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

Six healthy young volunteers were fed during two period of 9 days each by a strictly constantly liquid formula diet (Fresubin), on an ambulator basis. In a single blind cross-over randomized study, they were given either hydrochlorothiazide, 50 mg p.d., or a placebo during the first seven days of the two periods. The diuretic did not induce significant changes of either magnesemia or magnesiuria. In addition, the magnesium excretion after a challenging intravenous magnesium load remained unchanged. However, the thiazide normally increased the urinary excretion of sodium and potassium. It also induced hypocalciuria and hypercalcemia. The urinary excretion of cAMP and oxalic acid remained stable.
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PMID:[Short-term effect of thiazides on magnesium and calcium metabolism and secondarily on that of phosphorus, uric acid, oxalate and cyclic AMP]. 630 88

An oral calcium tolerance test was administered to 22 hyperparathyroid patients and 162 normal subjects to determine its value in the diagnosis of mild primary hyperparathyroidism. Basal urinary excretion of calcium was higher in patients [0.217 mg/100 ml glomerular filtrate (GF)] than in normal subjects (0.090 mg/100 ml GF), but there was 50% overlap between the two groups. Phosphorus excretion, expressed as the ratio of the maximal tubular reabsorption of phosphorus to the glomerular filtration rate, was lower in patients (2.77) than in normal subjects (3.7), but 38% of the patients fell within the normal range. Urinary excretion of total cAMP also failed to separate hyperparathyroid patients from normal subjects [5.8 +/- 0.32 (+/- SEM) nmol/100 ml GF in patients vs. 3.41 +/- 0.11 in normal subjects]. Determination of nephrogenous cAMP failed to increase the utility of cAMP as a predictor of hyperparathyroidism. In response to oral calcium, the elevation in serum calcium concentration was the same in both groups. The rise in urinary calcium was greater in patients, but showed 77% overlap with that in normal subjects. Conversely, serum immunoreactive PTH, measured with a midregion-specific RIA, was elevated in 90% of the patients. Some normal subjects also had high levels of PTH, but none of these had hypercalcemia. We conclude that the oral calcium tolerance test and measurement of urinary cAMP do not adequately distinguish hyperparathyroid patients from normal subjects. In the absence of renal insufficiency, the combination of hypercalcemia and elevated serum PTH concentration most accurately predicts the diagnosis of primary hyperparathyroidism.
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PMID:Assessment of adenosine 3',5'-monophosphate excretion and an oral calcium tolerance test in the diagnosis of mild primary hyperparathyroidism. 631 54

We evaluated nephrogenous cyclic adenosine monophosphate ( NcAMP ) levels in 61 normocalcemic patients with documented cancer of various organs and cell types. NcAMP levels were elevated in 17 (28%) and decreased in 13 (21%) of the cancer patients. Both high and low NcAMP levels were seen within the various cancer groups. There was a significant correlation (r = 0.383, P less than 0.01) between NcAMP and serum parathyroid hormone (PTH) levels, suggesting that tumor-related factors affecting NcAMP , may be partially related to native PTH. Alternatively, these factors might be altering the effect of endogenous PTH on renal tubules. A significant negative correlation was also observed between NcAMP and tubular maximum for phosphate (r = -0.356, P less than 0.02) suggesting that either cAMP per se or factors affecting NcAMP alter phosphate excretion. Follow up serum calcium data was available on 48 of the 61 patients. Subsequent hypercalcemia developed independent of the initial nephrogenous cAMP levels. It therefore appears that NcAMP elevation and development of hypercalcemia are two separate paraneoplastic phenomena.
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PMID:Nephrogenous cyclic adenosine monophosphate levels in normocalcemic cancer patients: its significance. 632 81

We performed graded calcium infusions twice in six normal young men, once without medication and a second time after they had received therapeutic doses of lithium carbonate for 5 days. The serum lithium level was 0.73 +/- 0.08 meq/liter (mean +/- SE) at the beginning of the calcium infusion and reached 0.97 +/- 0.13 150 min after receiving a lithium dose (210 min after beginning the test). There was no significant difference in mean basal serum calcium, plasma PTH, or nephrogenous cAMP for the untreated and treated periods. There was also no significant difference in calcium suppressibility of PTH secretion, as reflected by changes in nephrogenous cAMP. Changes in plasma PTH in response to calcium infusion likewise did not differ for the two periods, with the exception of a slightly greater degree of suppression in the unmedicated state (77% vs. 57% on lithium: P less than 0.02, by paired t test) at the last time point of the calcium infusion. The data show that short term administration of therapeutic doses of lithium does not alter the set-point for calcium suppression of PTH secretion in man. Further studies of calcium suppressibility of PTH secretion in subjects receiving long term lithium therapy will be needed to evaluate the pathophysiology of lithium-induced hypercalcemia.
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PMID:The effect of short term lithium administration on suppressibility of parathyroid hormone secretion by calcium in vivo. 633 Jan 56

