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

The authors investigated the effect of acute hypercalcaemia induced by a 2-hour intravenous infusion of calcium gluconate (8.9 mg Ca2+/kg b. w.) on the lactotrophic secretory reserve assessed by the test with insulin hypoglycaemia (delta PRL) and the effect of an intravenous bolus of 50 IU synthetic salmon calcitonin on the lactotrophic secretory reserve assessed by means of the TRH test (delta PRL). Acute hypercalcaemia inhibits PRL levels stimulated by insulin hypoglycaemia (p less than 0.01) as well as delta PRL (p less than 0.01). Calcitonin reduces PRL levels at rest and TRH stimulated levels (p less than 0.05 and p less than 0.01, respectively) as well as delta PRL (p less than 0.01). The prolactin inhibiting effect of calcitonin resembles markedly the effect of hypercalcaemia. The exact mechanism of these changes and the physiological impact of calcitonin on the regulation of PRL secretion is not known.
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PMID:Hypercalcaemia and calcitonin inhibit prolactin secretion. 644 27

In Sarotherodon mossambicus prolactin cell activity is related to ambient Ca2+ levels, and prolactin has hypercalcemic activity in this species. To study whether prolactin has a direct action on calcium metabolism, or whether prolactin's relationship with calcium is indirect and connected with control of gill permeability, the effects of external Ca2+ and Mg2+ on prolactin secretion and gill permeability were compared. It appeared that high external Mg2+ was associated with reduced prolactin secretion, even though high Mg2+ resulted in a marked hypocalcemia. Exposure of fish to high Ca2+ levels led to hypercalcemia. Both high Mg2+ and high Ca2+ concentrations in the ambient water reduced the osmotic water permeability of the gills. These results represent further evidence that prolactin secretion in S. mossambicus may be affected by any external factor that interferes with branchial permeability. It is concluded that prolactin's main function in this species is connected with control of branchial permeability rather than calcium metabolism, although internal calcium may be implicated in permeability control.
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PMID:Effects of external Mg2+ and Ca2+ on branchial osmotic water permeability and prolactin secretion in the teleost fish Sarotherodon mossambicus. 665 34

Neoplasia-induced hypercalcemia in the Fischer rat results in hypertension 1 wk after Leydig cell tumor transplantation. Systolic blood pressure, plasma catecholamine, prolactin, plasma renin activity (PRA), and aldosterone responses to immobilization stress were evaluated in Fischer rats 10 days after tumor transplantation and in age-matched nontransplanted controls. Basal systolic blood pressure, norepinephrine, and PRA levels at 10 days after tumor transplantation were higher in association with elevated calcium levels in tumor-transplanted rats than in controls. Systolic pressure, norepinephrine, and epinephrine responses to immobilization stress were greater in the hypercalcemia 10-day transplanted rats. Although basal levels of prolactin and aldosterone were similar in the two groups. These observations suggest that elevated levels of the vasoactive hormones norepinephrine and angiotensin may play a pivotal role in development of hypertension in association with neoplasia-induced hypercalcemia. Further, neoplasia-induced hypercalcemia in the Fischer rat is associated with a relative hyperreninemic hypoaldosteronism state.
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PMID:Hormonal changes associated with hypertension in neoplasia-induced hypercalcemia. 704 41

The serum prolactin response to acute hypercalcemia during calcium infusion was studied in 7 normal subjects. Prolactin, and calcium levels were determined at 30 minute intervals during the 210 minutes of the infusion. The infusion performed consisted of either normal saline at 3 ml/min for 210 minutes, or 15 mg calcium/kg at 3 ml/min for 180 minutes followed by normal saline infusion for the final 30 minutes. Calcium concentration increased from a base line of 10.0 +/- 0.26 (mean +/- SEM) to a maximal level of 13.6 +/- 0.26 (mean +/- SEM) mg/100 ml, in response to calcium level in response to normal saline infusion. Prolactin level decreased significantly (P less than 0.05) from 9.5 +/- 1.45 (mean +/- SEM) to 3.7 +/- 0.2 (mean +/- SEM) ng/ml at 180 minutes.
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PMID:The effect of acute hypercalcemia on prolactin release in man. 726 25

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

Osteopenia is an important clinical manifestation of hyperprolactinemia. Bone loss in these patients has mainly been attributed to concomitant deficiency of gonadal hormones rather than to hyperprolactinemia per se. Parathyroid hormone-related peptide (PTHrP) is expressed in human mammary tissue, and elevated circulating PTHrP levels as well as concomitant hypercalcemia have been described during lactation. We sought to determine circulating PTHrP levels in patients with long-standing hyperprolactinemia and whether PTHrP may exert possible systemic effects on bone and mineral metabolism. We studied 45 patients (30 women and 15 men) with persisting hyperprolactinemia 6 +/- 4 years (mean +/- SD) after trans-sphenoidal surgery for prolactin-producing pituitary adenomas. PTHrP levels in 117 healthy controls were 10.6 +/- 7.3 pmol-eq/l (mean +/- SD). In hyperprolactinemic patients, plasma PTHrP was elevated to 30.3 +/- 13.4 pmol-eq/l (p < 0.001, n = 45), and in patients with humoral hypercalcemia of malignancy PTHrP levels were 52.9 +/- 29.6 (p < 0.001 to controls and hyperprolactinemic patients). Fifty-three percent of hyperprolactinemic patients (n = 24) had clearly elevated PTHrP levels (> 2 SD). Retrospective immunocytochemical studies of the removed pituitary adenomas from 19 patients generally showed a higher degree of immunoreactivity for PTHrP (1-34) in all but one case when compared with normal pituitary tissue. Patients with elevated circulating PTHrP levels showed in most instances strong immunoreactivity to PTHrP in 70-100% of tumor cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma levels of parathyroid hormone-related peptide are elevated in hyperprolactinemia and correlated to bone density status. 763 11

