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)

We conducted a 7-month randomized, single, double, single-blind comparison of calcitriol (1,25(OH)2D3) with vitamin D3 in 22 hemodialysis patients to study the effects on the biochemical abnormalities associated with osteodystrophy. Calcitriol was given for 3 mo. All patients had initial prestudy calcium values less than or equal to 9.5 mg/100 ml, and phosphate values less than or equal to 4.5 mg/100 ml. Data were analyzed using the Normalized Trend Index (NTI). Calcitriol induced a rise in calcium (8.7 to 10.25 mg/100 ml) (p less than 0.001) and a fall in alkaline phosphatase (p less than 0.005), while D3 had no appreciable effect. The mean dose of calcitriol during treatment was 0.579 microgram/day while that for D3 was 706 IU/day. The effect on serum phosphate concentration was variable. Hypercalcemia as high as 13.2 mg/100 ml occurred in 2 of 13 patients on 1,25(OH)2D3, but in every instance promptly returned to normal with dose reduction. No other adverse effects were noted with therapy. We conclude that calcitriol reverses the biochemical abnormalities of osteodystrophy. Since its effects are rapidly reversed with discontinuation, the drug is probably safe as well as effective.
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PMID:Calcitriol in dialysis patients. 20 82

We evaluated the hypothesis that thiazide-induced hypercalcemia reflects potentiation of the cAMP response to parathyroid hormone (PTH) consequent to inhibition of phosphodiesterase in bone and kidney. A panel of thiazide diuretics did inhibit low-Km phosphodiesterase activity from bone homogenates. However, furosemide, a nonthiazide diuretic that does not promote calcium retention, was more potent a phosphodiesterase inhibitor than either chloro- or hydrochlorothiazide (CTZ, HCTZ). Thiazides did not influence basal or PTH-stimulated cAMP levels in incubated calvaria or renal cortical slices. Administration of CTZ or HCTZ to rats for 4 days did not affect basal cAMP, nor did such treatment potentiate the cAMP response in Calvaria to infusion of parathyroid extract in vivo. CTZ, HCTZ, and furosemide increased basal adenylate cyclase from renal cortex but did not affect PTH-stimulated activity. Adenylate cyclase from bone was not affected by thiazides but was inhibited by furosemide. Thiazide treatment potentiated the calcemic response to parathyroid extract in vivo but did not affect the calcemic response to dibutyryl cAMP. We conclude that potentiation of the cAMP response to PTH does not underlie the unique effects of thiazides on calcium metabolism.
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PMID:Thiazide diuretics do not potentiate cAMP response to parathyroid hormone. 20

The effects of vitamin D3 on rat kideney metabolism under conditions of experimental hypercalcemia. Acta Physiol. Pol., 1978, 29 (2) 153--159. The effect of vitamin D3 on renal gluconeogenesis processes was studied in the rat. The performed estimations of gluconeogenesis rate from malate and lactate demonstrated significant increases of glucose formation rate when kidney cortex slices of the vitamin D3 treated animals were analyzed. Further studies on the mechanism of the observed phenomenon were performed using kidney cell fractionation procedure and fluorometric estimation of the concentration of selected gluconeogenetic metabolites. Significant increases of phosphoenolpyruvate concentration in the cytosol fraction and citrate concentration in the mitochondrial fraction were observed. Comparison of the described action of vitamin D3 on gluconeogenesis and the effect of parathyriod hormone, as known from the literature suggests similar mechanism of both factor actions. A possibility of vitamin D3 action through the increase in intracellular calcium has been discussed.
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PMID:The effects of vitamin D on the rat kidney metabolism under conditions of experimental hypercalcemia. 20 82

