Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The long-term effects of the vitamin D metabolite, 25-hydroxycholecalciferol (25-HCC), were evaluated in 2 children with hypophosphatemic vitamin D-resistant rickets. Serial total balance studies demonstrated an apparent lack of correlation between the effects of the vitamin on intestinal absorption of calcium and phosphorus and both the onset of healing in 1 of the 2 patients treated with 5,000 to 7,500 u of the metabolite and the absence of demonstrable radiologic improvement in another patient in whom the final dosage was 20,000 u. per day. At first, the metabolite induced a positive calcium balance in both patients resulting largely from a reduction in intestinal calcium excretion. Despite a continued positive calcium balance, 1 of the 2 patients did not demonstrate further healing, while in the other patient healing was noted even when total calcium balance was negative. Serum phosphate levels did not return to normal in either patient, nor was phosphate excretion altered by 25-HCC. Serum alkaline phosphatase remained elevated in both. Serum immunoassayable parathyroid hormone levels were consistently normal to high-normal in the 2 patients throughout more than 24 months of observation. No instances of hypercalcemia and only occasional hypercalciuric episodes were noted.
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PMID:Long-term therapy of viramin D-resistant richets with 25-hydroxycholecalciferol. 16 13

Quantitative morphometric analyses of iliac crest biopsies from 20 epileptic patients receiving chronic anticonvulsant therapy have been performed before and after 4-8 months of vitamin D2 treatment with 9 000 U per day. Biochemical quantities, including serum 25-hydroxycholecalciferol (25-HCC) and serum parathyroid hormone (iPTH), were measured. The anticonvulsant osteomalacia found in the initial bone biopsies was characterized by an increased amount of ummineralized bone, an increased bone resorption and, contrary to vitamin D deficiency, an increased bone mineralization and bone formation. Bone resorption and bone formation were probably equally increased since the amount of cancellous bone was normal. Except for a slight increase in osteoidcovered surfaces and osteoclastic resorption surfaces, the bone changes were normalized after vitamin D2 treatment, leading to a mean serum level of 25-HCC 2.4 times above normal. Serum iPTH was normal before and unchanged during D2 therapy. The urinary calcium excretion remained decreased. The investigation characterizes anticonvulsant osteomalacia as a specific bone disease different from that of vitamin D deects of vitamin D metabolites on receptor cells.
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PMID:Effect of long-term vitamin D2 treatment on bone morphometry and biochemical values in anticonvulsant osteomalacia. 30 May 47

Serum 25-hydroxycholecalciferol (25-HCC) and serum parathyroid hormone (iPTH) were measured in 59 randomly selected adult epileptic outpatients receiving chronic anticonvulsant therapy. Quantitative morphometric analysis of iliac crest biopsies was performed. A mild degree of osteomalacia was found which was inversely correlated to dietary vitamin D intake. Serum 25-HCC was reduced in the epileptic patients compared to a control group, although dietary intake of vitamin D was higher than the mean daily intake in the Danish population. Serum 25-HCC was positively correlated to dietary vitamin D intake, but not correlated to the severity of bone changes, indicating that other factors than circulating 25-HCC are responsible for the development of anticonvulsant osteomalacia. Serum 25-HCG was inversely correlated to serum iPTH in patients with a low dietary calcium intake. The mean value of serum iPTH was not increased, and there was no correlation between serum iPTH and bone morphometry.
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PMID:The interrelationships between serum 25-hydroxycholecalciferol, serum parathyroid hormone and bone changes in anticonvulsant osteomalacia. 57 30

Mercuric chloride (HgCl2) was tested at 16 p.p.m. Hg for vitamin D sparing activity by presenting it dietarily in the presence and absence of 25-hydroxycholecalciferol (25-HCC) to Japanese quail (Coturnix c. japonica) for 25 days. No gross signs characteristic of mercury poisoning were observed, but some predictable effects of vitamin D deficiency on avian reproduction were manifested within 10 days. Rate of lay, egg shell thickness, and hatchability of fertile eggs decreased markedly for birds on vitamin D-deficient diets. Shell-less eggs were laid by these birds after 20 days and laying stopped entirely on the 23rd day. Laying resumed within 5 days after diets were refortified with 25-HCC. There was no detectable interaction between HgCl2 and vitamin D.
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PMID:Reproductivity of Japanese quail fed mercuric chloride in the absence of vitamin D. 60 45

Vitamin D has been proposed as a risk factor of ischaemic heart disease. In 12 patients with acute myocardial infarction the major circulating vitamin D metabolite, 25-hydroxy-cholecalciferol (25-HCC), did not show any fluctuations during the first 4 days after onset of symptoms. The serum 25-HCC level was then measured in 128 patients consecutively admitted because of chest pain, 53 of whom had myocardial infarction and 75 had angina pectoris. The values found did not differ from those measured in 409 normal persons. The seasonal variations of serum 25-HCC were less pronounced in heart patients than in normals, probably due to less sun exposure in the summer months. The levels of serum 25-HCC did not correlate with the concentrations of serum cholesterol, glycerides, calcium or magnesium. Low serum calcium and magnesium were observed in all patients. Serum calcium was further reduced in the course of acute myocardial infarctions while serum parathyroid hormone rose significantly. We conclude that patients with ischaemic heart disease are not ingesting or producing in their skin elevated amount of vitamin D.
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PMID:Vitamin D and ischaemic heart disease. 74 75

