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

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

The responses of TSH and PRL to intravenous doses of 500 micrograms of TRH were investigated in 26 patients with primary hyperparathyroidism. Fourteen patients (54%) showed low responses of TSH with peak values of less than 5 microU/ml (Group A). Twelve patients showed normal responses of TSH to TRH (Group B). Among the 26, 12 cases belonging to Group A and eight in Group B were reexamined after the correction of serum calcium level by parathyroidectomy. After successful treatment, the responses of TSH to TRH in six of the 12 patients in Group A returned to normal, whereas those in the remaining six were unchanged. The responses in the eight patients in Group B after surgery were not changed when compared to those before treatment. The basal values of PRL and the responses of PRL to TRH were normal in all patients and did not change after treatment. We showed that patients with primary hyperparathyroidism have a high incidence (54%) of suppressed TSH response to TRH. Hypercalcemia was obviously one of the causative factors in inducing this abnormality in six patients. However, persistently suppressed responses of TSH to TRH were observed in the other six patients in Group A even after the correction of the serum calcium level by surgery. This finding suggests a primary failure of the TSH-regulatory mechanism in some cases of primary hyperparathyroidism.
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PMID:The suppression of TSH in the presence of the normal PRL responses to TRH out of 26 patients with primary hyperparathyroidism. 641 19

To investigate the influence of calcium ions on the secretion of anterior pituitary hormones in response to stimulation by exogenous hypothalmic releasing factors in man, we measured serum concentrations of pituitary hormones serially during a continuous infusion of combined TRH (2 micrograms/min) and GnRH (1 microgram/min), with concomitant iv saline or calcium administration. Compared to saline, calcium administration was associated with a significant increase in GnRH-TRH-stimulated LH and FSH release and a corresponding rise in serum testosterone concentrations. The effect of calcium ions on gonadotropin secretion was specific, because releasing factor-stimulated secretion of TSH and PRL was suppressed by hypercalcemia. Serum concentrations of GH were not significantly altered under these conditions. In summary, the present results provide the first in vivo evidence that acute infusion of calcium ions augments GnRH-TRH-stimulated secretion of LH and FSH, with an accompanying increase in serum testosterone levels. In contrast, hypercalcemia did not alter serum GH concentrations, and it suppressed GnRH-TRH-stimulated release of PRL and TSH. We conclude that calcium ions can selectively influence releasing factor-stimulated secretion of certain anterior pituitary hormones in man.
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PMID:Divergent influences of calcium ions on releasing factor-stimulated anterior pituitary hormone secretion in normal man. 642 72

To investigate whether chronic endogenous hypercalcemia influences TSH and/or PRL release from pituitary thyrotrophs and lactotrophs in man, 10 patients with endogenous hypercalcemia, due either to cancer or to primary hyperparathyroidism, were injected with 25 micrograms TRH iv. The TSH and PRL responses were compared with those obtained in an age-, sex-, and weight-matched group of patients comprised of 10 normocalcemic individuals with other diseases. The mean maximal TSH response in the hypercalcemic group (3.7 +/- 0.4 microU/ml) was 46% lower than in the normocalcemic group (6.8 +/- 1.2 microU/ml; p less than 0.02). Similarly, the mean maximal PRL response was 45% lower in the hypercalcemic (31 +/- 5 ng/ml) than in the normocalcemic patients (57 +/- 9 ng/ml; p less than 0.05). Feasible mechanisms behind this inhibitory influence of chronic endogenous hypercalcemia on TSH and PRL responsiveness are discussed.
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PMID:Effect of chronic endogenous hypercalcemia on prolactin and thyrotropin responsiveness in man. 644 10

The effects of neoplasia-induced hypercalcemia on the hypothalamic-pituitary axis of the Fischer rat were determined by measuring the responses of TSH to TRH, PRL to TRH and haloperidol, and LH to LHRH in 3 groups of 8 rats prior to and at 4 and 8 days after transplantation of a Leydig cell tumor. The mean serum calcium was 8.2 +/- 0.2 mg/dl in 8 Fischer rats pretransplantation; had risen at 4 days posttransplantation to 9.8 +/- 0.2 mg/dl; and at 8 days was 11.2 +/- 0.1 mg/dl. TSH response to TRH was greater in the pretransplant rats than in the groups studied at 4 and 8 days posttransplant. Basal PRL levels and PRL responses to TRH and haloperidol were less in the groups studied at 4 and 8 days posttransplant. Basal LH values were similar in all 3 groups, but the LH response to LHRH was less for the posttransplant groups. The TSH response to TRH, PRL responses to TRH and haloperidol, and LH responses to LHRH were less in the 8 days posttransplants than in the groups studied at 4 days posttransplantation. There were significant negative correlations between TSH (r = -0.79) and PRL (r = -0.80) responses to TRH, PRL responses (r = -0.94) to haloperidol and LH responses (r = -0.91) to LHRH and the serum calcium. The results indicate that increasing levels of serum calcium following Leydig cell tumor transplantation are associated with suppression of adenohypophysial release of TSH, PRL, and LH; the degree of suppression is related to the magnitude of hypercalcemia achieved in this model.
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PMID:The effect of neoplasia-induced hypercalcemia on the neuroendocrine axis of the Fischer rat. 676 27

