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

Clinical and biochemical data are presented on 18 children with severe hyperinsulinaemic hypoglycaemia born to non-diabetic mothers. Thirteen presented within three days of birth, three by 20 months and two aged nine years. Diagnosis of hyperinsulinism (HI) was made in a single blood sample by showing inappropriate plasma insulin levels (23 +/- 3 mU/l) for glycaemia (1.2 +/- 0.1 mmol/l), with low blood ketone body, lactate, alanine and glycerol levels. All children showed increased glucose disappearance rates (KG 7.6% +/- 0.06) and glucose requirement (range, 9-25 mg/kg/min) and an exaggerated glycaemic response to glucagon when hypoglycaemic. Confirmatory tests included measurement of plasma insulin levels during leucine and arginine tolerance tests, during hypercalcaemia and after fish insulin. Coeliac angiograms were performed in three cases. Clinical progress could be divided into five categories. Four cases recovered normal insulin control spontaneously (transient neonatal HI); two children responded and remain on diazoxide therapy, two responded to diazoxide after partial pancreatectomy (diazoxide responsive HI); in three cases resolution of hypoglycaemia resulted from resection of isolated adenoma (insulinoma); total pancreatectomy was needed in five cases (nesidioblastosis) and two children were victims of drug administration (drug induced HI). This analysis allows the definition of a practical approach to diagnosis and management of this major clinical problem.
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PMID:Hyperinsulinaemic hypoglycaemia in infancy and childhood: a practical approach to diagnosis and medical treatment based on experience of 18 cases. 639 78

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

The effect of mild hypercalcaemia on the growth hormone (GH), C-peptide and glucose responses to arginine infusion in patients with insulin-dependent idiopathic diabetes mellitus (ID) was compared with that observed in patients whose diabetes was secondary to idiopathic haemochromatosis (IH) and chronic pancreatitis (CP). The summated GH responses to arginine infusion alone were similar in all three groups. Mild hypercalcaemia significantly diminished the GH response to arginine in patients with secondary diabetes, but not in those with ID. As the blood glucose and C-peptide responses were similar in the presence of a normal or raised serum calcium, the differences in GH response could not be ascribed to changes in blood glucose levels or to alterations in endogenous insulin release. For reasons as yet unknown, hypercalcaemia appears to have more of a stabilizing effect on the pituitary somatotrophic granules of those with secondary diabetes than in those with ID.
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PMID:The effect of acute hypercalcaemia on arginine induced growth hormone release in diabetic man. 653 33

Biochemical and other parameters in VX-2 carcinoma in rabbits were evaluated. VX-2 carcinoma not only produced hypercalcemia but also hypophosphatemia and 25-OH-vitamin D deficiency. An increased turnover of 25-OH-vitamin D seems likely. Serum parathyroid hormone and urinary cyclic AMP did not increase. Hypokalemia occurred in association with hypophosphatemia and lowered blood glucose within 1 week after tumor transplantation. At the end of the experiment glucose and insulin were both below the control range. It is concluded that VX-2 carcinoma in rabbits yields much more complex biochemical alterations than reported before on calcium metabolism.
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PMID:Electrolyte and glucose metabolism in VX-2 carcinoma of the rabbit. 668 51

The authors investigated in 19 healthy women changes in the plasma levels of cortisol and growth hormone during acute hypercalcaemia induced by a load of 8.9 mg Ca2+/kg body weight, administered as intravenous infusion and the effect of hypercalcaemia on the adrenocortical and somatotrophic secretory reserve assessed by the test with insulin hypoglycaemia. Hypercalcaemia causes a rise of the basal cortisol plasma level starting at the 90th minute from the onset of the infusion when the calcium level reaches values of 2.99 mmol/l. The adrenocortical secretory reserve is, however, significantly reduced by hypercalcaemia. Hypercalcaemia does not affect growth levels nor the somatotrophic secretory reserve.
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PMID:Effect of hypercalcaemia on adrenocortical and growth hormone secretion. 668 86

Gastric inhibitory polypeptide (GIP) is a candidate hormone for an incretin which stimulates or potentiates insulin secretion. We elucidated that, in five patients with hyperparathyroidism, GIP and insulin responded remarkably to glucose ingestion, and that hypercalcaemia appeared to have a stimulatory effect on glucose-induced GIP release as well as on insulin release. In nine healthy subjects a 2% calcium solution was continuously infused intravenously and a hypercalcaemic state was maintained. This caused GIP to respond significantly more to glucose ingestion. In spite of GIP being considered an incretin in the normoglycaemic state, GIP does not markedly stimulate insulin secretion. However, in the hypercalcaemic state in healthy subjects, glucose-induced GIP and insulin secretion is significantly greater than in the normocalcaemic state. The potentiated response of insulin to glucose may be caused, in part, by GIP.
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PMID:Release of gastric inhibitory polypeptide (GIP) during calcium infusion and in hyperparathyroidism. 675 Jul 3

