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

The diagnosis of primary hyperparathyroidism (PHP) depends increasingly on laboratory tests, since the majority of patients are elderly people without typical symptoms. A mean plasma calcium level close to the upper normal limit serves to diagnose hypercalcemia. To rule out malignant disease, the most common cause of hypercalcemia, measurement of plasma PTH is the most appropriate test. Determination of blood phosphorus, chloride, and alkaline phosphatase, and of urinary calcium and phosphorus, contribute to the investigation of the metabolic effects of the given disease but are not very useful for causal diagnosis. Urinary and nephrogenous cyclic AMP reflect PTH secretion but can be elevated in paraneoplastic hypercalcemia. Diagnosis of subtle forms of PHP by dynamic tests is largely of scientific interest, since they do not necessarily need treatment. The diagnosis of hypoparathyroidism is primarily clinical. PTH measurements rarely distinguish normal from low values. In severe hypocalcemia of non-parathyroid origin, plasma PTH is elevated (except in hypomagnesemia). In borderline cases, measurement of urinary cyclic AMP or of plasma PTH after attempted stimulation by EDTA infusion is helpful, especially in distinguishing between subtle hypoparathyroidism and tetany induced by hyperventilation.
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PMID:[Diagnostic tests in parathyroid diseases]. 300 36

A constant EDTA infusion of 24 mg/kg/h during 60-120 min was given to 26 patients with primary hyperparathyroidism (HPT), 8 patients with hypercalcaemia of other origin and 10 healthy control subjects. PTH and ionized calcium concentrations were measured at 5-10 min intervals. In all three groups the infusion caused a linear decrease in plasma ionized calcium. In both the HPT patients and the healthy subjects there was a prompt increase in the serum levels of parathyroid hormone (PTH) until a plateau was reached. The PTH response of the HPT patients appeared already within the hypercalcaemic range and the plateau value was attained at higher levels of PTH and ionized calcium than in the healthy subjects. The enhanced response distinguished half of the HPT patients with basal PTH values within the reference range from the healthy controls. The patients with nonhyperparathyroid hypercalcaemia displayed no increase in PTH values until the ionized calcium concentration was reduced far into or below the reference range. Thus the EDTA infusion permitted a complete differentiation between HPT and other causes of hypercalcaemia. In most cases an infusion over 30 min was sufficient for this purpose.
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PMID:Stimulation of parathyroid hormone secretion by EDTA infusion--a test for the differential diagnosis of hypercalcaemia. 308 18

We describe a clinical study comparing the value of measurements of intact human PTH [hPTH(1-84)] and total PTH immunoreactivity [hPTH-(1-84) plus fragments]. A two-step immunochemical method was used to separate plasma hPTH-(1-84) from all circulating PTH fragments. The first step involved extraction and concentration of plasma PTH using solid phase antiamino-terminal PTH antibodies. After elution, the PTH immunoextract was analyzed using a sensitive mid- and C-region immunoassay. Complete separation in the immunoextraction step was proven by Sephadex G-75 gel filtration. hPTH-(1-84) values in fasting patients showed a clear distinction between those with primary hyperparathyroidism and those with nonparathyroid hypercalcemia, in contrast with small overlap in total immunoreactive PTH values. The hPTH-(1-84) values increased faster and more substantially in response to long EDTA and calcium infusion tests, compared with total PTH immunoreactivity, in normal subjects. Infusion of EDTA (10 mg/kg BW) in 5 min) elicited a readily measurable response of hPTH-(1-84) between 5 and 10 min after starting the infusion. Ingestion of 1000 mg calcium caused a decrease in hPTH-(1-84) in 1 h or less. More than 50% of patients with terminal renal failure had normal hPTH-(1-84) values despite elevated total immunoreactive PTH concentrations. We conclude that the two-step hPTH-(1-84) assay is more specific and sensitive than most regional PTH assays. Measurements of hPTH-(1-84) levels may identify disorders of parathyroid function at an early stage and provide a useful tool for the study of parathyroid physiology.
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PMID:Clinical implications of estimation of intact parathyroid hormone (PTH) versus total immunoreactive PTH in normal subjects and hyperparathyroid patients. 308 25

The effect of 1,25-dihydroxy-vitamin D3 (1,25-(OH)2-D3) on the TRH induced TSH release was investigated. Wistar rats were injected with 1,25-(OH)2-D3 (0.05 microgram/kg/day) for three days, and TRH was injected iv on the third day. Blood was drawn every 10 min during the following 40 min, and TSH was determined. The TSH release was significantly higher in rats treated with 1,25-(OH)2-D3 than in controls. The rats treated with 1,25-(OH)2-D3 were hypercalcaemic and thus, in order to find out if the effect was mediated through hypercalcaemia rats treated as above, were infused with EDTA (30 mg/kg/100 min) starting 60 min before the TRH test. This treatment made the rats normocalcaemic, and the significant increase in the TSH release was still seen in the 1,25-(OH)2-D3 treated rats as compared to controls. The results thus indicate that 1,25-(OH)2-D3 enhances the TRH induced TSH release and that the effect is not mediated through an increase in the serum calcium concentration at the time of the TRH test. In order to find out if the effect could be mediated by changes in intracellular calcium the rats were treated with the calcium antagonist verapamil (25 mg/kg/day) and the adrenergic blocker propranolol (5 mg/kg/day) alone or together with 1,25-(OH)2-D3. In rats treated with verapamil or propranolol alone or 1,25-(OH)2-D3 + propranolol, no effect was observed on the TRH induced TSH release. Verapamil + 1,25-(OH)2-D3 significantly increased the TSH release as compared to both controls and rats treated with 1,25-(OH)2-D3 alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of 1,25-dihydroxy-cholecalciferol on the TRH induced TSH release in rats. 310 41