1,25 dihydroxycholecalciferol [1,25(OH)2D3] was studied in a double-blind controlled fashion in patients on chronic dialysis. Serum calcium was unchanged in 16 patients on vitamin D3 (D3) (400 to 1200 IU/day). In 15 patients on 1,25(OH)2D3 (0.5 to 1.5 microgram/day), serum calcium increased from 9.05 +/- .15 to 10.25 +/- .20 mg/dl (p less than 0.001), returning to 9.37 +/- .16 mg/dl (p less than 0.001) in the post control period. Patients on D3 showed no reversible decrease in immunoreactive parathyroid hormone levels, but patients on 1,25(OH)2D3 did, from a control of 1077 +/- 258 to 595 +/- 213 microliter equivalents/ml (p less than 0.01), and returned to 1165 +/- 271 microliter equivalents/ml (p less than 0.005). Nine of 12 patients on D3 who underwent serial iliac-crest biopsies showed histologic deterioration, and six of seven who received 1,25(OH)2D3 were improved or unchanged (p less than 0.025). Bone mineral and calcium decreased in patients on D3 (p less than 0.05) but not in those on 1,25(OH)2D3. Hypercalcemia occurred in five of 15 patients. We conclude that 1,25(OH)2D3 has a calcemic effect in chronic dialysis patients, decreases levels of immunoreactive parathyroid hormone, and is associated with histologic improvement in bone disease. Thus, 1,25(OH)2D3 is a valuable adjunct to the management of renal osteodystrophy but requires monitoring of serum calcium to avoid hypercalcemia.
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PMID:1,25 dihydroxycholecalciferol effects in chronic dialysis. A double-blind controlled study. 20 39

The effect of the light-darkness cycle on the efficiency of the ultimobranchial and parathyroid glands in altering duodenal calcium transport and plasma and urinary concentrations of calcium was examined in the adult male frog (Rana pipiens). Frogs were unfed, but were allowed access to 0.05 M-CaCl2 in the surrounding medium after ultimobranchialectomy or parathyroidectomy. Calcium transport, as assayed by the everted gut-sac technique, was increased in ultimobranchialectomized frogs at sunrise, concomitant with acute hypercalcaemia and hypercalciuria. An opposite but chronic response was observed in parathyroidectomized frogs with intact ultimobranchial glands. The maximum response observed at sunrise occurred when the concentration of calcium in the plasma of control frogs was decreasing; the minimum response, which occurred 6 h after sunrise, was coincident with a diurnal peak in the concentration of calcium. Vitamin D3 (500 microgram/frog) enhanced calcium transport in ultimobranchialectomized frogs, which resulted in chronic hypercalcaemia and hypercalciuria. The results suggest that diurnal variations in the plasma concentration of calcium do not initiate ultimobranchial activity, but are a response to endocrine control synchronized with the transition from darkness to light.
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PMID:Diurnal variations in the influence of the ultimobranchial glands on calcium homeostasis in the frog (Rana pipiens). 21 89

We have discussed in an earlier paper the value of estimating the circulating levels of biologically active parathyroid hormone. We consider here the importance of an evaluation of circulating calcitonin by showing the frequency of raised calcitonin secretion in hypercalcaemia of different origins. These results lead one to attribute to calcitonin a role which goes beyond the regulation of phospho-calcium metabolism and which in fact is that of a particularly sensitive indicator of tumours.
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PMID:[Calcitonin and hypercalcaemia (author's transl)]. 21 80

Renal handling of phosphorus was studied in the following groups of parathyroidectomized rats with maleate-induced Fanconi syndrome: 1) 6 rats receiving intravenous parathyroid hormone, 2) 6 rats receiving intravenous dibutyryl cyclic AMP (DBcAMP), 3) 6 rats undergoing volume expansion with saline, 4) 12 rats receiving intravenous 25 (OH)vitamin D3, 5) 12 rats with acute hypercalcemia induced by intravenous CaCl2, 6) 6 rats with phosphate deprivation, and 7) 6 rats receiving intravenous calcitonin. Parathyroid hormone and calcitonin failed to increase the urinary excretion of both cAMP and phosphorus. Likewise, DBcAMP failed to increase the urinary excretion of phosphorus. Extracellular volume expansion and hypercalcemia (serum calcium 12.9 +/- 0.7 mg/100 ml) did not alter the tubular reabsorption of phosphorus. In phosphate-deprived animals, the fractional excretion 0.16 +/- 0.05 (mean +/- SE) was lower than that in the control animals (maleate-treated without phosphate depletion), 0.46 +/- 0.04 (P less than 0.001). 25 (OH)vitamin D3 decreased the fractional excretion of phosphorus from 0.39 +/- 0.03 in the control (maleate-treated not receiving 25 (OH)vitamin D3) to 0.23 +/- 0.02 (P less than 0.001) in the experimental animals. The present study demonstrated an antiphosphaturic effect of 25(OH)vitamin D3 in experimental Fanconi syndrome; the mechanism of this action is not well understood.
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PMID:Antiphosphaturic action of 25 (OH) vitamin D3 in experimental Fanconi syndrome. 21 76

