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

Hyperparathyroidism is associated with abnormalities in glucose tolerance and insulin secretion. To assess the effects of hyperparathyroidism on the control of diabetes mellitus, 56 patients with concomitant hyperparathyroidism and diabetes mellitus were studied before and after parathyroidectomy. Fifty patients (89.3%) had hypercalcemia, and six patients (10.7%) had normocalcemia associated with inappropriately elevated parathyroid hormone. After surgery, three of five patients with insulin-dependent diabetes mellitus showed more than a 50% reduction in insulin requirement. Thirty-nine of 49 patients with noninsulin-dependent diabetes mellitus were followed. Of these, three patients had restoration of normal blood glucose levels without any diabetic treatment including diet restriction. Diabetes control improved in eight parents, remained stable in 18, and deteriorated in 10 patients. In the remaining two patients, impaired glucose tolerance disappeared in one patient and progressed to frank diabetes in the other. Overall 60.7% of the patients improved or remained stable in their diabetes control after parathyroidectomy. We conclude that in patients with hyperparathyroidism, the coexistence of diabetes mellitus might be a further indication for parathyroidectomy. Physicians should be alerted to the possible change in diabetic regimen and the risk of hypoglycemia in patients with diabetes after parathyroidectomy.
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PMID:Effect of hyperparathyroidism on the control of diabetes mellitus. 353 62

In order to investigate mineral and vitamin D metabolism in obese rats with hyperinsulinemia, plasma calcium and vitamin D metabolites were measured in Zucker fa/fa rats. Body weight, plasma insulin, and calcium in fa/fa rats were significantly increased compared to their lean littermates (p less than 0.01). However, no significant difference in plasma 25-hydroxyvitamin D (25(OH)D), 24,25-dihydroxyvitamin D, 1,25-dihydroxyvitamin D (1,25(OH)2D) or the ratio of 1,25(OH)2D to 25(OH)D was observed between fa/fa rats and their lean littermates. The hypercalcemia in the rats with hyperinsulinemia, therefore, might be caused by other calcium-regulating hormones or some factors other than 1,25(OH)2D. In addition, the hyperinsulinemia associated with obesity may not produce the accelerated conversion from 25(OH)D into 1,25(OH)2D.
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PMID:The role of vitamin D metabolites in hypercalcemia of Zucker fa/fa rats. 387 38

Previous studies have shown that there is an impairment in renal production of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the major biologically active metabolite of vitamin D3, in diabetes. This impairment is not due to a deficiency in the parathyroid hormone (PTH), a major stimulator of renal 1,25(OH)2D3 production. Therefore, we have investigated the capacity of PTH to stimulate 1,25(OH)2D3 production in insulin deficiency and with insulin replacement. Experiments were performed in rats fed a 0.6% calcium, vitamin D sufficient diet for 2 weeks. Thyroparathyroidectomy was performed on all rats. Rats to be rendered diabetic were injected with streptozotocin immediately after surgery. In non-diabetic rats, PTH administration significantly increased renal 1,25(OH)2D3 production (11 +/- 2 vs 46 +/- 5 pg/min/g; P less than 0.05). In diabetic rats, however, PTH caused only a modest increase in 1,25(OH)2D3 production (11 +/- 1 vs 19 +/- 4 pg/min/g; P less than 0.05). With insulin replacement, PTH stimulation of 1,25(OH)2D3 production was markedly increased over that seen in diabetic rats (48 +/- 12 vs 19 +/- 4 pg/min/g; P less than 0.05). PTH was equally effective in raising serum calcium, depressing serum phosphorus and tubular reabsorption of phosphate in non-diabetic as well as in diabetic rats. These results demonstrate that insulin is necessary for the maximal stimulation of renal 1,25(OH)2D3 production by PTH. However, insulin is not necessary for PTH action in terms of renal handling of phosphate and inducing hypercalcaemia. These results suggest multiple pathways for the action of PTH, only some of which are insulin requiring.
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PMID:Insulin modulates the stimulation of renal 1,25-dihydroxyvitamin D3 production by parathyroid hormone. 389 9

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 effect of streptozotocin-induced diabetes mellitus (DM) on the adaptive response to phosphorus depletion (PD) was investigated in order to examine if DM has any influence on the adaptation to PD in rats. PD for 7 days caused a marked reduction in serum phosphate (Pi) levels and increase in serum calcium (Ca) concentrations in control rats. In contrast, the increase in serum Ca concentration caused by PD was almost entirely eliminated in DM rats. Similarly, while bone Ca and P content was decreased by 7 days of PD in control rats, no significant changes in bone mineral contents were observed in DM rats during PD. There was a marked reduction in fractional excretion of Pi and an increase in fractional excretion of Ca during PD in both control and DM rats. Serum somatomedin A levels measured by radioreceptor assay were lower in DM rats compared to those in control rats, but PD caused no significant changes in either group of animals. These results demonstrate that the development of hypercalcaemia and reduction in bone mineral content in response to PD were inhibited while the renal tubular responses to PD were not affected in DM rats. It is suggested that the inhibition of the hypercalcaemic response to PD in DM rats is mainly due to an inhibition of the resorptive response of bone to PD, and that insulin either directly or indirectly may play a permissive role in the development of the resorptive response of bone to PD.
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PMID:Adaptation to phosphorus depletion: effect of streptozotocin-induced diabetes mellitus. 403 3

