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)

Clinical and experimental gerontologists are extremely interested in lipoproteins as well as in new methods for investigating and probing the apolipoprotein pattern. Using immunofixation electrophoresis, we separated free apolipoprotein A-1 from the apo A-1 associated with high-density lipoproteins. Free apolipoprotein A-1 is a low-molecular-mass form of apo A-1 that seems to contain an extremely low quantity of lipids. The use of IFE as a tool for probing free apo A-1 has revealed new and interesting findings, such as its "artificial" increase during serum conservation at temperatures between 0-4 degrees C. From the clinical point of view, we demonstrated a decrease to the point of disappearance of free apo A-1 in some patients with liver cirrhosis. Moreover, one of the main findings here reported is the failure of anti-human apo A-1 murine monoclonal antibody and monoclonal antibody mixture to precipitate free apo A-1 in agarose systems. This discovery has important implications both for basic knowledge on apolipoproteins and for practical reasons concerning variability in those immunoassays (radial immunodiffusion) utilizing monoclonal antibody mixtures.
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PMID:New in vitro findings on the "free" form of apolipoprotein A-1. 148 30

The existence of marked elevations of ascitic fluid cholesterol has been observed in patients with peritoneal carcinomatosis compared to patients with cirrhosis and has been found useful in differential diagnosis. This finding could be caused by an enhanced movement of plasma lipoproteins into the peritoneal cavity. To test this hypothesis we determined the fasting concentrations of total, high density lipoprotein (HDL)- and low density lipoprotein (LDL)-cholesterol, apolipoprotein-A1 (apo-A1) and apolipoprotein-B (apo-B) in serum and ascites of 17 patients with cirrhosis and 16 patients with peritoneal carcinomatosis. The movement of proteins from plasma to ascites was calculated from the ascites/serum concentration ratios of six different sized proteins with a molecular mass ranging from 54 kDa to 971 kDa. Mean values (mg/dl) for total cholesterol (92.6 vs. 21.0), HDL-cholesterol (15.6 vs. 1.8), LDL-cholesterol (63.4 vs. 16.1), apo-A1 (50.2 vs. 13.6) and apo-B (41.2 vs. 12.9) in ascites were significantly higher in peritoneal carcinomatosis than in cirrhosis. These differences could only partially be explained by the higher serum concentrations of these parameters in peritoneal carcinomatosis, but were mainly due to a lower selectivity for the movement of plasma proteins and lipoproteins into ascites (mean ascites/serum (A/S) ratio: 0.30-0.77) in peritoneal carcinomatosis as compared to cirrhosis (mean ascites/serum ratio: 0.11-0.21). In both groups about 85% of the total cholesterol in serum and ascites consisted of HDL- and LDL-cholesterol. These findings support the hypothesis that elevations in ascitic cholesterol in peritoneal carcinomatosis compared to cirrhosis are mainly caused by the increased movement of plasma HDL and LDL into the peritoneal cavity.
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PMID:Pathophysiology of elevated ascites fluid cholesterol in malignant ascites. Increased ascites to serum relation of proteins and lipoproteins in patients with peritoneal carcinomatosis as compared to patients with cirrhosis of the liver. 150 Jun 88

To make liver biopsy unnecessary in certain cases, PGA (P, prothrombin time; G, gamma-glutamyl transpeptidase; A, apoliprotein AI), a simple biological index combining a specific test for severe liver disease (prothrombin time), a sensitive test of alcoholic liver disease (serum gamma-glutamyl transpeptidase), and a test for liver fibrosis (serum apolipoprotein AI), was evaluated in a training sample of 333 drinkers and validated in 291 other drinkers. All patients underwent an intercostal liver biopsy, and the specimen was independently read by two pathologists. The PGA index varied from 0 to 12. When PGA was less than or equal to 2, the probability of cirrhosis was 0% and the probability of normal liver or minimal changes 83%. Conversely, when PGA was greater than or equal to 9, the probability of normal liver or minimal changes was 0% and the probability of cirrhosis 86%. These values did not vary between training and validation periods, between asymptomatic vs. symptomatic subjects or between PGA at admission vs. PGA 1 week later. This index could be useful for general practitioners in identifying subjects at high risk for severe alcoholic liver disease.
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PMID:A simple biological index for detection of alcoholic liver disease in drinkers. 179 91

