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-25-hydroxy-vitamin-D (25 OHD) concentration has been measured in 106 patients with untreated parenchymal and cholestatic liver disease. Low mean values were found in groups of patients with alcoholic hepatitis and cirrhosis, non-cirrhotic active chronic hepatitis, lupoid and cryptogenic cirrhosis, symptomatic primary biliary cirrhosis, and acute and chronic biliary disease. In a group of patients with presymptomatic biliary cirrhosis the mean value was not significantly different from normal. It is concluded that in the presence of significant parenchymal or cholestatic liver disease serum-25-OHD concentrations are usually low. The mechanisms for the reduction remain to be clarified, but low serum-25-OHD values may play a contributory role in the aetiology of osteomalacia in chronic liver disease.
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PMID:Serum-25-hydroxy-vitamin-D in untreated parenchymal and cholestatic liver disease. 6 May 15

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

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

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

A 61-year-old male with hepatocellular carcinoma (HCC) complicating liver cirrhosis presented hypophosphatemia progressing with HCC expansion and serum alpha-fetoprotein elevation. These changes were associated with an increased fractional excretion of phosphate and decreased theoretical phosphate threshold. There was increased nephrogenous cyclic adenosine monophosphate despite normal serum parathyroid hormone. Serum 1,25-dihydroxyvitamin D levels were markedly reduced with normal 25-hydroxyvitamin D levels. There were no symptoms of osteomalacia, however, a slightly increased osteoid seam was elicited on autopsy. The hypophosphatemia could be explained by presumed secretion from HCC of humoral factors which have a phosphaturic effect and also inhibit 25-hydroxyvitamin D-1 alpha-hydroxylase in renal tubular cells.
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PMID:Marked hypophosphatemia with decreased serum 1,25-dihydroxyvitamin D in a patient with hepatocellular carcinoma complicating liver cirrhosis. 171 78

We measured the concentrations of vitamin D-binding protein (DBP), total 25-hydroxyvitamin D, total 1,25-dihydroxyvitamin D [1,25-(OH)2D], and free 1,25-(OH)2D in sera of 107 patients with histologically proven chronic liver disease. Bone density measurements and dynamic skeletal histomorphometry were also performed. Osteoporosis, as defined by arbitrary criteria, was found in 42 patients (39%), while no patient had osteomalacia. Serum concentrations of vitamin D-binding protein, 25-hydroxyvitamin D, total 1,25-(OH)2D, and free 1,25-(OH)2D were reduced in patients with cirrhosis, but not in the noncirrhotic patients. Bone formation rates, which were low in 55 patients (51%), were correlated with liver functions, but not with the concentrations of either vitamin D metabolite. A subgroup of 44 patients with low serum 1,25-(OH)2D concentrations and low bone formation rates failed to show an appropriate increase in serum bone Gla protein after 1,25-(OH)2D3 administration even though serum concentrations of 1,25-(OH)2D rose normally. These data suggest that the bone disease in patients with hepatic disorders is not related to the serum concentrations of vitamin D metabolites or the effect of these metabolites on osteoblast function.
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PMID:Serum vitamin D metabolites are not responsible for low turnover osteoporosis in chronic liver disease. 258 58

1. Chronic alcoholism may be complicated by proximal muscle weakness associated with a selective atrophy of type II skeletal muscle fibres. The histopathological findings are non-specific as identical changes are seen in proximal muscle weakness associated with various metabolic myopathies, including osteomalacia. 2. The maximum voluntary contraction (MVC) of the dominant quadriceps and plasma 25-hydroxycholecalciferol [25-(OH)D] were measured in male alcoholics and control subjects to determine whether vitamin D deficiency contributed to proximal muscle weakness. 3. In both groups MVC declined with age and was related to body build. The distribution of plasma 25-(OH)D was skewed in alcoholics, with the mean significantly lower than in control subjects. Seventeen per cent of patients (but none of the control subjects) had pronounced biochemical deficiency [plasma 25-(OH)D less than 10 nmol/l]. 4. Alcoholics were significantly weaker than control subjects, even after correcting for the effects of age, height and weight. The severity of associated liver disease (cirrhosis vs no cirrhosis) did not influence muscle strength. Variation in plasma 25-(OH)D and albumin made an insignificant contribution to the difference in MVC observed between patients and control subjects. 5. We conclude that proximal muscle strength is reduced in chronic alcoholism but that this is not due to associated vitamin D [25-(OH)D] deficiency or alcoholic cirrhosis.
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PMID:Vitamin D deficiency and muscle strength in male alcoholics. 276 57

To study the pathogenesis of osteoporosis in patients with chronic liver disease, we performed dynamic bone histomorphometry and measured serum bone Gla-protein in 80 patients with various types of chronic liver disease. These results were compared with results obtained in 40 healthy controls. Mean trabecular bone volume and mean trabecular thickness were significantly reduced in both men and women with chronic liver disease (p less than 0.001 for both measurements in men and p less than 0.01 for both measurements in women). Osteoporosis as defined by histologic parameters was present in 17 (21%) patients with no significant differences in prevalence rates among the various hepatic disorders. No patient had histologic evidence of osteomalacia, although mineralization lag times were prolonged (p less than 0.01 for men and women). Bone formation rates were significantly reduced in 46 (57%) patients, and unlike the static measurements, were related to the type and severity of the underlying liver disease. Patients with alcoholic liver disease, hemochromatosis, and cholestatic liver disease had lower bone turnover rates and osteoblastic surfaces (p less than 0.001 and p less than 0.05, respectively) than patients with chronic active hepatitis. Furthermore, the presence of hepatic cirrhosis was associated with diminished bone formation and lower osteoblast surfaces. Serum bone Gla-protein levels were significantly correlated with bone formation rates and osteoblast surfaces (r = 0.585 and r = 0.434, respectively). A reduction in osteoblast surfaces has not previously been demonstrated in liver disease. This reduction and the associated impairment of osteoblastic activity may contribute to the pathogenesis of osteoporosis and can be assessed by the measurement of serum bone Gla-protein.
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PMID:Hepatic osteodystrophy. Static and dynamic bone histomorphometry and serum bone Gla-protein in 80 patients with chronic liver disease. 278 12


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