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

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

A personal series of 256 cases of acromegaly/gigantism seen over a 20-year period from 1963 is described. The insidious nature of the condition resulted in delay in diagnosis which was often made by a doctor when seeing the patient for an unrelated problem. Other features which commonly led to the diagnosis being made were headache, change in appearance, carpal tunnel syndrome, amenorrhoea and diabetes. The Hardy system for grading the radiological appearance of the pituitary tumour was used. Widely invasive tumours were not common but tended to occur in patients with younger age of onset and high GH levels. The occurrence of various symptoms and clinical features was noted and the changes resulting from reducing the GH level to normal. The incidence of hypertension, but not of coronary artery disease, is increased and the blood pressure may be reduced following successful treatment. The effects on the upper and lower respiratory tract are reported as well as sleep apnoea and problems associated with anaesthesia. Skin manifestations included sweating, pigmented skin tags, acanthosis nigricans and cutis verticis gyrata. In the skeletal system the incidence of kyphoscoliosis and osteoarthritis especially of the hip is reported: the question of hip replacement is discussed. Diabetes mellitus disappeared in most cases if the acromegaly was cured. In men but not in women the incidence of colloid nodular goitre was increased as was hyperthyroidism in middle-aged women. In two patients a parathyroid adenoma was present: hypercalcaemia was present in five additional patients, but the cause was not determined. The common occurrence of amenorrhoea in the younger women was noted, it was not always associated with hyperprolactinaemia, and often responded to successful treatment of the acromegaly. The association of acromegaly with hirsutism and galactorrhoea is confirmed. The incidence of impotence and loss of libid in the men is discussed: in a proportion of those in whom the acromegaly was cured, potency returned, but in a number depression occurred and what was believed to be psychogenic impotence persisted. Hyperprolactinaemia was found in 49 out of 151 patients with active acromegaly in whom the prolactin level was measured. Previous reports have indicated a doubling of death rates in acromegalics. In this series there were 47 deaths observed compared to 37.2 expected. The increased death rate was in women of all ages and in men under the age of 55, The increased deaths in the women were from cardiovascular and cerebrovascular causes and from breast cancer.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acromegaly. 330 90

Endocrinologic disorders occasionally manifest themselves by their associated or induced cutaneous abnormalities. In some instances the initial and most prominent complaints of the patient are related to alterations in the skin, and thus the dermatologist will at times be the first physician consulted. In this article we describe the cutaneous lesions that occur in patients with acromegaly, hypopituitarism, hypothyroidism, hyperthyroidism, diabetes mellitus, glucagonomas, hypercalcemia, hypoparathyroidism, and fibrous dysplasia. In addition, we also discuss the role of the skin in vitamin D metabolism. Whenever possible and where known, we have attempted to point out the pathophysiologic mechanisms that account for the cutaneous changes.
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PMID:Endocrine-skin interactions. Cutaneous manifestations of pituitary disease, thyroid disease, calcium disorders, and diabetes. 332 73

Since hypercalcemia is thought to have a modifying effect on glucose metabolism, the possible influence of experimental hypercalcemia on peripheral insulin reaction was investigated in 6 healthy control subjects by the euglycemic clamp technique. Each of these subjects was randomly tested twice, in the normocalcemic as well as in the hypercalcemic state (infusion of calcium gluconate 15 mg/kg body wt. over a period of 180 min). Infusion of calcium gluconate caused a 27% increase in plasma calcium levels, whereas the plasma phosphate levels were not significantly changed during the eucalcemic and hypercalcemic clamp protocol. Steady state plasma insulin levels and plasma glucose levels were nearly identical between the 2 clamp protocols. Exogenous hypercalcemia had no significant influence on peripheral glucose utilization measured by the M-value (M = 4.83 +/- 0.6 mg/kg body wt./min in the eucalcemic state, 4.77 +/- 0.7 mg/kg body wt./min in the hypercalcemic state, n.s.). The present data indicate that at least acute experimental hypercalcemia has no significant influence on peripheral glucose utilization.
Diabetes Res 1986 May
PMID:Influence of acute experimental hypercalcemia on peripheral insulin sensitivity in healthy subjects. 352 17

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

An unusual case of diabetes secondary to acute pancreatitis in a boy with end-stage renal failure receiving continuous ambulatory peritoneal dialysis (CAPD) is described. A hyperglycaemic, hyperosmolar pre-coma developed, aggravated by associated hypercalcaemia. The glucose content of the dialysis fluid contributed to the hyperglycaemia, which settled as the pancreatitis resolved and lower glucose concentration dialysis fluid was used. Our experience suggests that pancreatic dysfunction should be considered where significant hyperglycaemia occurs during peritoneal dialysis.
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PMID:Non-ketotic hyperosmolar diabetic pre-coma due to pancreatitis in a boy on continuous ambulatory peritoneal dialysis. 354 Jun 93

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

Twelve patients with pheochromocytoma have shown unusual clinical and laboratory presentation. These include three patients with cardiac manifestations (sick sinus syndrome, obstructive cardiomyopathy and ischemic ECG changes). Two patients with gastrointestinal problems (acute abdomen due to ischemic bowel and constipation). One child with sudden blindness and one, non diabetic patient with polyuria. Laboratory findings included four patients with diabetes mellitus, four patients with hypercalcemia two of them with concomitant hyperreninemia and one patient with hypokalemia. Awareness of the illness leads to the discovery of unusual cases and even a most severely sick patient can make a complete recovery.
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PMID:Uncommon presentation of pheochromocytoma: case studies. 390 36

The prevalence, distribution, and clinical associations of pancreatic ductal mucinous hyperplasia were studied in 102 non-malignant pancreases. Ductal mucinous hyperplasia was found in over 60% of specimens and was frequently associated with increased fibrosis--occasionally resembling pancreatitis. Significantly more ductal mucinous hyperplasia was found in pancreas from patients who were receiving corticosteroid treatment. Neither a history of hypercalcaemia in the three months before death, diabetes mellitus, alcoholism, tobacco smoking, nor the presence of gall stones was associated with an increase in ductal mucinous hyperplasia. The age of maximum prevalence, and the distribution of ductal mucinous hyperplasia in the pancreas were similar to those of pancreatic carcinoma. These similarities may be because both ductal mucinous hyperplasia and pancreatic carcinoma are proliferative responses, rather than because ductal mucinous hyperplasia is a precursor of pancreatic carcinoma.
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PMID:What is the significance of pancreatic ductal mucinous hyperplasia? 401 49

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


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