Squamous carcinomas are the most common cause of humoral hypercalcemia of malignancy (HHM) in humans. To develop an animal model of this syndrome, CD-1 female mice were painted with dimethylbenzanthracene, which produced cutaneous squamous carcinomas in the majority of those painted. Greater than 90% of tumor-bearing mice developed a syndrome of hypercalcemia, hypophosphatemia, hypercalciuria, elevated plasma 1,25-dihydroxyvitamin D, normal immunoreactive PTH, elevated urinary cAMP, and accelerated bone resorption compared to control mice. Tumor excision reversed the hypercalcemia and hypophosphatemia, and autopsies revealed no evidence of skeletal or other metastases. Dietary calcium restriction did not affect the hypercalcemia in tumor-bearing mice. Extracts of tumor tissue contained potent bioactivity paralleling that of bovine (b) PTH in a PTH-sensitive canine renal cortical adenylate cyclase assay. The activity was trypsin sensitive and partially inhibitable by Nle, Tyr bPTH amide. The activity coeluted with chymotrypsinogen (mol wt, 25,700) on Sephacryl S-200 chromatography, well ahead of bPTH. This is the first description of an animal squamous carcinoma that produces HHM. With the exception of elevated plasma 1,25-dihydroxyvitamin D levels, the syndrome precisely mimics that seen in human HHM. The presence of a biologically active protein larger than PTH in tumor extracts, similar to that extracted from human tumors, suggests a common mode of pathogenesis. This model should be useful in further studying the pathophysiology of HHM.
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PMID:Squamous carcinoma model of humoral hypercalcemia of malignancy. 649 73

Fifty patients with absorptive hypercalciuria (AH), 25 normal subjects (NS), and 25 nonhypercalciuric patients with stone disease (NHSF) were studied using an oral calcium tolerance test and 24-h urine collections on both a restricted and an unrestricted calcium intake. Mean (+/- SD) fasting fractional calcium excretion was increased in the patients with AH (2.7 +/- 1.1% vs. 1.4 +/- 0.6% in the NS; P less than 0.001) and was negatively correlated with fasting nephrogenous cAMP, suggesting that this renal calcium leak was secondary to parathyroid suppression. Plasma 1,25-dihydroxyvitamin D [1,25-(OH)2D] was elevated in 80% of patients with AH and was high normal in the remaining 20%. Ten patients, selected on the basis of results for 1,25-(OH)2D greater than 4 SD from the normal mean, displayed a particularly severe pattern of abnormalities, including mild hypercalcemia in two patients. Pooled data from the NS and patients with AH revealed a significant negative correlation between the plasma concentration of 1,25-(OH)2D and the renal phosphate threshold (r = -0.40; P less than 0.001), but this correlation lost significance when the NHSF were substituted for the NS as a control group (r = -0.07; P = NS). These findings 1) provide a pathophysiological basis for the increase in fasting calcium excretion commonly observed in hypercalciuric patients, and 2) stress the importance of circulating 1,25-(OH)2D in the pathogenesis of the syndrome, but 3) fail to support the phosphate leak theory of pathogenesis.
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PMID:A consideration of the hormonal basis and phosphate leak hypothesis of absorptive hypercalciuria. 654 92

Two patients with disseminated coccidioidomycosis and hypercalcemia are presented. One patient studied showed normal levels of 25-hydroxyvitamin D with depressed levels of 1 alpha,25-dihydroxyvitamin D. The serum calcitonin level was appropriate for the level of serum calcium, and the serum parathyroid hormone level was suppressed with elevation of the nephrogenous cAMP level. Intestinal absorption of calcium was elevated at 63 percent. Hypercalcemia and hypercalciuria persisted despite a 300 mg calcium diet. An osteotropic substance similar to the humoral hypercalcemia of malignancy is postulated.
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PMID:Hypercalcemia in coccidioidomycosis. 660 75

