urine concentration, an oral water load was given to induce a diuresis and provide urine specimens with a relatively wide range of creatinine concentration for each subject. In normal subjects the urinary calcium/creatinine ratio was found to be independent of urine concentration. In eight out of 10 patients with primary hyperparathyroidism and in two out of eight patients with hyper-calcaemia due to other causes, the urinary calcium/creatinine ratio was found to be high when the creatinine concentration was low, but usually normal when the creatinine concentration was high. The results suggest that if the urinary calcium/creatinine ratio of random urine specimens is used as a ;screening' procedure to detect hypercalciuria the latter cannot be excluded if the urinary creatinine concentration is more than 40 mg per 100 ml.
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PMID:The urinary calcium-creatinine ratio as a measure of urinary calcium excretion. 578 80

Others, using an Orion SS-20 ionised calcium analyser, noted that the ionised calcium concentration of a native serum sample was 8% greater than that of its ultrafiltrate. The experiments described here, using a Nova 2 ionised calcium analyser, confirmed a positive protein interference which was greater for human albumin than for IgG. Uncharged dextran showed no positive interference but dextran sulphate, which is highly charged and binds calcium, showed a large effect. Thus the interference is related to macromolecular charge. Dialysis experiments with normal and pathological human serum samples indicated that the ionised calcium of diffusible plasma water was overestimated by an average of 9.6% at an albumin concentration of 40 g/l and by 4.8% at 20 g/l. It is concluded that the measurement of ionised calcium with existing analysers can be clinically misleading in patients with abnormal plasma proteins. Hypocalcaemia is likely to be overdiagnosed and hypercalcaemia underdiagnosed in the presence of hypoalbuminaemia.
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PMID:Clinically significant effect of protein concentration on ion-selective electrode measurements of ionised calcium. 618 28

Calcium infusion imply a risk for cardiovascular complications. To avoid the risk, we have developed a new method for calcium infusion in man which can keep ionized calcium concentration in whole blood (WB-Ca++) in a steady state at a predetermined level. A solution of calcium chloride (Calcii chlor. Nord.), containing 0.117 mmol Ca++/ml water, is infused intravenously by means of an IMED 922H infusion pump. WB-Ca++ is determined every 5-10 min with a calcium ion-selective electrode, NOVA 2. The infusion rate is continuously adjusted. With the same initial infusion rate, 0.31 mmol Ca++/kg b.w./hour, hypercalcemia that is WB-Ca++ above 1.27 mmol/l was reached within 10 min in healthy volunteers, 8 females with a mean age of 26 years (range 19-36) and 7 males with a mean age of 29 years (range 25-34). The presettled WB-Ca++ level, 1.45 mmol/l, was obtained within 25 min and maintained in a steady state for 155 min at 1.45 +/- 0.01 mmol/l (mean +/- SE) in the female and at 1.46 +/- 0.01 mmol/l in the males. The range of the individual steady state mean WB-Ca++ was 1.42 +/- 0.02 mmol/l. No side-effects of the infusion were noted except for a slight increase in systolic and diastolic blood pressure 60 min after start of the infusion. In conclusion, the calcium clamp technique is safe and suitable for such situations where a presettled easily controlled WB-Ca++ level is required.
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PMID:A calcium clamp technique in man. 632 May 87

In 25 (33.8%) of 74 chronically haemodialysed patients a distinct osteopathy with bone pain, spontaneous fractures, arthralgias and weakness of the muscles due to dialysis was present. In comparison to a group without complaints the duration of the dialysis was longer by 6 months, the mineral contents of the bones was decreased in 38%, in the comparative group in 22%. A progressive demineralisation was found in 46%, in the comparative group in 20%. Hypercalcaemias under vitamin D2 caused a therapy resistance. In 1 exemplary case (type IIc, PTH 0.3 micrograms/l) in the 3rd year of dialysis a fracture of the neck of the femur took place and an endoprosthesis was implanted. There was a progressive demineralisation of about 16%. The suspicion of a typical combination with an encephalopathy due to dialysis did not confirm itself. A pseudocyst in the brain was found. The differential diagnosis to the hypercalcaemia-induced psychosis in the osteopathy due to dialysis is discussed. In a prophylactic application dihydrotachysterine proved favourable for avoidance of an osteopathy due to dialysis. Parallel to the clinical progressing of the osteopathy due to dialysis a progressive demineralisation could be demonstrated at the peripheral mineral contents of the bones. Extreme losses of minerals appeared from the 4th to the 59th month of dialysis from - 16% to - 37% and from the 22nd to the 87th month from plus 11% to minus 14% of the age-and-sex-specific normal values. Successful transplantations led to the stagnation of the progressive demineralisation, unsucessful transplantations increase them. The influence of the non-refined water for the production of dialysate by possible aluminium intoxications on the development of the osteopathy due to dialysis is discussed.
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PMID:[Dialysis osteopathy with spontaneous fractures, progressive demineralization and therapy resistance]. 635 38

