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

In the submitted review the author pays attention to mechanisms of control of insulin secretion and the mutual interaction of other messengers (cAMP, calcium and inisitol triphosphate) with special attention to the calcium signal which plays a most important role in the stimulation of the excitable B cell. The trigger of the two-stage insulin secretion is cyclic accumulation of calcium in the cytosol of the B cell and the mutual harmony between calcium of the intra- and extracellular compartment. In the early stage of insulin secretion in particular the intracellular compartment is the source of calcium; from there the ion is released due to the action of inositol triphosphate (IP3) activated by phospholipase C. Calcium of the extracellular compartment is mobilized also in the early secretory stage by opening of the depolarization-dependent calcium channels, it plays, however, a more important part during the second stage. Activation of the other messengers, incl. the calcium signal, depends on the type of secretagogue stimulus. During systemic changes of calcium homeostasis in vivo the calcium signal of the B cell is activated or inhibited in different ways. In the course of hypercalcaemia, in particular if acute, the direct influence of calcium ions on insulin secretion is modulated by further factors, e.g. somatostatin, calcitonin, cholecystokinin, glucagon, adrenocortical hormones, opioids and other substances released into the blood stream. In chronic hypercalcaemia which is the result of primary hyperparathyroidism or vitamin D intoxication the action of calcium on the metabolic and hormonal response is enhanced by the ionophoretic action of parathormone or active vitamin D metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The calcium signal in the regulation of insulin secretion]. 269 62

Thyroid glands from 64 bulls with hyperplastic and/or neoplastic changes in ultimobranchial remnants and in the parafollicular (C) cell system were studied structurally and with immunohistochemical methods. Antibodies against thyroglobulin, calcitonin, somatostatin, and neurotensin were used to detect these substances. Two different types of changes were observed. One change was hyperplasia and neoplasia of the ultimobranchial remnants that affected all their epithelial constituents. These included ultimobranchial follicles, cysts and tubules, as well as solid nests formed by basophilic immature cells which were functionally undifferentiated and unreactive with all the antisera used. Differentiated follicular cells that formed thyroid follicles and cribriform structures with immunohistochemical evidence of thyroglobulin production were also found. In addition, differentiated light and cytoplasm-rich cells were scattered in the walls of the thyroid follicles, ultimobranchial follicles, cysts and tubules as well as in the solid component. They were argyrophilic and reacted with antibodies against calcitonin and somatostatin. The other change was a diffuse or multifocal hyperplasia of the parafollicular (C) cells that was present in other parts of the thyroid parenchyma--sometimes with gradual development of sclerotic tumors that had been exclusively formed by these cells. They corresponded to light cytoplasm-rich cells seen in the ultimobranchial lesions that were argyrophilic and harbored material reactive with antibodies against calcitonin and/or somatostatin. The changes observed in the parafollicular cell system resembled lesions seen in human thyroid glands with the familial variant of medullary carcinoma as well as those reported in thyroid glands of patients with longstanding hypercalcemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperplastic and neoplastic changes in ultimobranchial remnants and in parafollicular (C) cells in bulls: a histologic and immunohistochemical study. 285 34

Hypercalcemia produced in healthy volunteers by intravenous infusions of calciumgluconolactobionate increased outputs of gastric acid, pepsin, and pancreatic enzymes. Hypercalcemia did not affect gallbladder emptying and serum gastrin values. Further, intravenous somatostatin (SRIF, 5 micrograms/kg.h) markedly inhibited secretion of gastric acid (p less than 0.01), pepsin (p less than 0.05), and pancreatic enzymes (p less than 0.02) stimulated by hypercalcemia. SRIF-inhibited outputs were below basal values. These results indicate that the inhibitory effect of SRIF on exocrine cells of the human gastrointestinal tract can not be reversed by extracellular hypercalcemia.
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PMID:[Effect of somatostatin on hypercalcemia stimulated gastric juice and exocrine pancreas secretion in the human]. 287 May 92

