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

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

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

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

The development of renal cell neoplasms ranging from adenoma to metastatic carcinoma is the most serious complication of acquired cystic kidney disease (ACKD). A comprehensive review of the pertinent literature shows that there is up to 50-fold increased risk of renal cell carcinoma in ACKD compared to the general population. The ACKD-associated renal cell carcinoma is seen predominantly in males, occurs approximately 20 years earlier than in the general population, and is frequently bilateral (9%) and multicentric (50%). Acquired cystic kidney disease-associated renal cell carcinoma is frequently asymptomatic (86%), but may be associated with bleeding, abrupt changes in hematocrit, fever, and flank pain or rarely with hypoglycemia, hypercalcemia, or metastases at presentation. Computed tomography seems to provide a better diagnostic yield than sonography or magnetic resonance imaging; nevertheless, large (up to 8 cm) tumors not visualized by any imaging techniques have been reported. It is generally agreed that there is a need for regular screening of symptomatic ACKD patients for early detection of renal cell carcinoma; however, whether screening is needed for asymptomatic patients remains controversial. Nephrectomy is indicated for tumors larger than 3 cm. Management for tumors smaller than 3 cm with persistent symptoms, such as back pain or hematuria, remains controversial, but nephrectomy may be recommended since many of these tumors turn out to be unequivocal renal cell carcinoma. Asymptomatic tumors smaller than 3 cm should be serially screened, and tumor enlargement may be an indication for nephrectomy. Acquired cystic kidney disease-associated renal cell carcinoma accounts for approximately 2% of deaths in renal transplant patients. A median length of survival of approximately 14 months and a 5-year survival rate of 35% are comparable to the same data for renal cell carcinoma in the general population. Successful renal transplant probably decreases the risk of renal cell carcinoma in ACKD patients, but this preliminary observation needs confirmation. The development of ACKD-associated renal carcinoma is a continuous process with evolving phenotypic expression, including damaged renal tubule, simple cyst, cyst with atypical lining, adenoma, and, finally, carcinoma. The pathogenesis of this continuous process is not entirely known, but growth factor-induced compensatory growth of tubular epithelium initiated by the changes of end-stage kidney disease, and probably perpetuated by activation of proto-oncogenes, seems to be the most significant factor.
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PMID:Renal neoplasm in acquired cystic kidney disease. 761 Dec 40

Possible new indications for the use of octreotide are discussed. In October 1988, octreotide received FDA-approved labeling for use in the management of carcinoid syndrome and vipomas. Since that time, research results and clinical experience have accumulated that suggest a potentially much broader therapeutic role for octreotide. Reports continue to be published on the use of octreotide for treating pituitary tumors, gastroenteropancreatic tumors, diabetes mellitus, AIDS-associated diarrhea, autonomic neuropathy, pancreatitis, pancreatic pseudocysts and ascites, complications of pancreatic surgery and transplantation, ileostomy-associated diarrhea, enterocutaneous fistulas, pancreatic fistulas, dumping syndrome, short bowel syndrome, and gastrointestinal bleeding. Other emerging indications for the use of octreotide include psoriasis, hypercalcemia, cancer-related pain, polycystic ovary syndrome, and certain cancers. In children, octreotide has been studied for use in treating hyperinsulinemic hypoglycemia of infancy. Along with the common adverse effects of octreotide, such as pain at the injection site and nausea, less frequent effects, such as cholelithiasis, gallbladder hypercontractility, and gastritis have now been described. Much of what has been learned is based on small uncontrolled studies and case reports, since the rarity of many of the conditions for which octreotide has shown promise has tended to preclude larger studies. As clinical experience with octreotide accumulates and better-designed trials are completed where possible, a broader therapeutic role for octreotide is likely to be recognized.
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PMID:Emerging indications for octreotide therapy, Part 1. 804 37

Seventy patients with primary liver cell carcinoma (PLC) were studied for the occurrence and relative incidence of paraneoplastic syndromes (PNS) between 1985 and 1990. Here we communicate results of the study involving hypercholesterolaemia, hypercalcemia, hypoglycaemia, gynaecomastia and polycythaemia. Hypercholesterolaemia occurred in 20% of our patients and is the most common PNS in our series; polycythaemia occurred in 15.6%, hypoglycaemia in 8.6% and hypercalcaemia in 7%. It is noteworthy that hypoglycaemia, which is one of the commonest and certainly the most dangerous PNS associated with PLC, occurred in few of our patients. The occurrence and incidence of PNS as obtained in the present study slightly differ from those in developed countries. The pathophysiological mechanisms underlying these systemic manifestations are discussed.
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PMID:Paraneoplastic syndromes in primary liver cell carcinoma in Nigeria. 816 31

