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)

In the present study we have investigated and also compared the biochemical nature of the platelet phospholipids in patients with portal liver cirrhosis and in normals. Normal platelets contained 10.88 +/- 0.83 microgram of phospholipid phosphorus per 10(9) platelets whereas the cirrhosis platelets contained 7.63 +/- 1.29 microgramP/10(9) platelets. In cirrhosis there was a 29.87% decrease of phospholipids compared to normal. However the percentage distribution of phospholipids in cirrhosis was similar to normal. But each phospholipid value in cirrhosis was found lower then normal. Estimated as microgram phosphorus per 10(9) platelets decreased amounts of phosphotidyl inositol (PI) (0.29 +/- 0.16), phosphotidyl serine (PS) (0.49 +/- 0.12), phosphotidyl ethanolamine (PE) (2.0 +/- 0.43) and spingomyelin (SPH) (1.42 +/- 0.31) and phosphotidyl choline (PC) (3.25 +/- 0.62) and total lipid phosphorus (7.63 +/- 1.29) were found in the patient group.
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PMID:Platelet phospholipids in liver cirrhosis. 60 16

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

In a retrospective analysis of 78 patients with liver cirrhosis, we found low serum levels of calcium and phosphorus. The low calcium levels showed a better correlation with high activity of aspartate aminotransferase than with low levels of albumin. In addition, there was a relationship between low calcium and low phosphorus levels. Therefore, factors other than, and in addition to, hypoalbuminemia seem to be responsible for the low calcium and phosphorus levels in cirrhosis patients. Although low levels of serum 25-hydroxyvitamin D were found in 23 of our patients, there was no indication that hypovitaminosis D was causative factor in the hypocalcemia and hypophosphatemia.
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PMID:Low levels of serum calcium, phosphorus and plasma 25-hydroxy vitamin D in cirrhosis of the liver. 68 Nov 62

Phosphorus-31 magnetic resonance spectroscopy of the human liver was undertaken in 28 healthy adult individuals and in 49 patients with liver disease of varying aetiology. Data localised to the liver were obtained using chemical shift imaging techniques. The mean (+/- 1 S.D.) of the peak area ratio phosphomonoesters (PME)/phosphodiesters (PDE) in healthy adult individuals, from spectra obtained with pulse angle 45 degrees and repetition time 1 s, was 0.24 +/- 0.07. The intra-examination variability of this ratio was 20%, the intra-subject variability 27% and the inter-subject variability 32%. An increase in the PME/PDE was observed in the 31P hepatic MR spectrum from primary or secondary tumours in all 17 patients studied, which invariably represented an increase in PME/ATP and, in some cases, a reduction in PDE/ATP. The spectra did not show aetiological characteristics. A non-specific elevation in PME/PDE was also observed in the 31P hepatic MR spectra of 10 (40%) of 25 patients studied who had diffuse liver diseases, such as cirrhosis and infiltrating malignancies. The spectral pattern did not distinguish between diseases of varying aetiologies, but there was a linear correlation between increasing PME/PDE and a reduction in plasma albumin concentrations (p = 0.03). In three patients with hepatic malignancy and abnormal hepatic 31P-MRS, marked spectral changes were observed after successful treatment to debulk the tumour. Only minor changes were observed in the abnormal spectrum of a fourth patient in whom treatment was unsuccessful. Hepatic 31P-MR spectroscopy may prove useful for monitoring disease processes and treatment effects in well characterised patient populations.
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PMID:Phosphorus-31 magnetic resonance spectroscopy of the human liver using chemical shift imaging techniques. 132 98

Cirrhotic patients have both impaired liver function and nutritional derangement. In fact, the prevalence of protein-energy malnutrition (PEM) is very high in these patients. The aim of the present study was to elucidate whether the nutritional status in cirrhosis could be an additional factor that would affect levels of plasma lipids. Plasma lipid phosphorus, cholesterol, and triglycerides (TG), and fatty acid profiles in plasma and plasma fractions were determined in 50 healthy subjects and 92 patients with liver cirrhosis. The cirrhotic patients were prospectively included in three groups according to the result of nutritional assessment: group 1 (n = 38), acceptable nutritional status (including well-nourished and mildly malnourished patients); group 2 (n = 29), moderate PEM; and group 3 (n = 25), severe PEM. The main findings of this study were that the decrease in plasma cholesterol and linoleic, dihomo-gamma-linolenic, and arachidonic acid levels of cirrhotic patients was related to the degree of PEM. Cholesteryl esters (CE) appeared to be the most sensitive indicator of lipid changes in cirrhosis. We consider that the role of malnutrition in the changes observed for polyunsaturated fatty acid (PUFA) profiles in plasma lipids of cirrhotic patients may be of major importance, since severe malnourished subjects exhibited the lowest levels of those compounds. Dietary supplementation of both essential fatty acids (EFA) and long-chain PUFA in adequate amounts to the cirrhotic patient might be of importance in the management of the disease.
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PMID:Malnutrition-related polyunsaturated fatty acid changes in plasma lipid fractions of cirrhotic patients. 151 24