The seasonal variations in circulating 25-hydroxycholecalciferol (25-HCC) were studied in 102 alcoholics with fatty liver disease without histologic signs of cirrhosis and in 35 patients with alcoholic cirrhosis. The mean levels were compared with those of normal persons. Alcoholics had generally lower 25-HCC values than the controls, particularly in the summer. This was primarily explained by insufficient diet and reduced exposure to sunshine. The ability of the liver to hydroxylate in the 25-position was studied in three groups of alcoholics with 1) fatty liver disease without cirrhosis, 2) compensated cirrhosis, 3) severely incompensated liver cirrhosis. All three groups exhibited a significant increase in serum 25-HCC following the peroral administration of cholecalciferol at a dose of 1 200 U daily for 7 days. Similar rises were seen 7 days after a single injection of 10 000 U cholecalciferol. This indicates a normal intestinal absorption of vitamin D, even in advanced alcoholic liver disease, and is inconsistent with a severely damaged 25-hydroxylation capacity in these patients. Osteomalacia due to impaired liver hydroxylation of vitamin D can hardly explain the increased fracture rate and the decreased bone mass, which have been described in alcoholics.
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PMID:The hepatic conversion of vitamin D in alcoholics with varying degrees of liver affection. 91 Jun 39

25-Hydroxycholecalciferol (25-HCC) levels were measured in 31 bedouin females and eight bedouin male tribesmen and compared with the levels in Jewish males and females in Beersheba. In nonpregnant bedouin women the mean 25-HCC level was 25.4 ng/ml +/- 9.78. In pregnant bedouin women the mean was 23.4 ng/ml +/- 8.52. In bedouin males the mean level was 25.7 ng/ml +/- 3.03. In Jewish females, both pregnant and nonpregnant, the levels were higher (32.7 ng/ml +/- 6.02 and 44.3 ng/ml +/- 9.24). Jewish males had levels of 32.8 +/- 6.29 ng/ml. No bedouin had plasma levels below 10 ng/ml, and there was no evidence to suggest deficiency of vitamin D in bedouin males or females.
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PMID:25-Hydroxycholecalciferol levels in bedouins in the Negev. 97 99

The effect on phosphate excretion of graded doses of parathyroid hormone (PTH) and the biologically active vitamin D3 metabolite, 25-hydroxycholecalciferol (25-HCC), administered singly and in combination, were studied in the nonexpanded, vitamin D-depleted thyroparathyroidectomized rat. Infusion of 1 unit of 25-HCC per hour for 6 hours induced an antiphosphaturia only when administered with 0.2 units of PTH per hour, while neither agent alone changed phosphate excretion. A dose of 2.0 units of PTH per hour did not cause phosphaturia unless given with 1 unit of 25-HCC per hour. In pharmacologic dosage (5 units per hour), PTH produced phosphaturia in the absence of the metabolite.
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PMID:Parathyroid hormone and 25-hydroxy vitamin D3: synergistic and antagonistic effects on renal phosphate transport. 116 16

The metabolism of vitamin D3-3H was studied in a small group of controls and subjects with tropical sprue after the oral or intravenous administration of 8 to 10 microCi of D3-3H. The biological half life of D3-3H upon the administration of the isotope by the intravenous route was normal in 2 controls, very low in a subject with tropical sprue who had steatorrhea, and decreased in a subject with tropical sprue who did not present steatorrhea. After the administration of the isotope by the oral route, the biological half life was 35 hours in the control and no radioactivity could be detected in the plasma of the subject with tropical sprue who had steatorrhea. Twenty four hours after the intravenous dose the percentage of radioactivity in the plasma as HCC-3H was two times higher in the tropical sprue subjects than in the controls. When the dose was given orally the net absorption was 50.5% in the subject with tropical sprue and steatorrhea and 86.8% in the subject with tropical sprue who was partially treated. These results showed rapid clearance of the D3-3H in the subject with tropical sprue and steatorrhea indicating depletion of vitamin D stores in the tissues and decrease in the net absorption of the dose when given orally. The presence of a higher percentage of the dose in the plasma as HCC-3H after the intravenous and oral administrations in the tropical sprue subjects when compared to controls indicates that the diseased state does not alter vitamin D3 metabolism.
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PMID:The kinetics of D3-3H metabolism in tropical sprue. 300 14

Plasma levels of 25-hydroxycholecalciferol (25-HCC) were measured by a specific competitive protein-binding assay. Mean levels in both normal London adults and adolescent schoolchildren were 16 ng/ml and the mean level in a group of epileptic patients on high-dosage anticonvulsant therapy was 5 ng/ml, (difference from normals P < 0.001). Two further epileptic patients, with well-marked anticonvulsant osteomalacia, were treated with small doses of 25-HCC during full metabolic balance studies; rapid healing followed administration of 25-HCC by mouth in doses of 10-45 mug daily, which is well below the effective dose range of calciferol in this condition. These findings provided further evidence that anticonvulsant osteomalacia results from hepatic enzyme induction which, by increasing the metabolism of cholecalciferol to inactive compounds, lowers 25-HCC levels in patients whose dietary vitamin D intake and exposure to sunlight are otherwise adequate. Results also indicated that under certain circumstances 25-HCC may have considerably stronger antirachitic potency in man than has hitherto been recognized.
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PMID:Plasma levels and therapeutic effect of 25-hydroxycholecalciferol in epileptic patients taking anticonvulsant drugs. 434 60


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