It has been suggested that cyclic nucleotides (cAMP and cGMP) participate in the regulation of cardiac contractility and glycolysis. In the present study, this possible involvement was examined in spontaneously beating rat atria during hypoxia (50% oxygen saturation). Thirty seconds after reduction of high oxygen saturation (HiOxSa) in the incubation medium, the contraction amplitude declined to 50% of the initial level. The decline was partly antagonized by norepinephrine (NE) or hypercalcemia. The cAMP level remained unchanged during hypoxia, but the cGMP content gradually increased. Paradoxically, the production of lactate decreased after 30 sec of hypoxia but had increased by 2 min, when depletion of creatine phosphate and ATP stores was also initiated. Sodium nitroprusside (nitroprusside) and NE elevated the cGMP and cAMP, respectively, in both HiOxSa and hypoxia. Nitroprusside and NE also showed a positive inotropic effect in HiOxSa. Verapamil decreased contractility without changing the levels of cAMP or cGMP. In HiOxSa, both nitroprusside and verapamil decreased lactate production but were not able to resist the increase in atrial lactate level brought about by NE. In hypercalcemia the amplitude increased, but lactate production was slightly reduced in HiOxSa. Between 5 and 10 min of hypoxia, 45Ca uptake was reduced to about one-third of that in the control. It is suggested that lack of oxygen has direct and parallel effects on the sarcolemma and the mitochondria. The former induces deterioration of contractility, the latter termination of aerobic energy production. Cyclic nucleotides are not involved in either of these phenomena. However, at a low rate of anaerobic glycolysis, e.g., in HiOxSa or at the very early stage of hypoxia, cGMP could inhibit and cAMP accelerate lactate production.
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PMID:Regulation of cardiac contractility and glycolysis by cyclic nucleotides during hypoxia. 685 62

The effects of two models of chronic hypercalcemia on renal acid-base metabolism were studied in rats. In the first series of experiments, rats were rendered hyperparathyroid by the autologous grafting of 20 to 24 parathyroid glands into a single recipient. Hypercalcemia (5.48 +/- 0.03 mEq/liter in high PTH animals, 4.96 +/- 0.06 mEq/liter in pair-fed controls, P less than 0.001) occurred as did metabolic alkalosis (plasma total carbon dioxide 25.44 +/- 0.47 mEq/liter vs. 23.84 +/- 0.57 in controls, P less than 0.05). The rise in total carbon dioxide was in part a renal tubular effect since urine pH was lower (6.77 +/- 0.04 vs. 6.95 +/- 0.04, day 5, P less than 0.01) bicarbonaturia less (165 +/- 26 vs. 283 +/- 28 mumoles/24 hr, day 5, P less than 0.01) and titratable acid (TA) excretion increased (164 +/- 43.4 vs. 48.2 +/- 2.53 mEq/24 hr, day 5, P less than 0.01) in hyperparathyroid animals vs. pair-fed controls. To test the specific role of hypercalcemia versus PTH in this effect, normoparathyroid animals were treated with 1.25 (OH)2 vitamin D3 or SHAM injected, Urinary cAMP was reduced in these animals (0.030 +/- 0.004 mumoles/8 hr) compared to hyperparathyroid rats (0.055 +/- 0.01 mumoles/8 hr P less than 0.05) suggesting differences i PTH levels. Hypercalcemia occurred in 1,25(OH)2 vitamin D treated animals as did increased plasma total carbon dioxide and urinary TA while urinary bicarbonate excretion and urinary pH were reduced. Because hypercalcemia was associated with elevated total carbon dioxide in both models, it is proposed that chronic hypercalcemia stimulated renal acid excretion and in a sustained manner results in metabolic alkalosis, at least in part, on a renal basis.
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PMID:Effects of two models of hypercalcemia on renal acid base metabolism. 689 40

Responsiveness of the sheep fetus to parathyroid hormone (PTH) infusion was studied in the unanesthetized fetus in situ and the results were compared with those obtained in the newborn lamb, PTH, 0.5 USP U/min per kilogram body weight was infused intravenously to four sheep fetuses in utero (gestational age 127-141 days) and 10 newborn lambs (1-20 days of age). PTH infusion increased plasma Ca in the fetus and the PTH-induced hypercalcemia increased plasma calcitonin although the maternal levels of Ca and calcitonin did not change. In the fetus, as well as in the newborn lamb, PTH decreased the percentage tubular reabsorption of phosphate (TRP) and increased urinary excretion of cAMP. These results indicate that the sheep fetus has developed the target organ responsiveness to PTH and a normal calcitonin secretory mechanism by the last trimester of gestation.
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PMID:Parathyroid hormone responsiveness in the sheep fetus and newborn lamb. 722 32


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