Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To establish a dose-effect relationship for the xipamide diuretic in double-blind trials 0, 5, 10, 20 and 40 mg of xipamide were administered to 5 groups of 6 to 14 healthy test persons in each group. Before, during and after the 15-d period of application all the blood electrolytes as well as the metabolism parameters of glucose, uric acid, cholesterol, neutral fats as well as creatinine and urea were determined. Similarly during the entire period of investigation the 24-h urine samples were collected daily and from these the electrolyte excretion as well as the endogenic creatinine clearance were determined. It was found that diuresis and natriuresis significantly enhanced in comparison with placebo were already achieved with 5 mg xipamide per day, they could no further be increased by higher doses. Much rather at 40 mg xipamide per day a significant hypokalaemia as well as a light hypercalcaemia developed. Independently of the dose, during the period of investigation a light, fully compensated hypochloraemic alkalosis developed. Regarding the metabolic processes a slight increase in the uric acid and cholesterol blood levels was observed, while the blood-sugar level, the triglycerides as well as the endogenic creatinine clearance remained unaffected. It can be concluded from the investigations that maximum natriuresis and diuresis can already be achieved with a daily xipamide dose of 5 mg, while side effects can be kept at a minimum.
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PMID:[Dose-response relationship of xipamide in healthy subjects]. 700 20

Thirty-seven cases of canine hypoadrenocorticism were compared with 39 previously reported cases. The 2 series were compared because it was believed that a study of 37 consecutive cases diagnosed at 1 institution (Michigan State University) and compiled by 1 group of veterinarians would yield data that were more representative of the disease than multiple cases from various institutions. Age, sex, and breed data were similar in both series. The frequency of anorexia, vomiting, depression, and the mean values for the clinicopathologic data were similar for both series except for blood glucose concentration (P less than 0.025). The Michigan State University series was different in that it had a lower frequency of eunatremia, increased plasma total solids, and hypoglycemia but a higher frequency of lymphocytosis, lymphopenia, hyponatremia, hyperglycemia, and hypercalcemia. Further, 3 dogs in the Michigan State University series had azotemia plus near isosthenuric urine, suggesting renal disease, but they seemingly responded to therapy for hypoadrenocorticism. Only 1 such case was identified in the literature. Finally, we detected fewer instances of P waves not being evident in lead II of an electrocardiogram.
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PMID:Canine hypoadrenocorticism: report of 37 cases and review of 39 previously reported cases. 703 23

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

Although IAPP was first discovered and isolated from amyloid deposits in an endocrine pancreatic tumour (EPT), surprisingly few reports have investigated the potential use of IAPP as a marker for neuroendocrine tumour growth. In this study we present results from plasma measurements of IAPP in 102 patients with neuroendocrine tumours. Four of 35 patients (11%) with midgut carcinoid tumours, but none of the patients (4 and 5, respectively) with lung carcinoids or with rectal carcinoids displayed elevated plasma levels of IAPP. Five of 31 patients (16%) with sporadic EPT and 3 of 27 patients (11%) with EPT and multiple endocrine neoplasia type 1 syndrome disclosed elevated IAPP levels. Within the different syndromes, 1/11 individuals with insulinoma, 2/16 with gastrinoma, 0/2 with glucagonoma, 0/3 with VIPoma and 5/26 with non-functioning tumours showed elevated plasma levels of IAPP. In two patients, the plasma IAPP levels were extremely elevated. These patients also exhibited altered glucose homeostasis. In response to a standardised mixed meal test, IAPP increased in parallel to the insulin, pancreatic polypeptide, gastrin and glucose responses. In MEN1 patients with hypercalcaemia due to increased secretion of parathyroid hormone, the plasma levels of IAPP were significantly higher before than after surgical removal of the parathyroid adenomas. However in normocalcaemic patients, no correlation between the blood calcium and plasma IAPP levels was found. Immunocytochemical staining of tumour tissue showed that 9/13 (69%) of insulin producing tumours, 4/14 (29%) of non-functioning tumours and 1/9 (11%) of gastrin producing tumours were IAPP immunoreactive. Amyloid deposits were always IAPP immunoreactive. In conclusion, increased circulating levels of IAPP occurred in 12% of 102 patients with neuroendocrine tumours. In 2 patients with extremely elevated plasma levels of IAPP, effects on glucose homeostasis were recorded. Thus, IAPP may be useful as an additional marker for neuroendocrine tumour growth in selected cases.
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PMID:Islet amyloid polypeptide (IAPP) in patients with neuroendocrine tumours. 775