Plasma insulin dynamics were evaluated in 10 patients with primary hyperparathyroidism before and after parathyroidectomy and correction of hypercalcemia. Before surgery fasting plasma insulin concentrations and insulin responses to administered glucose, tolbutamide, and glucagon were significantly greater than postoperative values. Hyperinsulinemia was not associated with altered glucose curves during glucose or glucagon tolerance tests, but a relatively greater insulin response to tolbutamide resulted in an increased hypoglycemic effect following its administration. The glucose-lowering action of intravenous insulin was slightly impaired before treatment. Intramuscular injections of parathormone to six normal men for 8 days induced mild hypercalcemia and hypophosphatemia and reproduced augmented plasma insulin responses to oral glucose and intravenous tolbutamide. 4-hr intravenous infusions of calcium to another group of six normal men raised serum calcium concentrations above 11 mg/100 ml. This did not alter glucose or insulin curves during oral glucose tolerance but markedly accentuated insulin responses to tolbutamide and potentiated its hypoglycemic effect. When highly purified parathormone was incubated with isolated pancreatic islets of male rats, glucose-stimulated insulin secretion was unaffected. These findings suggest that chronic hypercalcemia of hyperparathyroidism sustains a form of endogenous insulin resistance that necessitates augmented insulin secretion to maintain plasma glucose homeostasis. This state is insufficient to oppose tolbutamide-induced hypoglycemia because of an additional direct, selective enhancement of hypercalcemia on pancreatic beta cell responsiveness to the sulfonylurea. The possible direct role of parathormone in these events has not been established.
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PMID:Plasma insulin disturbances in primary hyperparathyroidism. 512 11

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

Calcium homeostasis was studied in freely fed control, streptozotocin diabetic, long-term and short-term insulin-treated diabetic rats 7 wk after the induction of diabetes. In contrast to the short-term (5-12 day) diabetic rat model, intestinal absorption of calcium was markedly enhanced in chronically insulin-deficient animals. Moreover, conventional balance studies showed that these animals were in positive calcium balance despite severe hypercalciuria. Intestinal hyperabsorption of calcium in long-standing diabetic rats occurred despite low levels of circulating 1,25-dihydroxyvitamin D and hypercorticosteronism and was attended by hypercalcemia and suppression of both plasma parathyroid hormone (PTH) and urinary cyclic 3',5'-AMP (cAMP). Long-term insulin replacement completely normalized the intestinal hyperabsorption of calcium, corrected the plasma calcium, and significantly increased circulating PTH and urinary cAMP excretion. Insulin therapy also corrected the decreased plasma 1,25-dihydroxyvitamin D observed in untreated diabetic animals. Intestinal hyperabsorption of calcium appeared to be only partially corrected by short-term insulin therapy. The accumulated results reveal decided differences in calcium homeostasis and hormonal response between the rats with long-standing diabetes and those with diabetes of short duration.
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PMID:Calcium homeostasis in chronic streptozotocin-induced diabetes mellitus in the rat. 628 97

A case of a 65-year-old woman with a pancreatic tumor secreting insulin, glucagon, and associated with high PTH levels and hypercalcemia is reported. The patient underwent two Streptozotocin (STZ) treatments (1 g iv/week for 10 weeks) after liver metastases were found. Hormonal and metabolic parameters were monitorized . Before the first STZ treatment insulin levels ranged between 78 and 132 microU/ml. After STZ administration insulin decreased and then remained lower (8-48 microU/ml) until the death of the patient. Pre-treatment glucagon levels ranged between 1.3 and 3.9 ng/ml. STZ induced a decrease of glucagon to 0.5 ng/ml. Glucagon chromatography revealed the prevalence of high molecular weight (greater than 6,000 mol wt) immunoreactive glucagon (0.9 ng/ml) drastically reduced by STZ treatment (0.15 ng/ml). Hypoaminoacidemia was observed before STZ administration, but at the end of the therapy plasma amino acid concentrations were normal. Hypercalcemia too was sensitive to STZ, but not PTH value, which remained high. The second STZ treatment performed a year later was less effective and so a chemotherapeutic protocol was started. Our findings suggest a cytolitic effect of STZ on malignant A-cell, with reduction of glucagon levels and restoration of amino acid metabolism. This effect would be useful for medical treatment of non-operable glucagon secreting tumors.
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PMID:Effect of streptozotocin in a case of glucagon-secreting malignant islets-cell tumor. 632 96

Carbohydrate metabolism was investigated in 9 patients with symptomatic primary hyperparathyroidism. Before and after parathyroidectomy intravenous and oral glucose tolerance test, tolbutamide test, arginine infusion test and insulin tolerance test were performed. During intravenous and oral glucose tolerance tests, patients with primary hyperparathyroidism exhibited hyperinsulinemia and impaired glucose tolerance without normalization after surgery. Tolbutamide-induced induced insulin release did not differ pre- or postoperatively. After restoration of normocalcemia and normocalcemia and normophosphatemia we found significantly lower glucose and insulin levels following arginine infusion and a significantly increased hypoglycemic response to parenterally administered insulin, probably indicating partial improvement of glucose tolerance after surgery. Our findings suggest that biochemical abnormalities associated with primary hyperparathyroidism, like hypercalcemia, hypophosphatemia, and elevated parathyroid hormone levels may cause and sustain a form of endogenous insulin resistance, which consequently leads to hyperinsulinemia and to impaired glucose tolerance. Since hyperinsulinemia as well as impaired glucose tolerance seem to be only slowly and partially reversible in symptomatic primary hyperparathyroidism, these data could be considered as an additional argument for early surgical intervention in this disorder.
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PMID:Peripheral insulin resistance in primary hyperparathyroidism. 634 5


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