Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum Group-specific component (a probable vitamin D transport protein) concentrations have been measured in 72 patients with chronic liver disease. Low mean values were found in groups of patients with cirrhosis and metastatic liver disease. In a group of patients with biliary tract disease the mean value was not significantly different from normal except for seven patients with severe bone disease who were found to have the lowest levels. The mechanism for the reduction remains to be clarified, but low Group-specific component values may play a contributory role in the osteodystrophy of chronic obstructive liver disease.
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PMID:Group-specific component [Gc] levels in chronic liver disease. 7 53

To assess the role of hepatic function and alcohol on vitamin D metabolism, serum 25-hydroxyvitamin D (25-OHD) levels were measured in 20 healthy nonalcoholic control subjects, 31 "inactive" cirrhotics whose alcoholism was in remission, 8 alcoholic cirrhotics, and 15 alcoholics with normal liver function. Cirrhosis but not alcoholism, was assoicated with low serum 25-OHD levels. The aminopyrine breath test (ABT) was performed because aminopyrine, like vitamin D3, is metabolized by hepatic microsomes; the ABT correlated highly (r = 0.74, rho less than 0.01) with serum 25-OHD in the inactive cirrhotics. After an intravenous injection of 120 mug vitamin D3, serum 25-OHD rose significantly within 24 hr in 6 healthy controls and 2 patients with celiac disease but not in 6 inactive cirrhotics. The data suggest impaired 25-hydroxylation of vitamin-D impaired in patients with cirrhosis, related predominantly to the degree of hepatic dysfunction.
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PMID:Abnormal vitamin D metabolism in patients with cirrhosis. 18 83

Despite regular long-term parenteral vitamin D2 treatment, four patients with biliary cirrhosis had multiple symptoms of bone disease and bone biopsy specimens showed osteomalacia without osteoporosis. Three patients also had a proximal myopathy. Plasma calcium values (after correction for albumin), phosphorus, magnesium, and serum 25-hydroxy-vitamin D were within normal limits. Treatment with 1,25-dihydroxy-cholecalciferol (1,25-(OH)2D3) relieved symptoms in three of the four patients and improved those in the fourth. Histological examination of bone showed improvement in all four patients, but serum and urinary biochemical changes were not pronounced. We conclude that 1,25-(0H)2D3 treatment has a beneficial effect on bone and muscle in hepatic osteomalacia, either because vitamin D 1-hydroxylation fails in biliary cirrhosis or because hepatic osteomalacia is resistant to vitamin D2 metabolites.
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PMID:Parenteral 1,25-dihydroxycholecalciferol in hepatic osteomalacia. 62 Feb 4

This study deals with 29 patients with cirrhosis, caused by alcohol in 23 cases, at a stage of edematoascitic decompensation. Calcemia was low 88 +/- 7 mg/l) as well as calciuria 87 +/- 92 mg/24 h). Phosphoremia and hydroxyprolinuria were within normal limits. A moderate diminution of 25 OH D3 (29,5 +/- 18 ng/ml) was observed in most patients but one third of them had no or very low levels of parathormone and 10 out of 27 had an elevated level of calcitonin. Bone histomorphometry which was done in 24 cases showed a discrete osteoporosis, a relative hyperosteoidosis and a hyperosteoclasis. There was a very significant relationship between hypocalcemia, and hypoalbuminemia but the other abnormalities could not be correlated significantly with either the duration or the severity of the disease. Hypocalcemia and bone histomorphometric abnormalities of cirrhosis can certainly not be explained only by a lack of liver hydroxylation of vitamin D.
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PMID:[Vitamin D, parathormone, calcitonin and bone histomorphometry in patients with cirrhosis]. 75 54

The concentration of the vitamin D-binding protein was measured in human serum by single radial immunodiffusion. Normal serum concentrations were slightly higher in normal women than in normal men. No race-related difference was found between white people from Belgium and black people from Zaire. Lower concentrations were found in cord serum and in patients with cirrhosis of the liver. Increased serum levels were observed during pregnancy or during the intake of estro-progestogens. The serum level of the vitamin D-binding protein was not altered in various diseases of calcium metabolism (primary osteoporosis, primary and secondary hyperparathyroidism, rickets, osteomalacia or vitamin D intoxication). No correlation was found between serum levels of 25-hydroxy vitamin D and those of its binding protein. From these data the following conclusions can be drawn: 1) The serum concentration of the vitamin D-binding protein (about 6.10(-6)M) largely exceeds the normal serum concentration of 25-hydroxy vitamin D (about 4.10(-8)M), so that this protein is normally for less than 1% saturated, 2) Normal serum levels of the vitamin D-binding protein were observed in several diseases of calcium metabolism, and 3) The free concentration of 25-hydroxyvitamin D is not regulated at a constant level.
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PMID:The measurement of the vitamin D-binding protein in human serum. 88 87