Assessment of the relative transcription rates and mRNA steady-state levels for apolipoprotein genes E, A-I, and A-II has been performed in normal rat liver, during liver regeneration and following induction of cirrhosis, as well as in rats with inherited analbuminemia associated with hyperlipidemia. Apo E exhibits primarily transcriptional control with an additional component of posttranscriptional control, whereas Apo A-I is controlled primarily at the posttranscriptional level, thus indicating that these genes are regulated independently. The level of control for Apo A-II has not been determined, because of difficulty experienced in measuring the transcription rate of this gene. During liver regeneration, cirrhosis, and analbuminemia, there is a marked increase in the ratio of Apo A-I to Apo E mRNA, resulting from an increase in the Apo A-I mRNA steady-state level and a decrease in Apo E mRNA. These changes are similar in the three pathophysiologic states and seem to occur through a combination of transcriptional and posttranscriptional mechanisms.
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PMID:Transcriptional and posttranscriptional regulation of apolipoprotein E, A-I, and A-II gene expression in normal rat liver and during several pathophysiologic states. 212 16

The serum apolipoprotein A (Apo A) and alpha-fetoprotein (AFP) were evaluated in histologically verified 30 cases of alcoholic cirrhosis and 18 cases of hepatocellular carcinoma (HCC). The latter were also divided into subgroups depending on the presence or absence of associated cirrhosis. Serum Apo A levels were found to be significantly decreased in cirrhotics (p less than 0.001) compared to controls and non-cirrhotic HCC patients. In 22 cases of alcoholic cirrhosis (AFP less than 10 ng/ml) and 12 cases of HCC (AFP greater than 600 ng/ml), the AFP levels itself were diagnostic, but in the remaining cases, AFP levels (100-600 ng/ml) were not able to differentiate between cirrhosis and malignancy. In this later group of patients with low pathological range of AFP, serum Apo A levels found to be significantly decreased in alcoholic cirrhotic patients (p less than 0.001) compared to HCC patients. Thus, estimation of Apo A levels may be helpful to interpret the AFP values at lower pathological range due to suspected liver pathology.
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PMID:Diagnostic significance of estimation of serum apolipoprotein A along with alpha-fetoprotein in alcoholic cirrhosis and hepatocellular carcinoma patients. 245 72

A prospective study of apolipoprotein AI has been undertaken in 581 alcoholic patients and in 100 controls in order to describe the changes of apolipoprotein AI according to the different stages of the alcoholic liver disease, to correlate the changes to serum liver tests and to estimate its diagnosis and prognostic value. Results showed that apolipoprotein AI concentration is highly related to the degree of liver injury, reaching a maximum in patients with steatosis (229 +/- 90 mg per dl), beginning to decrease in patients with fibrosis (188 +/- 88 mg per dl) and reaching a minimum in patients with severe cirrhosis (91 +/- 46 mg per dl). Apolipoprotein AI had an independent and discriminative value for the diagnosis of fibrosis (p less than 0.001) vs. steatosis and for the diagnosis of cirrhotic vs. noncirrhotic fibrosis (p less than 0.001) or vs. acute alcoholic hepatitis without cirrhosis (p less than 0.001). Cirrhotic patients with apolipoprotein AI less than 100 mg per dl had a lower survival rate at 1 year (62 +/- 7%) than patients with greater value (80 +/- 6%; p less than 0.05), but this prognostic value disappeared in multivariate analysis when other known prognostic factors were taken into account.
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PMID:Apolipoprotein AI and alcoholic liver disease. 309 67

