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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

Early reports of patients with metabolic bone diseases such as nutritional osteomalacia, Fanconi syndrome, indicated an association with aminoaciduria. This association has since been described in osteomalacia of G. I. or hepatic origin, secondary to anticonvulsant therapy, tumors, and chronic renal failure. Aminoaciduria also occurs in primary hyperparathyroidism. In nutritional osteomalacia, vitamin D deficiency was thought to be responsible for the renal tubular abnormality, since it responded to treatment with vitamin D. However, since the description of aminoaciduria in hyperparathyroidism, the literature has been divided concerning the etiology of aminoacidura in conditions associated with abnormal vitamin D metabolism because secondary hyperparathyroidism often occurs in these conditions. Recently, some cases of Fanconi syndrome and a case of tumor-associated osteomalacia have been described with low or absent plasma 1,25-dihydroxycholecalciferol levels, normal serum PTH, and aminoaciduria. In one of these cases, and more recently in patients with chronic renal failure, it has been demonstrated that treatment with 1,25(OH)2D3 can improve amino acid transport independently from changes in serum PTH levels. 1,25(OH)2D3 therefore normally opposes the aminoaciduric effect of PTH. This is an agreement with observations which demonstrate that 1,25(OH)2D3 also opposes the phosphaturic action of parathyroid hormone.
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PMID:Aminoaciduria--its relationship to vitamin D and parathyroid hormone. 699 53

The case is reported of a 32-year-old female Asian immigrant admitted with incapacitating pain and suspected diffuse malignant neoplasia. A detailed history and typical laboratory and radiological findings confirmed the diagnosis of osteomalacia caused by lack of sun exposure and a diet poor in vitamin D. Pathogenetic, diagnostic and therapeutic aspects of "immigrant osteomalacia" are discussed.
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PMID:[Immigrant osteomalacia]. 707 75

Measurements of 1,25 (OH)2D3 and other metabolites of vitamin D in a patient with oncogenic osteomalacia confirm the selective, reversible deficiency of 1,25 (OH)2D3 in this syndrome, and indicate the rapidity of normalization (within days) of the hormone level and associated hypophosphatemia after resection of the tumor. In this patient, the tumor was an intranasal hemangiopericytoma.
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PMID:Vitamin D metabolite levels in oncogenic osteomalacia. 740 81

A 15-year-old boy was treated for nonfamilial hypophosphatemic rickets. Treatment with ergocalciferol, 100,000 units/day, and phosphorus, 2 to 4 g/day, failed to alleviate the rickets. Levels of 1 alpha, 25-dihydroxyvitamin D were low while levels of 25-hydroxyvitamin D were elevated. After removal of a benign fibroma, the level of 1 alpha, 25-dihydroxyvitamin D increased, the serum phosphorus level became normal, and the osteomalacia was cured. The alteration of vitamin D metabolism and associated hypophosphatemia in oncogenic osteomalacia is a potentially reversible cause of bone disease mediated by the tumor.
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PMID:Tumor-induced osteomalacia. Evidence of a surgically correctable alteration in vitamin D metabolism. 745 73

The expression of the six known insulin-like growth factor binding proteins (IGFBPs) and their corresponding messenger RNAs has been examined in three cell lines established from surgical and biopsy specimens of human prostate carcinoma. All three cell lines produced both IGFBP-4 and IGFBP-6 and the respective mRNAs; expression of IGFBP-6 has not been previously demonstrated in human prostate tumor cells. No other binding proteins were detected. The levels of IGFBP mRNAs were not regulated by androgens or IGF-1, but the level of IGFBP-6 mRNA was sharply increased by 1,25-dihydroxyvitamin D3 (1,25(OH)D3). The stimulation was dose-dependent with a maximum effect at 10 nM 1,25(OH)D3 and a clearly discernible effect at 0.1 nM. The results support a role for vitamin D in the control of prostate tumor growth, mediated at least in part by interaction with IGFs and specific IGFBPs.
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PMID:IGF-binding proteins in human prostate tumor cells: expression and regulation by 1,25-dihydroxyvitamin D3. 753 47

A case of hypophosphatemic osteomalacia with recovery after removal of a plantar neurilemoma is reported. One hundred cases of osteomalacia with a connective tissue tumor were found in the medical literature. Both sexes and all age groups were affected. Patients often had severe osteomalacia with decreased serum 1,25 (OH)2 vitamin D and phosphate levels and renal phosphate wasting. These abnormalities resolved immediately after complete excision of the tumor, which was often a small lesion found after the diagnosis of osteomalacia. Of the 100 tumors, 87 were benign and half were vascular (e.g., hemangiopericytoma, hemangioma, angiofibroma). A large number of tumors could not be readily classified because they contained vascular structures, giant cells, spindle-shaped cells, and cartilage. Many other histologic variants were observed, including giant cell tumors, nonossifying fibromas, cartilaginous tumors, and osteosarcomas. The tumor was usually located in a limb, generally a lower limb, and was skeletal in nearly half the cases. The tumors produced one or more substances with a capacity for blocking intracellular phosphate transfer and inhibiting renal tube 1 alpha hydroxylase. The link between these two abnormalities remains unclear.
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PMID:Hypophosphatemic osteomalacia with plantar neurilemoma. A review of the literature (100 cases). 755 13

