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

To investigate the effects of acute hypercalcemia on exocrine pancreatic secretion, anesthetized cats were given calcium intravenously. Increasing hypercalcemia (3.7-6.3 mmol/L) evoked a dose-dependent increase in enzyme output that was 12 times greater than in normocalcemic controls (p less than 0.001) and was 60% of subsequent maximal stimulation with intravenous cholecystokinin (CCK). The effect of hypercalcemia on enzyme secretion was abolished when CCK was administered 60 min before calcium and at a dose to cause maximal enzyme output. Atropine did not prevent the calcium-induced increase in enzyme secretion. Pancreatic fluid and bicarbonate outputs were not influenced by hypercalcemia during intravenous administration of small amounts of secretin, but were increased by addition of CCK to the secretin infusion. Hypercalcemia did not induce macroscopic or light-microscopic changes in pancreatic morphology. Plasma levels of both CCK and gastrin were increased (p less than 0.01) during hypercalcemia, with and without precalcium administration of CCK; atropine significantly inhibited (p less than 0.05), but did not abolish the calcium-induced releases of both peptides. These data suggest that in the anesthetized cat, acute hypercalcemia induced by intravenous calcium infusion stimulates pancreatic secretion of enzymes, but not fluid and bicarbonate. Acute hypercalcemia also causes release of CCK and, as shown previously, gastrin. The findings suggest that the stimulatory effect of hypercalcemia on pancreatic enzyme secretion is not dependent on intact cholinergic pathways and is probably not exclusively mediated by release of CCK or gastrin.
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PMID:Effects of acute hypercalcemia on exocrine pancreatic secretion in the cat. 257 66

A family of multiple endocrine neoplasia type I with five confirmed cases in three generations is described. All of them have primary hyperparathyroidism in common. The propositus is 51 year-old male. After a year of symptoms of gastroduodenal ulcer, he was found to have elevated levels of serum gastrin and PTH. The serial imaging studies revealed a tumor in pancreatic head, and Zollinger-Ellison syndrome was diagnosed. The gastrin level was reduced into normal range after extirpation of the tumor, but post surgical elevation of Calcium put the patient under parathyroidectomy, which normalized serum PTH and Calcium levels. His two sisters (I and II), the mother of them, and the daughter of sister I, had neither signs nor symptoms until family study showed hypercalcemia in all. Sister I is a 54 year-old female with enlarged parathyroid. The hyperparathyroidism is of chemical type, but no other endocrinological abnormality is found. The Calcium level decreased after parathyroidectomy. Sister II is a 56 year-old female. The only sign was galactorrhea. Serum PTH and Calcium decreased after parathyroidectomy. The prolactinoma was diagnosed by the increased prolactin levels and enhanced mass lesion in sella turcica. Her serum prolactin levels is now within normal range since she is on bromocryptine. The mother of the above three siblings and the daughter of the sister I are now under further study.
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PMID:[A family with multiple endocrine neoplasia type I presenting prolactinoma, Zollinger-Ellison syndrome and hyperparathyroidism]. 286 39

In patients with hypercalcemia with abdominal symptoms, gastrin concentration is often measured to exclude the Zollinger-Ellison syndrome. We found that interpretation of such measurements is clouded by a contradictory literature. We therefore measured serum gastrin concentrations in 78 patients with primary hyperparathyroidism, 36 with nonparathyroid hypercalcemia, 13 with hypocalcemia, and 33 normocalcemic controls. Gastrin values above normal occurred in 22% of those with primary hyperparathyroidism and 28% of those with nonparathyroid hypercalcemia. Values above 250 pg/mL occurred only in those with hypochlorhydria or multiple endocrine neoplasia, type 1 (MEN 1). After parathyroidectomy, gastrin levels fell significantly, but elevated values tended to recur in those with MEN 1 if hypercalcemia recurred. Thus, chronic hypercalcemia of either parathyroid or nonparathyroid origin may elevate serum gastrin concentrations, but marked elevations suggest either achlorhydria or MEN 1.
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PMID:Serum gastrin level is increased by chronic hypercalcemia of parathyroid or nonparathyroid origin. 286 39

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 treatment of choice for gastric acid hypersecretion in MEN type I has now changed from total gastrectomy to the long-term administration of H2 receptor blockers or similar agents. However, the importance of parathyroidectomy for the concomitant hypercalcaemia is not fully realized. A case is reported of a subject with MEN type I, who was initially treated with parathyroidectomy and H2 receptor blockade. Following parathyroidectomy, there was a rapid fall of the markedly elevated gastrin levels to the upper limit of the normal range. During follow-up of 2.5 years, there has been no increase in serum gastrin, and the subject's gastric symptoms have resolved, despite the cessation of H2 blockade. Infusion of calcium to pre-operative levels and superimposed secretin stimulation after this period of time closely reproduced the pre-operative hypergastrinaemia. On screening, the subject's only child was found to have hypercalcaemia but normal serum gastrin levels and pituitary function; parathyroidectomy has been carried out. No abnormality of gastrin secretion has been found during follow-up. This case highlights the importance of early parathyroidectomy in this syndrome.
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PMID:Resolution of hypergastrinaemia after parathyroidectomy in multiple endocrine neoplasia syndrome type I (MEN type I). 288 48