Corticosteroids are extensively prescribed in advanced cancer for various specific indications (e.g. spinal cord compression), for pain relief, as hormone therapy and to stimulate appetite and wellbeing. Choice of corticosteroid is dictated largely by local fashion, and times of administration are more traditional than pharmacological. Corticosteroids have many potential disadvantages, some life-threatening (e.g. masked septicaemia). Others are seriously debilitating (e.g. myopathy, avascular bone necrosis). Oropharyngeal candidiasis is a common complication. Corticosteroids are withdrawn in about 5% of patients because of unacceptable adverse effects, including moon-face and diabetes mellitus. Corticosteroid hypersensitivity occurs, and the succinate salts have been associated with bronchospasm. Steroid pseudorheumatism may occur with high dose therapy or when tailing off after a prolonged course. Important drug interactions with corticosteroids relate to salt and water retention, and decreased glucose tolerance. Some anticonvulsants cause an increased clearance of corticosteroids and, with dexamethasone, up to a 50% reduction in the anticipated effect. The benefit of corticosteroids in terms of increased appetite, mood and activity has been demonstrated in several controlled trials. The effect may well be time-limited in most patients. In several studies, corticosteroids have resulted in an analgesic-sparing effect. Some centres use very high doses of dexamethasone in cases of spinal cord compression, although the justification for these is not obvious. Corticosteroids are used to help relieve nerve compression pain and in symptomatic raised intracranial pressure. Corticosteroids are also injected locally into or around bone metastases, particularly ribs and the sacro-iliac joints. Epidural injections are used for patients with troublesome intractable low back pain. Corticosteroids are now used less often in hypercalcaemia because of poor response rates. More benefit is obtained, however, if high dosages are used, e.g. prednisolone 60 to 80 mg/day. Dexamethasone is widely used as an antiemetic in association with chemotherapy. Some centres use dexamethasone by continuous subcutaneous infusion in selected patients when the oral route is not feasible. The choice of starting dose of a corticosteroid is largely arbitrary. It is important, however, not to miss a possible treatment benefit by prescribing too low a dose. For most patients, an initial dosage of prednisolone of 30 to 60 mg/day (dexamethasone 4 to 8 mg/day) is appropriate. In patients with anorexia, there are several alternative options that should be considered. There is evidence to suggest that patients with advanced cancer receiving a corticosteroid are not as closely monitored as other patients. There is a need to state clearly in writing the reason(s) for prescription and to review after 1 or 2 weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The risks and benefits of corticosteroids in advanced cancer. 781 99

Lower dialysate calcium concentrations were recently proposed to overcome the risk of hypercalcemia in continuous ambulatory peritoneal dialysis (CAPD) patients on calcium-containing phosphate binders and/or vitamin D metabolites using the standard dialysate calcium concentration (SCa) of 1.75 mM. To assess transperitoneal calcium mass transfer (CaMT) in CAPD patients using a dialysate with a low calcium concentration (LCa, 1.00 mM), 18 stable patients were randomly allocated to receive either LCa or SCa. CaMT was assessed over 4 hours using 2L dialysate bags with three different dialysate glucose concentrations (1.5%, 2.3%, 4.25%). Total serum calcium (tCa), ionized calcium (iCa), and the exact dialysate volume were measured before and after the 4-hour dwell. A sample of the drained dialysate was obtained to measure the dialysate calcium concentration. The tCa and iCa levels were not significantly different in both groups prior to and did not change throughout the test. CaMT (median/range) was -0.64 mmol/exchange (-0.35(-)-1.29 mmol/exchange) using LCa with 1.5% glucose compared to 0.23 mmol (-0.18-0.87 mmol) with SCa (p < 0.0001). CaMT was negatively correlated to iCa and ultrafiltration volume [4.25%: LCa-1.22 (-0.84(-)-1.9); SCa -0.43 (-1.35-0.13); p < 0.001]. In summary, LCa results in a loss of calcium into the dialysate even at low ultrafiltration volumes and serum iCa levels. This might facilitate the prevention and therapy of renal osteodystrophy with calcium-containing phosphate binders and calcitriol. However, patients using LCa must be carefully monitored for calcium homeostasis and bone turnover.
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PMID:Transperitoneal calcium mass transfer using dialysate with a low calcium concentration (1.0 mM). 839 41