The authors compared the effect of synthetic salmon calcitonin and synthetic somatostatin (SRIF) and hypercalcaemia on an oral glucose tolerance test (OGTT) in healthy subjects in relation to changes of insulin (IRI), somatotrophin (HGH) and cortisol levels. Calcitonin--100 U--in an intravenous infusion in the course of OGTT markedly altered the pattern of the blood sugar curve and of IRI levels. After the initial retardation of the rise of the blood sugar and IRI levels during the 15th and 30th min, the values of both variables increased parallel during the 120th and 180th min, as compared with the control examination after saline. SRIF--500 micrograms--administered in an intravenous infusion altered the pattern of the blood sugar and IRI curves in a similar way as calcitonin, however during the 120th and 180th minute when the blood sugar levels rose significantly the IRI levels did not rise. The curve of HGH levels on infusion with calcitonin displayed a typical three-phase course, as during the control OGTT. During infusion of SRIF the HGH levels were insignificantly but constantly reduced during the first 60 mins. of the OGTT and thus the typical three-phase shape of the curve was impaired. Calcitonin significantly raised the cortisol levels throughout the OGTT, while SRIF caused their slight decline during the 120th min. Hypercalcaemia induced by infusion of 13.3 mg Ca/kg body weight did not alter significantly the blood levels of glucose, IRI and HGH, but caused a significant rise of the cortisol level throughout the OGTT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of calcitonin, somatostatin and hypercalcaemia on metabolic and hormonal indicators during an oral glucose tolerance test (OGTT). 288 8

A case of prostatic carcinoma with the cellular patterns of an adenocarcinoma and carcinoid tumor is reported. The tumor contained ultrastructural dense core neuroendocrine granules, and immunoperoxidase staining revealed prostatic acid phosphatase, prostatic-specific antigen, chromogranin, neuron-specific enolase, serotonin, adrenocorticotrophic hormone (ACTH), somatostatin, parathormone, calcitonin, bombesin, and glucagon but no insulin. The patient had exhibited hypercalcemia that may have been related to hormone production by the tumor. The literature on the endocrine aspect of the prostate and its tumor is reviewed.
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PMID:Prostatic carcinoma with endocrine features. A report of a neoplasm containing multiple immunoreactive hormonal substances. 289 Dec 93

Hypercalcemia was induced in rats by the administration of A.T.10. We then determined the levels of total and ionized calcium and calcitonin in the serum, as well as performed ultrastructural observations and histochemical investigations of the calcitonin and neuron-specific enolase immunoreactivities in the stimulated parafollicular cells. The main aim of the study was to apply histochemical procedures to determine the immunoreactions of calcitonin gene-related peptide (CGRP), somatostatin and secretory protein-I in stimulated parafollicular cells. Immunoreactions of CGRP and calcitonin decreased strikingly in A.T.10-treated animals, whereas no visible changes were noted in somatostatin immunoreactivity. In the case of secretory protein-I, an insignificant increase of its immunoreactivity was observed in the treated animals. The cytophysiological significance of these results is discussed.
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PMID:Effect of hypercalcemia on parafollicular cells in the rat thyroid gland. 289 47

A female patient with acromegaly, hypercalcemia, and Zollinger-Ellison syndrome was found to have a very high plasma concentration (average 2,300 pmol/liter; normal less than 50 pmol/liter) of growth hormone-releasing factor as measured by a radioimmunoassay to human pituitary growth hormone-releasing factor-1-44. The plasma concentration of growth hormone averaged 25 mIU/liter (normal less than 5 mIU/liter) and there was no rise following an intravenous 100 micrograms bolus of human pituitary growth hormone-releasing factor-1-44. Plasma growth hormone and growth hormone-releasing factor levels were unaffected by bromocriptine, insulin-induced hypoglycemia, and sleep. A long-acting somatostatin analogue lowered both the growth hormone-releasing factor and the growth hormone levels. Thyrotropin-releasing hormone stimulation and oral glucose tolerance tests produced significant increases in plasma growth hormone levels whereas the growth hormone-releasing factor level remained unchanged, suggesting that when normal somatotrophs are exposed to maximal growth hormone-releasing factor stimulation, thyrotropin-releasing hormone becomes a secretagogue of growth hormone from the pituitary. It is proposed that in the absence of a radioimmunoassay for growth hormone-releasing factor, a lack of growth hormone response to growth hormone-releasing factor in a patient with acromegaly is compatible with a source of ectopic growth hormone-releasing factor production.
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PMID:Growth hormone secretion dynamics in a patient with ectopic growth hormone-releasing factor production. 392 80