A 26-year-old man with Graves' hyperthyroidism associated with central diabetes insipidus (DI), initially showed hypercalcemic crisis. Initially, very low serum levels of intact parathyroid hormone (PTH) and 1,25-dihydroxy vitamin D3 and a moderate rise of serum C-terminal PTH related protein (C-PTHrP) were observed which strongly suggested a humoral hypercalcemia of malignancy due to PTHrP. However, the serum C-PTHrP level later became normal. Mild hyperprolactinemia, no responses of growth hormone (GH) to insulin-induced hypoglycemia despite a normal growth hormone releasing hormone (GRH) test and mild thickening of the pituitary stalk on magnetic resonance imaging were observed. Thus, an autoimmune nature of his central DI is considered; it is noteworthy that the serum C-PTHrP level may be elevated by renal failure in patients with hypercalcemia due to causes other than PTHrP.
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PMID:Development of hypercalcemic crisis in a Graves' hyperthyroid patient associated with central diabetes insipidus. 858 May 71

Many complications are frequently associated in patients with cancer which require immediate treatment. Oncologic emergencies are widely varying, which include superior vena cava syndrome, intracranial hypertension, spinal cord compression, metabolic emergencies, surgical emergencies, urologic emergencies, etc. In the treatment of these emergencies, the decision is most difficult because the usual responses and criteria for decision making are altered, and specific expertise is necessary. In patient with cancer, a situation in which complex problems are frequent, and the use of more sophisticated studies may be critical in defining and following acute, emergent problems. Furthermore, poor host "reserve" may make earlier decision-making essential, even though apparent risks are greater and diagnosis may be less certain. In this review, pathogenesis, manifestation, diagnosis, and treatment of principal oncologic emergencies (hypercalcemia, hyponatremia, tumor hypoglycemia, DIC, and cardiac tamponade) were evaluated from the view point of medical oncology.
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PMID:[Oncologic emergencies]. 905 Nov 26

Cachexia consists of a constellation of metabolic changes that occur in cancer patients, including the reduction of muscle and fat tissue, asthenia, anorexia, hypoglycemia and hypercalcemia. These syndromes complicate therapeutic intervention and decrease the quality of life of the patient. This review discusses the involvement of cytokines in cancer cachexia and describes the contribution of IL-6 and other cytokines to the wasting of C-26-bearing mice. The neutralization of IL-6 by antibody, or IL-6 receptor antagonism by suramin, significantly reduce the severity of key parameters of cachexia. The participation of several other factors (PGE2, IL-1, IL-10 and TNF-alpha) in the cellular communication between the C-26 tumor cell and tumor-infiltrating macrophages is also described.
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PMID:Inhibition of experimental cancer cachexia by anti-cytokine and anti-cytokine-receptor therapy. 938 67

Murine colon 26 carcinoma growing at either subcutaneous (s.c.) or intramuscular (i.m.) inoculation sites causes cachexia in mice. Such animals show extensive loss of body weight, wasting of the muscle and adipose tissues, hypoglycaemia, and hypercalcaemia, even when the tumour weight comprises only about 1.9% of carcass weight. In contrast, the same tumour when inoculated into the liver does not cause any sign of tumour-related cachexia even when the tumour becomes much larger (6.6% of carcass weight). Interleukin 6 (IL-6), a mediator associated with cachexia in this tumour model, is detected at high levels both in the tumour tissues and in the circulating blood of mice bearing colon 26 tumour at the s.c. inoculation site. In contrast, only minute levels of IL-6 are detected in the tumour grown in the liver. The colon 26 tumour grown in the liver does not lose its ability to cause cachexia, because the tumour when re-inoculated s.c. is able to cause extensive weight loss and produce IL-6 as did the original colon 26 cell line. Histological studies revealed differences in the composition of tumour tissues: the tumours grown in the subcutis consist of many polygonal tumour cells, extended-intercellular space, and high vascular density, whereas those grown in the liver consist of spindle-shaped tumour cells. Thus, the environment where tumour cells grow would be a critical factor in determining the cachectic phenotype of cancer cells, including their ability to produce IL-6.
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PMID:Tumour inoculation site-dependent induction of cachexia in mice bearing colon 26 carcinoma. 1007 Aug 67


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