To determine the cause of reduced urea synthesis in cirrhosis, absolute concentrations of phosphorus metabolites in the human liver have been measured in vivo with magnetic resonance (MR) spectroscopy. One-dimensional chemical shift imaging was used to obtain phosphorus-31 spectra from five healthy volunteers and five patients with alcoholic cirrhosis. A reference standard included in all studies enabled the calculation of absolute concentrations. In contrast to hepatic metabolite ratios, absolute concentrations reveal that in the cirrhotic patients, concentrations of adenosine triphosphate (ATP) were significantly reduced and concentrations of phosphomonoesters slightly reduced. Intracellular pH was unchanged. Histologic evidence suggests that the amount of ATP per cell was unchanged and could not account for the reduced urea production. Instead, urea synthesis depends on the functional liver cell mass, which was reduced by 31% in alcoholic cirrhosis. Quantitative in vivo P-31 MR spectroscopy of liver has potential clinical applications and can supplement the more generally used P-31 metabolite ratios.
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PMID:Quantitative P-31 MR spectroscopy of the liver in alcoholic cirrhosis. 156 69

We have previously reported that monocyte aryl hydrocarbon hydroxylase (AHH) activity is depressed in patients with liver disease and is decreased more in cirrhosis than in early stage liver disease. To determine if monocyte AHH activity reflects liver AHH activity, we studied an animal model of cirrhosis, i.e., yellow phosphorus induced cirrhosis in the pig. AHH activity was detectable in monocytes isolated from peripheral blood of normal pigs (0.32 +/- 0.13 nmol.mg-1 P.h-1, n = 11) and was comparable to the level of AHH activity in hepatic Kupffer cells isolated from wedge or needle biopsies of livers of normal pigs (0.38 +/- 0.21, n = 7). The AHH level in pig Kupffer cells was approximately 10% of the AHH level in hepatocytes and microsomes. To induce liver disease, pigs were administered yellow phosphorus (0.6 mg/kg) 5 days per week for 16 weeks. At 4 weeks of treatment, monocyte AHH activity was not different from control and liver histology was normal. Depression of monocyte AHH activity was evident at 8 weeks of treatment when liver fibrosis was seen histologically. At 12 weeks of treatment when histology revealed extensive liver fibrosis and collagen levels were elevated, the level of monocyte AHH activity was decreased 67% compared with controls. Similar changes were observed at 12 weeks in Kupffer cell AHH activity (86% decrease) and hepatocyte AHH activity (70% decrease) compared with controls. These results suggest that monocyte AHH activity reflects liver AHH activity and may be a good indicator of change in liver enzyme function in liver disease in the pig model of cirrhosis.
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PMID:Monocyte aryl hydrocarbon hydroxylase (AHH) activity mimics Kupffer cell and hepatocyte AHH activity in an animal model of liver disease. 180 52

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

Fatty acid (FA) profile of plasma total lipids, phospholipids (PL), cholesteryl esters (CE), and triglycerides (TG) were measured in 101 patients with advanced liver cirrhosis and in 44 age- and sex-matched healthy controls. Plasma levels of lipidic phosphorus, esterified cholesterol, and TG also were measured, and the unsaturation index (UI) was calculated for each fraction. Total plasma concentrations of saturated FA, linoleate, and polyunsaturated FA (PUFA) were lower in cirrhotics than in controls. This profile was also found in plasma levels of PL- and CE-associated FA. No detectable amounts of C20:3n9 were found in cirrhotic patients. Percent FA distribution of lipid fractions showed a lower percentage of linoleate and PUFA and a higher relative amount of saturated and monoenoic FA in cirrhotics than in controls. As a consequence, the UI of PL and CE was diminished in liver cirrhosis. Linoleate and PUFA deficiency was more marked in CE than in PL, as shown by the number of patients with values below the 5th percentile of the control group, suggesting an attempt to maintain the unsaturation of PL as the most important component of cell membranes. Hepatic failure, poor essential FA intake, and malnutrition are some of the possible etiologic factors for PUFA deficiency in cirrhosis. Their relative contribution to plasma FA abnormalities, as well as the clinical and pathophysiological consequences of PUFA deficit in cirrhotic patients, requires further investigation.
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PMID:Plasma fatty acid profile in advanced cirrhosis: unsaturation deficit of lipid fractions. 225 24

Elevated serum levels of intact parathyroid hormone (PTH) have been reported in severe versus mild biliary cirrhosis. The aim of this study was to determine whether hyperparathyroidism was present in severe liver disease on the basis of the inability of the liver to catabolize the hormone. Because biologic activity resides in the amino terminal, and amino terminal PTH determinations have not been routinely made in liver disease, it is possible that hyperparathyroidism was previously missed in these patients. Accordingly, we obtained fasting blood from 11 patients with severe liver disease and 8 age-matched controls. We measured intact, amino terminal, and mid-region PTH, vitamin D metabolites, bone gamma carboxyglutamic acid protein (BGP), ionized calcium, phosphorus, magnesium, and liver function tests. Serum levels of PTH were normal with all assays and 1,25(OH)2D levels were not elevated. These findings argue against the possibility that hyperparathyroidism plays a role in the pathogenesis of hepatic osteodystrophy.
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PMID:Absence of hyperparathyroidism in severe liver disease. 249 4


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