Radioimmunoassay for parathyroid hormone (PTH) in equids was performed on blood samples from healthy equids and equids with hypercalcemia and hypophosphatemia. The assay was validated for equine carboxy-terminal PTH. Manipulation of serum ionized Ca in healthy equids by infusing Na2 EDTA and CaCl2 produced an expected increase and decrease, respectively, in measurable immunoreactive PTH. Intra-assay and interassay coefficients of variation were 2.6% and 11.7%, respectively. The range of PTH valves for healthy mature horse mares and geldings maintained on pasture was less than 0.27 ng/ml to 0.92 ng/ml and for horse colts fed grain was 0.61 to 1.25 ng/ml. Serum PTH values were measured on 2 equine patients with hypercalcemia, 1 pony with primary hyperparathyroidism and 1 horse with pseudohyperparathyroidism. Both patients had increased serum PTH values.
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PMID:Radioimmunoassay for parathyroid hormone in equids. 359 56

The influence of serum calcium concentration on total circulating parathyroid hormone (PTH) and on the relative amount of intact PTH-(1-84) and large carboxyterminal fragments was studied in the canine and bovine species and in man. Serum calcium was modified through infusions of CaCl2 or EDTA and samples obtained in time for the measurement of serum calcium and PTH concentrations. Pools of serum, corresponding to specific serum calcium concentrations, were analyzed by gel chromatography in all species. PTH was measured with a carboxyterminal radioimmunoassay. In basal conditions, total serum PTH was composed mostly of large carboxyterminal fragments, intact PTH-(1-84) representing less than 25% of the hormone in any species. With hypercalcemia, (greater than or equal to 2.0 mg/dl), total serum PTH decreased only to 40% of the original value measured in all species, despite serum calcium concentrations of over 13 mg/dl. The relative amount of intact PTH-(1-84) remained unchanged in the bovine and canine species and slightly decreased in man. Hypocalcemia (less than or equal to 2.0 mg/dl) induced a 300-450% increase in the basal PTH value measured. The relative amount of intact PTH-(1-84) became as or more important than carboxyterminal fragments in the canine species and in man, respectively, and remained slightly less in the bovine species. Despite small quantitative variations between species, these results indicate that changes in serum calcium concentration induced acute modification in PTH secretion or PTH peripheral metabolism, altering the ratio of intact hormone to carboxyterminal fragments in circulation.
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PMID:Influence of serum Ca concentration on circulating molecular forms of PTH in three species. 378 37

Experimental hypercalcaemia was induced in rats by (1) transplantation of the solid Walker 256 tumour, and (2) intraperitoneal injections of calcium gluconate. Whole blood clotting was studied by means of thromboelastography and whole blood clotting times in polystyrene and glass test tubes. At serum calcium levels between 10.3 and 11.5 m-equiv/l a slight delay in clot formation was found which was reversible by the addition of EDTA to whole blood. Acute, calcium-gluconate-induced hypercalcaemia, however, leads to a significant shortening of the clotting time in the polystyrene tube and to a lesser degree in the glass tube. Maximal factor XII activation in vitro with ellagic acid levels the difference of clotting times again. From these experiments it is concluded that acute hypercalcaemia induces a hypercoagulable state, possibly by partial contact activation, and thus may favour thrombus formation in vivo.
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PMID:Experimental hypercalcaemia and whole blood clotting. 420 Mar 24

A method is described for the quantitation of total skeletal activity during bone scans. The method requires a single plasma sample only, taken at the time of imaging. The ratio of % injected dose of 51Cr EDTA to that of 99Tcm MDP is calculated from this sample following combined injection of the two radiopharmaceuticals. The 51Cr EDTA level corrects for the glomerular filtration of 99Tcm MDP. Using this method, which only requires a gamma counter, significant differences from normal controls have been shown in patients with osteomalacia, renal osteodystrophy, Paget's disease and hypercalcaemia. The method provides routine quantitative data to add to the imaging information in the bone scan.
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PMID:Chromium 51 EDTA/technetium 99m MDP plasma ratio to measure total skeletal function. 623 85

FBH is characterized by symptomless hypercalcemia, low urinary calcium excretion, normal iPTH values, generally normal parathyroid histology, and failure of subtotal parathyroidectomy is normalize serum calcium. We studies six patients with FBH from three kindreds, six patients with sporadic 1 omicron HPT, and six healthy volunteers. To characterize the renal response to PTH, 14 of the subjects had infusions of bovine PTE (300 U intravenously over 15 min) and, separately, stimulation of endogenous PTH release by infusion of disodium EDTA (50 mg/kg over 2 hr). PTE induced striking increases of UcAMP (nM/100 ml of GF) that were indistinguishable between controls and subjects having FBH. However, the rise of UcAMP in 1 omicron HPT was significantly reduced (p < 0.001) compared to controls or the FBH group. EDTA-induced hypocalcemia raised serum iPTH and UcAMP in all three groups; the increases of iPTH (two assays of differing specificity) were greatest in 1 omicron HPT and least in FBH. In contrast, increases of UcAMP were greatest in FBH and 1 omicron HPT and indistinguishable from one another. The increase of UcAMP considered as a function of the increase in PTH showed significantly greater UcAMP responses in FBH than in the other groups. These results are consistent with primary or secondary alterations of renal responsiveness to PTH in both FBH and 1 omicron HPT, which may in part explain the different renal tubular calcium handling in the two conditions.
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PMID:Urinary cyclic 3',5'-adenosine monophosphate responses to exogenous and endogenous parathyroid hormone in familial benign hypercalcemia and primary hyperparathyroidism. 625 80

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


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