The present investigation was carried out in 16 healthy subjects in order to study whether calcium antagonism would affect the hypoglycemic response to insulin, and/or whether it would affect the insulin and glucose responses to glucagon. For this purpose verapamil, a potent calcium-blocking agent, was used. Verapamil infused alone did not affect the basal insulin or glucose concentrations. However, such infusion reduced the hypoglycemic response to insulin. Furthermore, the glucose response to glucagon was augmented by simultaneous infusion of verapamil, whereas the insulin response to glucagon was unaffected. When healthy volunteers were simultaneously infused with both calcium and verapamil the glucose response to glucagon was no longer augmented. The insulin response to glucagon also remained unaffected. These findings indicate that intravenous verapamil has hyperglycemic effects, unrelated to insulin, under certain conditions. They also imply that exogenous hypercalcemia counteracts the augmentative effect of verapamil on the glucose response to glucagon.
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PMID:Effect of verapamil on glucose response to intravenous injection of glucagon and insulin in healthy subjects. 699 47

Insulin secretion in response to an oral glucose challenge during acute hypercalcaemia was studied. Oral glucose tolerance tests (OGTT) were performed in 12 non-diabetic, non-obese human volunteers, aged 20-28 years. Blood samples were collected for calcium, glucose and insulin determination. The next day the same volunteers received a 4 h infusion of calcium gluconate (15 mg/kg/4 h) and were administered glucose 1 h after starting the infusion. Serum calcium, glucose and insulin concentrations were measured again. Infusion of calcium gluconate resulted in an increase in serum calcium concentration of 5 mg/100 ml over 4 h. During these infusions no significant changes in glucose concentrations were noted. On the other hand, the total mean insulin concentration, expressed as the area under the 3 h glucose tolerance curve, and the insulin peak at 30 min were significantly increased during hypercalcaemia (P < 0.001). These data indicate that acute hypercalcaemia does not affect carbohydrate tolerance but increases insulin secretion in human beings.
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PMID:Effect of acute hypercalcaemia on glucose tolerance and insulin release in human beings. 699 45

The present investigation was carried out in order to study the acute effects of hypercalcemia on the carbohydrate metabolism in healthy subjects and in patients with non insulin-dependent diabetes mellitus (NIDDM). The combined effect of hypercalcemia and a calcium-antagonistic agent (verapamil) was also studied in healthy subjects, in patients with chronic hypercalcemia, e.g. primary hyperparathyroidism (PHPT). Calcium, infused intravenously to fasting diabetic patients, induced a significant decline in the blood glucose concentration. This was not the case in healthy individuals. When glucose was administered orally during exogenous hypercalcemia, glucose tolerance decreased significantly in the diabetic as well as in the healthy individuals. Verapamil, however, abolished this hypercalcemia effect, and even improved the tolerance for oral glucose when administered intravenously together with calcium in the patients with NIDDM. No such effect of verapamil was seen in the healthy subjects or in the patients with PHPT. Insulin activity was left unaffected by hypercalcemia and/or verapamil in all experimental situations. These findings thus imply that hypercalcemia decreases the tolerance for oral glucose in normoglycemic subjects, and further deteriorates the glucose tolerance in patients with an already impaired carbohydrate metabolism. Verapamil, on the other hand, appears to counteract this effect of hypercalcemia in diabetic patients. Since insulin remains unaffected by calcium and verapamil in the above mentioned situations, it is reasonable to assume that the calcium- and verapamil-induced effects on the glucose tolerance are due to glucose-regulatory factors other than insulin.
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PMID:Hypercalcemic and calcium-antagonistic effects on insulin release and oral glucose tolerance in man. 704 21

Plasma gastric inhibitory polypeptide (GIP), insulin, glucagon concentrations and blood glucose levels in response to the ingestion of 100 g glucose were measured in 5 patients with hyperparathyroidism in order to elucidate the effect of hypercalcemia on the release of these hormones. In addition, the effect of acute hypercalcemia on the release of these hormones in response to glucose ingestion was investigated in normal subjects. Fasting plasma GIP concentration in patients with hyperparathyroidism was significantly greater than the value in seventeen normal subjects. Significantly higher responses of plasma GIP and insulin were observed after the glucose ingestion in the patients with hyperparathyroidism as compared with the values in the normal subjects, and integrated GIP and insulin responses to the glucose ingestion for 120 min in the patients with hyperparathyroidism were significantly greater than the values in the normal subjects. On the other hand, plasma glucagon concentration after the glucose ingestion in the patients with hyperparathyroidism remained unchanged, although plasma glucagon concentrations after the glucose ingestion decreased significantly from the basal value in the normal subjects. Blood glucose levels after the glucose ingestion in two groups increased significantly from the basal value in the same manner. In nine normal subjects calcium infusion (4 mg/kg bolus injection followed by continuous infusion of 4 mg/kg/hr for 3 hr) caused a significantly high concentration of plasma calcium (11.5 approximately 13.0 mg/dl) from the basal value. Significantly higher responses of plasma GIP and insulin to the glucose ingestion were observed during calcium infusion as compared with the values during saline infusion. On the other hand, plasma glucagon concentration after the glucose ingestion was not significantly changed during calcium infusion in contrast with a significant decrease of plasma glucagon after the glucose ingestion during saline infusion. Consequently, calcium was considered to play a major part in the release of GIP and insulin. The characteristic response of plasma glucagon during calcium infusion was considered, at least in part, to protect the hypoglycemia caused by hyperinsulinemia.
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PMID:[The effect of calcium on the release of gastric inhibitory polypeptide (GIP) - with reference to the release of GIP in patients with hyperparathyroidism (author's transl)]. 704 44


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