A ninth Japanese patient afflicted with lecithin-cholesterol acyltransferase (LCAT) deficiency is described with emphasis on renal pathology. The most striking feature is massive deposition of lipid material in the glomeruli, particularly in the glomerular basement membrane (GBM) and in the mesangial region. The glomerular changes appear to be similar to that seen in some cases with cirrhosis of the liver. Lipid material contains a large amount of apolipoprotein-B detected by immunohistology. In two renal biopsies, taken three years apart, renal pathology is essentially the same and glomerular pathology is most characteristic. It is suggested that lipid deposition in glomeruli in this patient is rather slow. Family study of the present case reveals consanguinous marriages in the previous two generations suggesting the exaggerated gene expression of LCAT deficiency in this family.
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PMID:Nephropathy of familial lecithin-cholesterol acyltransferase deficiency: report of a case. 351 May 35

To assess the sensitivity, specificity and clinical value of prealbumin as liver test, prealbumin plasma levels were measured in 100 patients with liver disease and in 65 patients without clinical evidence of liver impairment. The sensitivity of prealbuminemia was higher than that of albumin, pseudocholinesterase, apolipoprotein and prothrombin activity. Its specificity was higher than that of pseudocholinesterase and comparable with the specificity of other liver tests. Prealbumin plasma levels were progressively decreasing in patients with liver cirrhosis graded as Child's A, B and C, respectively. In these patients prealbuminemia was correlated with galactose elimination capacity, assumed to be an index of maximal liver functional capacity.
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PMID:Value of prealbumin plasma levels as liver test. 362 40

Apolipoproteins A-I, A-II and B were evaluated in 18 chronic active hepatitis and 27 liver cirrhotic patients. The latter were also divided into compensated and decompensated subgroups. Significantly low values of apolipoproteins A-II and B were seen in chronic active hepatitis and liver cirrhotic patients, while apolipoprotein A-I was decreased in liver cirrhotic patients only. Chronic active hepatitis had higher apolipoprotein values than liver cirrhosis and in the latter one decompensated subgroup showed lower apolipoprotein levels than the compensated one. Apolipoproteins A-I, A-II and B correlated also well with prothrombin activity (Normotest) in liver cirrhotic patients, especially the apolipoprotein A-II values. This study suggests that serum values of apolipoproteins are affected by the type of liver damage and that their decrease could be partly due to impaired liver synthesis.
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PMID:Apolipoproteins A-I, A-II and B in chronic active hepatitis and in liver cirrhotic patients. 642 13

12 patients with unequivocal post-alcoholic end-stage liver cirrhosis were compared with 12 healthy controls with regard to the plasma concentrations of lipids, lipoproteins (by rate zonal ultra-centrifugation) and apolipoproteins of high-density-lipoproteins (HDL) (by disc electrophoresis), as well as to the activities of lecithin-cholesterol acyltransferase (LCAT) in plasma and of hepatic lipase (HL) in post-heparin plasma. The cirrhotic group showed the following differences (all significant at the p less than 0.01 level) from the control group: Total cholesterol, HDL-cholesterol, very-low-density-lipoproteins (VLDL), HDL, and HL were decreased. Intermediate-density-lipoproteins (IDL) were not detectable in the cirrhotic group. Low-density-lipoproteins (LDL) did not differ significantly from controls. However, LDL from cirrhotic patients contained more triglycerides but less esterified and free cholesterol (all p less than 0.01). The percentage apolipoprotein composition of HDL did not differ significantly between controls and cirrhotics. Surprisingly, LCAT activity in plasma as well as the ratios between esterified and free cholesterol in plasma, LDL, and HDL were nearly identical in both groups. It seems likely that LCAT activity decreases only in the states of acute or subacute liver injury or of biliary obstruction. Severe chronic liver injury or of biliary obstruction. Severe chronic liver damage as in our cases of end-stage liver cirrhosis without any signs of acute liver injury exhibits apparently no defect in cholesterol esterification.
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PMID:Lipoproteins, HDL-apolipoproteins, activities of hepatic lipase and lecithin-cholesterol acyltransferase in the plasma of patients with post-alcoholic end-stage liver cirrhosis. 663 32


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