Homologous recombinant tilapia prolactin-188 (PRL-I) and tilapia prolactin-177 (PRL-II) were tested for calcitropic activity in tilapia, Oreochromis mossambicus. Injection of PRL-I and PRL-II (4 injections, 12.5 pmol/g, over an 8-day period) induced hypercalcemia that resulted from an enhanced calcium influx via the gills and a decreased calcium efflux. Both PRLs increased the density of the Ca(2+)-transporting Ca(2+)-adenosinetriphosphatase in a plasma membrane preparation of the branchial epithelium. Dose-response studies (doses tested: 0.75-12.5 pmol/g) demonstrated that PRL-I was roughly twofold more potent than PRL-II in inducing hypercalcemia, in enhancing basal levels of cortisol, and in stimulating opercular ionocyte density. PRL-I and PRL-II were equipotent in stimulating the dermal mucocyte frequency. We conclude that in this species PRL-I and PRL-II have calcitropic effects, and that PRL-I is more potent than PRL-II in this respect. We postulate that PRL has corticotrophic activity in this fish.
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PMID:Calcitropic effects of recombinant prolactins in Oreochromis mossambicus. 818 75

Administration of estrogen as well as prolactin to B. melanostictus resulted in hypercalcemia. Parathyroids and ultimobranchials of the toad were hypertrophied and the secretory epithelium reflected hyperplasia. Histophysiological manifestation of the parathyroids of treated toads suggests that estrogen and prolactin bring about hypercalcemia by stimulating the parathyroids. Changes in the ultimobranchials suggest hyperactivity of the gland to combat estrogen- and prolactin-induced hypercalcemia.
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PMID:Histophysiological evidence for parathyroid mediation of estrogen- and prolactin-induced hypercalcemia in the toad Bufo melanostictus (Schneider). 858 4

This study investigated the influence of calcium on serum prolactin (PRL) in hyperprolactinemic and healthy women. Previous studies have shown an inhibitory effect of Ca2+ on serum PRL, related to the degree of hypercalcemia. Serum PRL levels were measured by immunoradiometric assay (IRMA) in subjects before and one hour after 1375 mg Ca2+ injection. Serum PRL level was significantly decreased by calcium injection in hyperprolactinemic women (89.2 +/- 29.1 and 63.3 +/- 35.8 ng/ml; p < 0.01) while it was not significant (p > 0.05) in women with normal PRL levels (12.6 +/- 5.1 ng/ml and 11.3 +/- 4.0 ng/ml). These results indicate that acute alterations in serum calcium levels affect PRL secretion in hyperprolactinemic women.
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PMID:The influence of calcium infusion on serum prolactin in hyperprolactinemic women. 885 76

Multiple Endocrine Neoplasia type 1 (MEN 1) syndrome comprises tumors or hyperplasia of different glands, including parathyroid, pituitary, adrenal cortex and the gastroenteropancreatic system. The vast majority of MEN 1 are found in familial clusters, although a few cases are sporadic. Hypercalcemia and/or nephrocalcinosis are the first and most common clinical manifestation in familial MEN 1 syndrome, followed by islet cell tumors (especially those secreting gastrin or insulin) and pituitary dysfunction due to either functioning or non-functioning microadenomas. Genetic studies indicate that familial MEN 1 syndrome is inherited through a dominant gene with incomplete penetrance and variable expression. The diagnosis of MEN 1 syndrome is mainly based on the careful assessment of the clinical history, symptoms physical evaluation along with the assay of serum electrolytes (i.e., calcium, phosphorus, etc.) and hormonal substances (i.e., gastrin, insulin, pancreatic polypeptide, prolactin, adrenocorticotropic hormone, etc.). In addition, several provocative tests have been used to identify endocrine tumors (particularly those of the gastroenteropancreatic system) and imaging techniques play a crucial role for the diagnostic approach in MEN 1 syndrome. Even though in the long term, the prognosis of MEN 1 syndrome is unfavourable. Recently, however, many therapeutic strategies, including both surgical and pharmacological options, have been developed to reduce the size of the neoplasm and control symptoms associated with hormone oversecretion.
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PMID:[New etiopathogenic, clinical and therapeutic findings in multiple endocrine neoplasia type 1]. 892 87


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