Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Our knowledge of the cellular changes that lead to liver cell carcinoma in humans is limited by proper and necessary ethical restriction on clinical research. We know rather more about risk factors, the most important of which is cirrhosis, it seems that both the causative agent and the time of duration of the cirrhotic process are relevent to the magnitude of this risk. According to present knowledge, alpha1-antitrypsin deficiency, alcoholism, naturally occurring carcinogens, drugs, and the hepatitis B virus seem to carry the greatest risk of cancer developing in a cirrhotic patient. Cirrhosis, however, is not an essential prerequisite, and some or possibly all of these agents can also induce cancer without cirrhosis. Bile duct carcinoma commonly follows infestation with liver flukes. Cirrhosis is usually absent but duct epithelial hyperplasia is present prior to the development of cancer. Many cellular changes have been observed in patients and among populations considered to be at risk from liver cancer. Of these, liver cell dysplasia is the most striking and studies of its prevalence, natural history, and association with cirrhosis suggest that it is a precancerous change.
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PMID:Precursor lesions for liver cancer in humans. 77 94

We have studied the ultrastructure of histamine-containing cells in the bronchial lavage of normal rhesus monkeys. These cells were recognized by the similarities of their specific cytoplasmic granules to those in tissue mast cells and basophilic leukocytes of other species. According to cell shape, two forms of bronchial lavage histamine-containing cells (BL-HCC) were observed. One was round and small, and the other pleomorphic and large. However, the subcellular structures, especially the specific cytoplasmic granules, were identical for both forms of HCC. With available evidence, we now consider both types of BL-HCC to be one cell species. The difference in cell shape may be an inherent variation within this cell population, or a reflection of the maturity of individual cells. Most BL-HCC had long slender pseudopods, and the majority of them were mononucleated. Some HCC appeared binucleated; multinucleated cells were not encountered. The ultrastructure of mast cells, in tissue fragments biopsied from three sites, was in many ways similar to that of BL-HCC, but there were clear morphological dissimilarities between these two cell groups. It is unlikely that tissue mast cells are the direct precursors of BL-HCC. Attempts to compare BL-HCC with blood basophilic leukocytes were unsuccessful due to the failure to detect the latter in monkey peripheral blood with electron microscopy in the present study. The possible origin of BL-HCC is discussed.
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PMID:Histamine-containing cells in bronchial lavage fluid. I. Ultrastructural characterization and comparison with mast cells in three types of tissues of rhesus monkeys. 82 49

In a series of 18 patients suffering from varying degrees of chronic renal failure treated by diet alone, there was a statistically significant positive correlation between plasma magnesium levels and plasms 25 hydroxycholecalciferol (25 HCC) levels. This is thought to be due either to the direct action of 25 HCC on the bone liberating magnesium from bone crystal, or to an increased intestinal absorption of magnesium caused by 25 HCC.
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PMID:Interrelation between plasma magnesium and 25 hydroxy-vitamin D3 levels in chronic renal failure. 87 18

In 37 patients with Crohn's disease the 25-hydroxycholecalciferol (25-HCC) serum level, serum concentration of calcium and inorganic phosphate, and the enzyme activity of alkaline phosphatase were measured. Furthermore the activity index of Crohn's disease was determined in every patient. There was no statistically significant difference of 25-HCC serum levels in these patients compared to a healthy control group. Correspondingly most patients showed normal alkaline phosphatase enzyme activity and normal serum concentration of calcium and inorganic phosphate. No correlation between 25-HCC concentration and site of inflammation or activity index was found.
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PMID:25-hydroxycholecalciferol serum levels in patients with Crohn's disease. 90 78

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

Low doses of 1,25-DHCC cause a significant increase in trabecular and cortical bone mass of the mature rat skeleton by stimulated endosteal bone formation. The increased serum contents of calcium and inorganic phosphate give rise to a moderate nephrocalcinosis. An increased bone resorption occurs upon toxic dose levels causing profound nephrocalcinosis. Similar doses of 25-HCC do not affect the mature bone.
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PMID:Low doses of 1,25-dihydroxycholecalciferol increase mature bone mass in adult normal rats. 91 86

The blood levels of 25-hydroxyvitamin D (25-HCC) in 26 patients with nephrotic syndrome (proteinuria of 6.5 g/24 h +/- 0.8 SEM) ranged between 1 and 18.6 ng/ml (8.6 +/- 1.0 SEM). This value was significantly lower (P less than 0.01) than that in normal subjects (21.8 +/- 2.3 ng/ml) and patients with chronic renal failure (24.8 +/- 2.3 ng/ml). There was inverse correlation (P less than 0.01) between levels of 25-HCC and magnitude of proteinuria and a direct relation (P less than 0.01) with serum albumin. Reduction in proteinuria was rapidly followed by a rise in blood 25-HCC toward normal. Ionized calcium levels were low in 16 of 26 nephrotic patients irrespective of degree of renal failure. In four of seven nephrotic patients with normal renal function, ionized calcium levels were low and showed an inverse relation with levels of parathyroid hormone. These data show that patients with nephrotic syndrome have low blood levels of 25-HCC probably due to its loss in urine. This derangement is probably responsible for the disorders of calcium metabolism in nephrosis.
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PMID:Blood levels of 25-hydroxyvitamin D in nephrotic syndrome. Studies in 26 patients. 93 Dec 2

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


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