The influence of acute hypercalcemia induced by i.v. infusion of calcium gluconate on basal TSH and T3 levels in plasma and on their response to TRH stimulation (TRH test) was investigated in 10 healthy subjects. TRH test under normal conditions without hypercalcemia was carried out in the same subjects. Under acute hypercalcemia the basal T3 levels were evaluated markedly up to levels occurring after TRH stimulation. However, the relative increase of T3 following TRH challenge was of the same degree as in normocalcemia. Basal TSH levels did not differ from those found under normocalcemia, but the response to TRH was decreased. The results suggest that hypercalcemia affects the mechanisms regulating the levels of the thyroid hormones and TSH.
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PMID:Hypercalcemia influences TRH-stimulated TSH and T3 response. 680 Jul 77

To investigate whether exogenous hypercalcemia influences the release of TSH from the anterior pituitary, 25 microgram TRH were injected iv in six healthy subjects who were pretreated orally with either 10 mg metoclopramide or placebo and infused iv with either calcium or saline. Under normocalcemic conditions, TRH raised the serum TSH level from 1.1 +/- 0.1 to 8.0 +/- 3.3 microU/ml (P less than 0.01). Exogenous hypercalcemia reduced this TSH response to TRH by 37 +/- 11% (P less than 0.02). Although metoclopramide was without effect on basal TSH release in an additional five healthy subjects and also left TRH-stimulated TSH release unaffected under normocalcemic conditions, oral pretreatment with the drug counteracted the inhibitory effect of hypercalcemia and restored a normal TSH response to TRH in hypercalcemic subjects. These results indicate that exogenous hypercalcemia may potentiate dopaminergic TSH inhibition in normal individuals.
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PMID:Influence of metoclopramide on calcium inhibition of thyrotropin response to thyrotropin-releasing hormone. 680 Oct 79

A number of previous investigations have indicated that the pituitary may directly stimulate secretion of parathyroid hormone. Others have disagreed. With the recent development of an in vitro bovine parathyroid perfusion system, the direct effect of suspected secretagogues can be assessed on a dynamic, ongoing basis. A partially purified pituitary extract (preparation A) was injected into calves. The plasma calcium increased an average of 1.1 mg/100 ml plasma. No increase of immunoreactive parathyroid hormone (iPTH) was detected, however, in the peripheral plasma prior to the increase in plasma calcium concentration. Since the peripheral plasma iPTH concentration has been shown to be relatively insensitive to changes in the secretion rate, the inability to detect a change in the iPTH concentration does not preclude a direct stimulating effect of the pituitary on the parathyroid. When preparation A was tested on in vitro perfused bovine parathyroid glands, a 30% average increase in secretion of c-iPTH (carboxy terminus) and a 56% average increase in secretion of n-iPTH (amino terminus) was observed under normocalcemic conditions. Under conditions of hypercalcemia, there was an average increase in the c-iPTH secretion rate of 60% and an average n-iPTH secretion rate increase of 88%. A failure of TSH, LH, GH, ADH, oxytocin, and prolactin to stimulate iPTH was observed. Previous reports have eliminated ACTH, MSH, and lipotropin as possible parathyroid secretagogues. The concept of a parathyroid stimulating hormone (PTSH) located in the pituitary that can directly stimulate the parathyroid gland to secrete parathyroid hormone is consistent with the results of this investigation.
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PMID:Pituitary stimulation of parathyroid hormone secretion: evidence in cattle for a parathyroid stimulating hormone. 742 44

The cholecalciferol analogues 1(S),3(R)-dihydroxy-20(R)-[3'(S)-cyclopropyl-3'-hydroxyprop-1'(E)- enyl]-9,10-secopregna-5(Z),7(E),10(19)-triene (calcipotriol, MC 903), 1(S),3(R)-dihydroxy-20(R)-[3'-ethyl-3'-hydroxy- pentoxy]-9,10-secopregna-5(Z),7(E),10(19)-triene (KH 1060) and 1(S),3(R)-dihydroxy-20(R)-[5'-ethyl-5'-hydroxy-hepta- 1',3'(E)-diene-1'-yl]-9,10-secopregna-5(Z),7(E),10(19)-triene (EB 1089) have been modified in the side chain to increase their effects on cell differentiation and proliferation and to reduce the risk of inducing hypercalcemia. The effects of these analogues were tested on FRTL-5 cells, a strain of continuously growing and well-differentiated rat thyroid cells. FRTL-5 cells express a normal vitamin D receptor (VDR), and 1,25-(OH)2D3 potently attenuates the thyrotropin (TSH) stimulated production of the intracellular signalling molecule 3',5'-cyclic adenosine monophosphate (cAMP), iodide uptake and cell growth of these cells. These effects were also induced by the cholecalciferol analogues after 4 days of incubation. KH 1060 was the biologically most potent of the analogues and, compared to KH 1060, the IC50 values were 1.2-, 2.7- and 14-fold higher when 1,25-(OH)2D3, EB 1089 and MC 903, respectively, were used for the displacement of receptor bound [3H]1,25-(OH)2D3. As indicated by their VDR binding, 1,25-(OH)2D3 and EB 1089 were equipotent inhibitors of the TSH stimulated adenylyl cyclase activity, iodide uptake and FRTL-5 cell growth. The analogue MC 903 was the second most potent inhibitor of cell growth in spite of expressing the lowest affinity for the VDR and the weakest inhibition of TSH-stimulated adenylyl cyclase activity and iodide uptake. In conclusion, the biological effects of these cholecalciferol analogues in rat thyroid FRTL-5 cells seem to be mainly determined by their binding affinity for the VDR, although non-genomic effects can not be excluded.
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PMID:Vitamin D receptor binding and biological effects of cholecalciferol analogues in rat thyroid cells. 804 43


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