The problem of hypergastrinemia in patients with the syndrome of multiple endocrine neoplasia (MEN type 1) has become increasingly controversial since the introduction of the antisecretory H2 antagonists for the treatment of the Zollinger-Ellison syndrome (ZES). One of the questions in the management of ZES is whether the malignant potential of the gastrinomas or the recurrent complications of ulcer will be the ultimate cause of death. Another problem is whether the association of MEN is a favorable or unfavorable factor to the prognosis of patients with ZES. Hypercalcemia contributes to excessive gastrin secretion, thereby casting doubt on the diagnosis of ZES in the presence of MEN. Patients with MEN are also more likely than patients with ZES not to have gastrinoma on an exploratory laparotomy. The existing controversy concerns the choices of therapy in instances of progressive ZES associated with MEN or when there is a failure to detect a primary gastrinoma when exploration is performed. To highlight the debate, the clinical courses of two patients, observed during two and three decades, respectively, are presented. These patients were receiving high doses of cimetidine; in addition, conventional surgical treatment for ulcer and repeated biopsies for gastrinoma were performed. After total gastrectomies (as life saving procedures), both patients are well.
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PMID:The progressive Zollinger-Ellison syndrome in multiple endocrine neoplasia. 290 96

Management of patients with multiple endocrine neoplasia type I (Wermer's syndrome) who have concurrent hypercalcemia and hypergastrinemia is controversial. The usual therapeutic approach has been to perform parathyroidectomy first before surgery for ulcer disease in an effort to decrease serum calcium concentration and presumably remove one of the stimuli for both gastrin and gastric acid secretion. We present the history of a 48-year-old man with primary hyperparathyroidism and Zollinger-Ellison syndrome who underwent acid secretory studies and secretin stimulation tests before and after parathyroidectomy. We also studied the effect of calcium channel blockade on gastrin and gastric acid secretion, since calcium influx into endocrine cells, such as the gastrinoma cell, is thought to be critical in hormone secretion. Although parathyroidectomy reduced serum calcium and parathormone levels to normal, basal serum gastrin concentration and basal acid output remained unchanged. The peak rise in serum gastrin concentration after secretin injection was less after parathyroidectomy than before parathyroidectomy but was still abnormal. During administration of verapamil, a calcium channel antagonist, no change was seen in the serum gastrin concentration, secretin test response, or acid secretion. Basal acid output was 45.4 mmol/hr before parathyroidectomy or verapamil and 54.0 and 50.4 mmol/hr after parathyroidectomy or verapamil, respectively. In contrast, a small but significant decrease (p less than 0.05) in serum parathormone concentration occurred during treatment with verapamil, an observation that to the best of our knowledge has not been previously reported in humans.
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PMID:Lack of effect of parathyroidectomy or calcium channel blockade on serum gastrin concentration and gastric acid secretion in a patient with hyperparathyroidism and Zollinger-Ellison syndrome. 379 19

Thirteen cases of patients with the Zollinger-Ellison syndrome were reviewed. In two cases the diagnosis was made by incidental biopsy of small liver nodules at operation for peptic ulcer disease. Seven patients had gastric secretory tests which showed a basal acid output to maximum acid output ratio of more than 65 percent. Five patients had bao:mao ratios less than 50 percent.A 30-month interval between incidental discovery of tumor and clinically evident disease was observed in two patients. Recurrence of symptoms after excision of tumor was noted after a similar interval in another case. Serum gastrin levels, before total gastrectomy, were elevated in all cases. The lowest preoperative level in this series of patients was 550 picograms per ml (normal 100 to 150 picograms). They were diagnostic in two patients with normal gastric secretory studies. The levels fell to normal following total gastrectomy in six patients. Two patients still had elevated levels five years and 14 years after total gastrectomy. One was discovered to have a parathyroid adenoma with hypercalcemia. Total gastrectomy was curative in all the patients with the Zollinger-Ellison syndrome; lesser operations were not.
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PMID:Acid secretion and serum gastrin levels in the Zollinger-Ellison syndrome. 503 40

A family with Multiple Endocrine Adenomatosis Type 1 (MEA 1) is described. Of the 59 members, 15 were affected. Zollinger-Ellison syndrome was present in six individuals of whom the five available for study had hyperparathyroidism. The youngest of these patients with Zollinger-Ellison Syndrome was 25 years old. Hyperparathyroidism alone was present in nine individuals of whom the eldest was 30 years old. Three other members had raised serum gastrin levels but lacked symptoms suggestive of Zollinger-Ellison syndrome and in these individuals, the serum calcium levels were normal. A review of the literature confirms the finding that, in MEA 1, Zollinger-Ellison syndrome has not been shown to occur in the absence of hypercalcaemia. Screening of affected members of such families can therefore be restricted to the measurements of serum calcium levels.
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PMID:Hyperparathyroidism: a prerequisite for Zollinger-Ellison syndrome in multiple endocrine adenomatosis Type 1--report of a further family and a review of th literature. 610 54

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


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