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

The levels of circulating 25 OH-D were determined by a direct radio-competition methods both in normal subjects and in subjects with various pathological conditions. In normal subjects, the average level of 25 OH-D was higher in summer (42.3 ng/ml) than in winter (29.1 ng/ml), P less than 0.005. Monthly variations in the 25 HO-D levels were found in relation to insolation The level of 25 OH-D was practically normal in osteoporosis (28.9 ng/ml), clearly lower in the mixed forms called "osteoporomalacia" (13.5 ng/ml, P less than 0.005) and very low in osteomalacia (5.8 ng/ml, P less than 0.001). In cases of cortisone osteopathy the average level was 22.8 ng/ml (NS). The level of 25 OH-D was also found to be lower in hepatic cirrhosis (11.7 ng/ml, P less than 0.01), in subjects treated with anticonvulsants (P less than 0.01), and in the course of hyperparathyroidism (P less than 0.002). There was no corelation between the level of 25 OH-D and calcaemia, phosphoraemia, circulating immunoreactive parathyroid hormone, or the relative osteoid volume. In contrast, there seemed to be a good correlation with the level of alkaline phosphatasaemia. The level of 25 OH-D was also determined in 4 subjects with vitamin-resistant osteomalacia: in 3 cases hepatic hydroxylation seemed normal, indicating the possibility of a subsequent disorder of vitamin D metabolism; in one case the absence of hepatic hydroxylation was noted.
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PMID:[Study of circulating 25 hydroxyvitamin D]. 98 30

Competitive protein-binding assay of 25-OH-D was developed by the use of specific vitamin D-binding proteins from vitamin D-deficient rat serum. Ether extract of serum sample which was dried and dissolved in ethanol, or standard solution of 25-OH-D3, was incubated with 3H-25-OH-D3 and vitamin D-binding protein for 2 hours at 4degreesC. Free and bound 3H-25-OH-D3 were separated through dextran-coated charcoal. The sensitivity of the assay system was 0.22 ng/tube. Percent cross reaction in the assay was 2.18% in vitamin D3, 0.70% in 1, 25-(OH)2-D3, less than 0.28% in 1alpha-OH-D3, and less than 0.06% in dihydrotachysterol, cholesterol and cortisol. Human serum 25-OH-D is 28.9+/-2.9 ng/ml in 19 normal subjects. Serum 25-OH-D in the old-age group (50-70 years of age) was significantly decreased, compared with that in the young-age group (20-40 years of age). Serum 25-OH-D was significantly decreased in gastrectomized and osteoporotic patients as well as in the patients with liver cirrhosis, in comparison with their age-controls.
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PMID:Effects of age and diseases on human serum 25-hydroxycholecalciferol determined by competitive protein-binding assay. 99 36

Enteral calcium absorption was determined in 18 patients with non-obstructive liver disease (16 with liver cirrhosis, 2 with chronic hepatitis). There was no significant difference in comparison with healthy persons. Osteoporosis in patients with chronic liver disease probably is not due to impaired calcium absorption but to other complications of liver disease as immobility, muscle atrophy, chronic pancreatitis, alcoholism and malnutrition. Osteomalacia on the other hand, is a complication of long standing obstructive liver disease. In these cases vitamin D treatment is indicated.
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PMID:[Osteopathies and calcium absorption in chronic liver diseases]. 122 54

The long-term prognosis of extrahepatic biliary atresia after surgical restoration of bile flow is still controversial. An ongoing process of cirrhosis and the development of portal hypertension continue to create frequent and frustrating management problems. Clinical features, hepatic function, echotomography aspect, calcium-phosphorus metabolism and serum levels of 25-OH-D-3 were evaluated in 12 anicteric patients with extrahepatic biliary atresia successfully treated in a period from 1974 through 1987. Seven of these children had a total of 21 episodes of cholangitis. In five patients liver biopsy, obtained at the time of the external diversion closure, showed a biliary cirrhosis. Growth, development and hepatic function were normal in all children studied; one patient had esophageal varices. The serum levels of 25-OH-D3 in patients without oral supplementation of vitamin D are lower than normal. This deficit can be corrected by oral administration of vitamin D. Our study revealed that the children with successful portoenterostomy appeared to thrive normally and that they tolerated the relatively mild liver damage. We believe that Kasai operation should be done in all patients with extrahepatic biliary atresia and that the liver transplantation is to be reserved only in those with unsuccessful Kasai. In our experience external diversion was not useful to prevent cholangitis and moreover it complicates the hepatectomy in case of transplantation.
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PMID:[Long-term prognosis of patients with extrahepatic biliary atresia successfully treated with surgery. Our experience]. 194 2


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