It is generally known that patients with primary hyperparathyroidism (pHPT) feature disturbances in carbohydrate metabolism and hypertension. The incidence and prevalence of frank diabetes mellitus is significantly increased in these patients. The etiology and pathogenesis of the vascular and metabolic aberrations in this condition are still unclear. Glucose intolerance in pHPT is characterized by severe insulin resistance associated with pancreatic beta cell hypersecretion of insulin. Hypercalcemia is thought to be mainly responsible for the impaired glucose metabolism. However, several studies demonstrated that hypophosphatemia can also induce insulin hypersecretion and impair peripheral glucose uptake. Hypertension in primary hyperparathyroidism is mainly attributed to hypercalcemia. However, high peripheral insulin levels are also proposed to contribute to the development of essential hypertension and hyperinsulinemia per se is regarded as an important independent cardiovascular risk factor. After parathyroidectomy and decrease of the calcium levels to within the normal range, the blood pressure levels of the patients with pHPT normalised very quickly, whereas normalization of the high peripheral insulin levels was only found in a subgroup of patients. Thus, hypercalcemia seems to be mainly responsible for hypertension in primary hyperparathyroidism. Another important, yet unresolved issue is the question as to whether or to which extent the disturbances in glucose homeostasis are reversible after surgical correction of pHPT. At an early stage of the disease, insulin resistance and insulin hypersecretion are fully reversible after parathyroidectomy, whereas in patients with long-standing primary hyperparathyroidism and severely impaired glucose tolerance the metabolic disturbances will only partially improve. These results argue for improved screening to identify asymptomatic patients with primary hyperparathyroidism and for early surgical intervention in this disease.
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PMID:[Diabetes mellitus and carbohydrate metabolism in primary hyperparathyroidism]. 847 26

A 44 year old Japanese woman with adult T-cell leukaemia (ATL) was admitted to Kyushu University hospital to receive a course of alpha-interferon treatment. She experienced a sudden onset of hypercalcaemia and epigastric pain associated with an increase in the level of pancreatic enzymes. Her serum parathyroid hormone related protein level was above normal although her high sensitive PTH level was within the normal range. Ultrasonography and computed tomography (CT) of the abdomen showed enlargement of the pancreas with indistinct margins and massive accumulation of extrapancreatic fluid. Cullen's sign was observed. A few days after the onset of acute pancreatitis, the serum amylase level increased to 3400 IU/L, and the serum calcium level fell to 4.2 mg/dL from 13.3 mg/dl. Her fasting blood glucose level increased to 242 mg/dL. Although the first episode of pancreatitis appeared to respond to treatment, she experienced a second episode of pancreatitis accompanied by an elevation of the serum calcium level. These findings suggest that acute pancreatitis was caused by hypercalcaemia associated with ATL.
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PMID:Acute pancreatitis induced by hypercalcaemia associated with adult T-cell leukaemia: a case report. 867 68

A missense mutation in the Ca(2+)-sensing receptor (CaSR) gene was previously identified in a Japanese family with familial hypocalciuric hypercalcemia. Five members of this family with the mutation in the CaSR gene also showed abnormal glucose tolerance, whereas family members homozygous for the wildtype CaSR gene were normal in this respect. The potential relation between mutations in the CaSR gene and the incidence of diabetes mellitus was therefore investigated in 27 non-insulin dependent diabetic and 40 normal Japanese subjects. Each exon of the CaSR gene was amplified by the polymerase chain reaction and subjected to single-strand conformation polymorphism (SSCP) analysis. The region of the gene containing the sixth exon showed three distinct patterns on SSCP analysis in both diabetic patients and normal subjects. Direct sequencing of DNA revealed a T/C polymorphism in the fifth intron. The TT genotype was apparent in 59.3% of diabetic patients and in 45.0% of normal subjects. The CC genotype was present in 25.9% of diabetics and in 22.5% of normal subjects. The diabetic patients were divided into three groups on the basis of genotype for the polymorphism (TT, TC, or CC). However, there was no significant difference among the three groups with regard to the method of therapy, the incidence or severity of diabetic complications, duration or family history of disease, HbA1c level, or laboratory data. The polymorphism in the fifth intron of the CaSR gene does not therefore appear to be associated with non-insulin dependent diabetes mellitus.
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PMID:Polymorphism of the human Ca(2+)-sensing receptor gene in Japanese individuals: no relation to non-insulin dependent diabetes mellitus. 893 12


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