Prostaglandin E concentrations were measured in a patiet with breast carcinoma, hypercalcemia, undetectable parathyroid hormone (PTH) and no evidence of bone metastases. Catheterization of the drainage bed of her tumor documented production of E series prostaglandins. Treatment with the largest recommended doses of indomethacin for 10 days failed to lower her plasma prostaglandin E (PGE) concentrations or to correct the hypercalcemia, but it normalized urinary excretion of PGE. Subsequent chemotherapy reduced prostaglandin concentrations toward normal values concomitant with a reduction of clinically estimated tumor burden. During this period of time, serum calcium concentrations had no consistent relationship to the plasma PGE levels. We suggest that PGE merely reflected the tumor burden of this patient and did not directly contribute to the genesis of her hypercalcemia. The pertinent literature relating PGE and hypercalcemia is reviewed.
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PMID:Prostaglandin E and hypercalcemia in breast carcinoma: only a tumor marker? A need for perspective. 21 52

On the basis of a dramatic hypercalcemia revealed by digestive and neuropsychic symptoms and related to a primary hyperparathyroidism, the authors recall all the clinical circumstances which should lead to determination of plasma calcium as well as the clinical and biological particularities which, in front of a hypercalcemia, suggest a primary hyperparathyroidism. The stress the usefulness and the limits of the dosage of plasma immunoreactive parathyroid hormone as well as the difficulties to differentiale primary from paraneoplasic hyperparathyroidism. The recent pathophysiological concepts of malignant hypercalcemia reviewed.
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PMID:[Primary hyperparathyroidism. Current aspects of its diagnosis apropos of a case with digestive and neuropsychiatric manifestations]. 21 10

The question of parathyroid autonomy in primary hyperparathyroidism has been the subject of conflicting immunoassay data. We studied the effects of calcium infusion (12 mg/kg/3h) and calcium injection (3 mg/kg/10 min) on peripheral plasma parathyroid hormone (iPTH) determined with a multivalent antiserum and on the excretion of nephrogenous cyclic AMP in normal subjects and in 7 patients with primary hyperparathyroidism who displayed only mild, intermittent hypercalcemia. In control subjects, calcium administration resulted in small (13-20%) reductions in iPTH, whereas some 4/5 (77-81%) of the nephrogenous cyclic AMP was rapidly and uniformly suppressed. In the patients with primary hyperparathyroidism, both analyses revealed a lack of absolute parathyroid autonomy in response to calcium, with overlapping iPTH responses between a majority of the patients and the control group. In contrast, the nephrogenous cyclic AMP responses provided a clear separation of the 2 groups after both calcium infusion and calcium injection (mean values for both studies, patients: 2.93 nmol/100 ml GF vs. normal sugjects: 0.38 nmol/100 ml GF), and measurements of total cyclic AMP excretion also clearly distinguished the 2 groups. When a sensitive antiserum with predominantly carboxy-terminal reactivity was employed, the iPTH responses to calcium injection provided an improved separation of patients and normal subjects. The data suggest that 1) although parathyroid autonomy is not, in general, a feature of primary hyperparathyroidism, abnormal parathyroid suppressibility is easily demonstrated even in patients with a subtle form of the disorder; 2) the determination of nephrogenous cyclic AMP provides an optimal method for assessing rapid changes in parathyroid function; and 3) the interpretation of iPTH results from such studies is dependent on a number of technological features of the assay employed.
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PMID:Effects of the intravenous administration of calcium on nephrogenous cyclic AMP: use as a parathyroid suppression test. 22 21


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