The release of immunoreactive gastrin and somatostatin form the gastric antrum was studied in anesthetized pigs after parathyroid hormone (PTH) infusion into the antral circulation. PTH (40 units/20 min) was infused into the right gastro-epiploic artery. Blood was sampled from the right gastro-epiploic vein (antral venous blood) and from the superior vena cava (mixed venous blood). The basal gastrin concentration in antral venous blood was 17 times higher than that in mixed venous blood (1220 + 367 versus 71 +25 pmol/1, mean +SE). The somatostatin concentrations in antral and mixed venous blood were 127 +20 and 82 +23 pg/ml (mean +SE), respectively. After PTH infusion the gastrin level both in antral and mixed venous blood increased significantly without inducing systemic hypercalcemia. PTH infusion did not significantly influence the somatostatin level either in antral venous blood or in mixed venous blood. The findings demonstrate that PTH can induce gastrin release from the gastric antrum without concomitant systemic hypercalcemia and that this release of gastrin is not accompanied by a change in the somatostatin level in antral venous blood.
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PMID:Effect of parathyroid hormone on gastrin and somatostatin release from the gastric antrum. 611 27

Clinical and laboratory data, histologic, electron microscopic and immunocytochemical findings of the tumors of eight patients suffering from Cushing's syndrome and of one patient with hypercalcemia are described. The unlabeled antibody enzyme method was used for the detection of insulin, glucagon, somatostatin, pancreatic polypeptide, corticotropin, beta-lipotropin, calcitonin, parathyroid hormone, and gastrin. Ectopic Cushing's syndrome was caused by pancreatic endocrine tumors, medullary thyroid carcinoma, a bronchial, a gastric and a thymic carcinoid, and a carcinoid of the mediastinum. Hypercalcemia in one patient was related to a pancreatic endocrine tumor. After surgery the clinical symptoms disappeared in two patients, but persisted or relapsed in five patients. ACTH-immunoreactivity could be demonstrated in six of eight tumors; calcitonin-immunoreactivity was found in the tumor of the patient suffering from hypercalcemia. ACTH-immunoreactivity could be localized to secretory granules by immunoelectron microscopy, and the presence of ACTH and beta-LPH in the same tumor cells could be shown in one pancreatic tumor. A combination of production of orthotopic and ectopic hormones was found in one, and secretion of two ectopic hormones was detected in another pancreatic endocrine tumor.
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PMID:Ectopic hormone production by endocrine tumors: localization of hormones at the cellular level by immunocytochemistry. 627 90

In exceptional cases, acromegaly develops as the clinical expression of an ectopic secretion of Growth Hormone (GH) or Growth Hormone-Releasing Factor (GRF), tumorous in origin. In the present report, we describe an instance of acromegaly caused by the secretion of GRF from a voluminous pancreatic tumor. The resection of this tumor resulted in a temporary disappearance of the biological and clinical symptoms of acromegaly, which then reappeared in conjunction with a rise in plasma GRF. From this pancreatic tumor, substances displaying a potent GRF activity were isolated and characterized. Amino acid analyses revealed that they were related to 3 peptides containing respectively 44, 40 and 37 aminoacids. The largest (hp GRF (1-44)-NH2) referred as hp GRF or somatocrinin is considered to be the primary molecule. The pancreatic tumor was multisecreting as proved by high plasma levels of somatostatin, pancreatic polypeptide and glucagon, normalized after the tumor removal, taken together with the immunocytochemical demonstration of the presence of these peptides in the tissue and with the isolation of somatostatin. In contrast hypercalcemia associated with an elevated plasma level of IR-PTH was unmodified by tumor removal. Diagnosis of acromegaly as ectopic endocrine syndrome will probably be facilitated by plasma GRF radioimmunoassay, as a result of production of anti synthetic GRF antibodies.
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PMID:[Acromegaly, clinical expression of the production of growth hormone releasing factor in pancreatic tumors]. 643 Feb 7


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