To determine the impact of induced hypo- and hypercalcemia on TRH (400 micrograms)-stimulated TSH and PRL release, healthy subjects (n = 11) were infused with 5% glucose in water (n = 11), disodium EDTA (n = 11), or calcium gluconate (n = 7). TRH was given as an iv bolus 60 min (5% glucose and EDTA) and 120 min (calcium) after initiation of the respective infusion. Basal plasma concentrations of TSH remained unchanged during induced hypo- and hypercalcemia, whereas those of PRL fell during the latter (P less than 0.05). The mean sum of increments (0-90 min) in PRL and TSH was considerably greater during hypocalcemia than during hypercalcemia (PRL, P less than 0.002; TSH, P less than 0.005). The increments in the plasma hormone concentration above basal after iv TRH were increased compared to those in normocalcemia (PRL, 98.4 +/- 37.9 ng/ml; TSH, 38.9 +/- 11.8 microU/ml) during hypocalcemia [PRL, 128 +/- 47.8 ng/ml (P less than 0.002); TSH, 46.7 +/- 12.8 microU/ml; (P less than 0.005)], but were impaired during hypercalcemia [PRL, 70.1 +/- 27 ng/ml (P less than 0.002); TSH, 28.9 +/- 8.5 microU/ml (P less than 0.025)]. The mean sum of increments in PRL was related to concentrations of both serum calcium (r = -0.59; P less than 0.01) and PTH (r = 0.51; P less than 0.05). A relation was also seen between the incremental responses of TSH and serum calcium (r = -0.52; P less than 0.05), PTH (r = 0.55; P less than 0.01), and phosphorus (r = -0.55; P less than 0.01). We conclude that in healthy man, TRH-mediated release of both PRL and TSH are inversely related to serum calcium concentrations in such a manner that hormone secretion is enhanced by acute hypocalcemia, but blunted by hypercalcemia.
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PMID:Effects of disodium EDTA and calcium infusion on prolactin and thyrotropin responses to thyrotropin-releasing hormone in healthy man. 640 62

The influence of changes in the serum calcium concentration on TSH secretion was evaluated in patients with primary hyperparathyroidism and idiopathic hypoparathyroidism and in normal subjects. Serum calcium concentrations were 12.7 +/- 0.8, 9.0 +/- 0.4, and 5.7 +/- 0.5 mg/100 ml in hyperparathyroid, normal, and hypoparathyroid subjects, respectively, and were significantly different from each other. Serum T3 and T4 concentrations were comparable among the three groups. The basal serum TSH concentration was highest in hypoparathyroid, lowest in hyperparathyroid, and intermediate in normal subjects. However, all values were within normal limits and were not significantly different from each other. TRH-stimulated TSH secretion was significantly greater in hypoparathyroid patients and significantly less in hyperparathyroid patients than in normal subjects, respectively. The TSH response to TRH was normalized when the serum calcium concentration was normalized by parathyroidectomy in a hyperparathyroid patient or by 1 alpha-hydroxyvitamin D3 administration in a hypoparathyroid patient. To further clarify the mechanism responsible for the modified TSH response to TRH in the hypercalcemic state, rats were made chronically hypercalcemic by the administration of 1 alpha-hydroxyvitamin D3 (0.2 micrograms/100 g BW, ip, for 10 days) and 3% calcium chloride in drinking water. The pituitary TSH content of hypercalcemic rats was significantly greater than that of control rats. The results suggest that decreased TSH secretion produced by chronic hypercalcemia is due to diminished TSH release, rather than to decreased pituitary TSH reserve.
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PMID:Thyrotropin secretion in patients with hyperparathyroidism or hypoparathyroidism: effect of serum calcium on thyrotropin release. 640 63

Therapy of the malabsorption syndrome centers on adequate diagnosis of the underlying pathology, with vigorous therapeutic efforts directed at correcting this and thereby preventing ongoing losses of nutrients. Dietary therapy includes a high-protein, high-calorie, low-fat diet often supplemented with MCTs in an effort to minimize steatorrhea. Water-soluble vitamin deficiency is rare, but supplementation with small daily doses is innocuous and probably should be prescribed. Significant fat-soluble vitamin deficiencies are seen more commonly and can be monitored by physical examination and the prothrombin time. Calcium, magnesium, and vitamin D deficiencies are more common than originally suspected. Adequate therapy requires monitoring of the serum calcium, magnesium, parathyroid hormone levels, and, optimally, 24-hour urinary collections for calcium. Supplementation of these mineral deficiencies requires ongoing close observation to prevent hypercalcemia. Iron deficiency can be easily diagnosed by available serum iron determination, and replacement with oral supplements is curative. Trace metal deficiencies occur, but our capabilities of detecting and treating them is still in its infancy. Figure 3 outlines our approach to the evaluation and treatment of the patients suspected of having the malabsorption syndrome.
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PMID:Nutritional aspects of malabsorption syndromes. 641 33


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