The modifying effects of 22-oxa-calcitriol (OCT), a synthetic analog of 1 alpha,25-dihydroxyvitamin D3, were assessed in a multi-organ carcinogenesis model using male F344 rats initially treated with five kinds of carcinogens. In experiment 1 the rats were given OCT intraperitoneally at doses of 30 micrograms/kg (25 rats) or 3 micrograms/kg (25 rats), three times a week for 24 weeks after initial carcinogen exposure over 4 weeks and a 2 week non-treatment period. Twenty-two rats received the five carcinogens and were given the vehicle intraperitoneally as a control. A further group of 10 rats was given the 30 micrograms/kg dose of OCT without prior carcinogen application. At the end of the total observation period of 30 weeks the carcinoma incidence in the small intestine of rats given 30 micrograms/kg OCT after carcinogen treatment was 0%. This incidence was significantly smaller when compared with the control group. The incidence of large intestine carcinomas in the 30 micrograms/kg OCT group showed a tendency to decrease. The numbers of small and large intestinal carcinomas per rat were also significantly lower in the group given 30 micrograms/kg OCT than after 3 micrograms/kg OCT or carcinogens alone. Attention was, therefore, focused on colon carcinogenesis and in experiment 2 30 micrograms/kg OCT administered six times a week to rats for 8 weeks after the last injection of N,N'-dimethylhydrazine (DMH) exposure. OCT significantly reduced the formation of DMH-induced aberrant crypt foci, considered to be putative preneoplastic lesions. In experiment 3 30 micrograms/kg OCT was administered six times a week to rats for 4 weeks without prior carcinogen treatment. The proliferating cell nuclear antigen labeling index for the colonic epithelium of rats given 30 micrograms/kg OCT was decreased. Ornithine decarboxylase and spermidine/spermine N1-acetyltransferase activities in colonic epithelium, assayed as indicators of cell proliferation, were not significantly decreased as compared with control group values. Furthermore, vitamin D receptors in colonic epithelium were not significantly increased. Thus the present study indicates that OCT can exert inhibitory effects on tumor development in the small and large intestines, although the mechanism is unclear.
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PMID:Inhibition of intestinal tumor development in rat multi-organ carcinogenesis and aberrant crypt foci in rat colon carcinogenesis by 22-oxa-calcitriol, a synthetic analogue of 1 alpha, 25-dihydroxyvitamin D3. 755 59

A Western-style diet containing high-fat and phosphate, and low calcium and vitamin D was fed to mice for 20 weeks. Starting at week 8, subgroups of animals received the Western-style diet supplemented by two different calcium sources: tricalcium phosphate and calcium citrate malate. Hyperproliferation (increased [3H]thymidine-labelled cells/colonic crypt) and hyperplasia (increased total epithelial cells/crypt) developed in the sigmoid colon after 8 weeks of feeding the Western-style diet confirming previous results, and these were reversed at later periods by the addition of the two calcium sources to the Western-style diet. Findings indicate that the modified colonic epithelial cell hyperproliferation and hyperplasia which have been associated with subsequent development of colonic neoplasia, are induced in mice fed a Western-style diet, and the addition of calcium to the diet inhibited their development in the colonic mucosa.
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PMID:Inhibition of Western-diet induced hyperproliferation and hyperplasia in mouse colon by two sources of calcium. 758 87

The Caco-2 cell line was utilized to analyze the role of nutrient factors such as calcium, vitamin D and epidermal growth factor (EGF) in epigenetic control of human colon carcinoma cell growth. Proliferative signals from either low extracellular calcium or EGF, respectively, are transduced in Caco-2 cells via an increase in c-myc proto-oncogene mRNA and nuclear protein expression levels. Activation of the EGF receptor is associated also with down-regulation of the cytoplasmic high-affinity vitamin D receptor (VDR). This would allow colon carcinoma cells to escape from the VDR-mediated anti-mitogenic action of 1 alpha, 25-dihydroxyvitamin D3 (1 alpha,25(OH)2D3). However, Caco-2 cells have the unique property to synthesize the vitamin D hormone from 25-hydroxyvitamin D3. 1 alpha,25(OH)2D3, in turn, counteracts the negative effect of EGF on VDR abundancy and slow down tumor cell proliferation through a c-myc-independent pathway.
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PMID:Growth regulation of human colon adenocarcinoma-derived cells by calcium, vitamin D and epidermal growth factor. 760 83


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