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)

For the evaluation of certain differences in the diminution of export proteins of the liver we examined some exactly defined groups of liver diseases with the aim of further differentiation of the pathogenetic mechanisms. We measured the activity of glutamate-oxalacetate transaminase, glutamate-pyruvate transaminase, glutamate dehydrogenase, lactate dehydrogenase, alkaline phosphatase, cholinesterase and lecithin-cholesterol acyltransferase, the Quick value, the coagulation factors I, II, V, VII, VIII, IX and X. Clotting factors were determined by a Schnitger-Gross Coagulometer. Prothrombin, antithrombin III, plasminogen, factor VIII associated antigen and activated factor XIII were measured by immunoelectrophoresis according to Laurell. Lipoprotein electrophoresis in agarose gel was performed to evaluate changes in lecithin-cholesterol acyltransferase activity. Except of the rising diminution of export proteins in the course of liver disease from acute hepatitis to cirrhosis we found also specific changes of the patterns of the plasma specific enzymes. These proteins were diminished dependent on their half life time and the inflammatory activity--measured as the height of the transaminases. Lecithin cholesterol acyltransferase and factor VIII did not participate in the general diminution of the most export proteins; some details were found to explain this differing behaviour. Results are critically discussed with regard to new aspects in the biochemistry of the damaged liver cell.
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PMID:[Correlations between the diminished secretion of export proteins from the liver and the plasmatic activity of liver cell enzymes (author's transl)]. 42 91

The morphology of red blood cells was studied in 30 patients with severe liver cirrhosis, in 10 patients with extrahepatic jaundice, and in 10 control subjects. In all the patients with extrahepatic jaundice more than 30% of red blood cells were target cells with increased resistance to osmotic lysis. In 12 patients with liver cirrhosis more than 30% of red blood cells were spur cells. The cholesterol: phospholipids (C/PL) molar ratio was 0.89 in target cells, 1.33 in spur cells, and 0.74 in normal red blood cells. The red blood cell membrane cholesterol and phospholipids exchanged with plasma lipoproteins, the lipid composition of which was studied in eight patients with spur cells; the free cholesterol: phospholipid (FC/PL) molar ratio was 0.33 (0.16 in the controls) in high density lipoproteins (HDL) and 1.40 (0.82 in the controls) in low density lipoproteins (LDL); in these patients the polyunsaturated fatty acid content was low in both phospholipids and cholesterol esters of lipoproteins. The irregular folds of the spur cells regressed when polyunsaturated lecithin was infused (2 g daily for five days) in eight patients with spur cell anaemia; the infusions decreased both C/PL ratio in RC to 0.88 and the concentration of unconjugated bilirubin (104.3 to 82.0 mumol/l (6.1 to 4.8 mg%)), whereas the activity of the plasma lecithin:cholesterol acyltransferase (LCAT) increased from 31.2 to 54.4 mumol/l/h. Polyunsaturated fatty acid content of RC lecithin increased after the infusion as it did in HDL, the FC/PL ratio of which decreased to 0.23.
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PMID:Membrane lipid composition of red blood cells in liver disease: regression of spur cell anaemia after infusion of polyunsaturated phosphatidylcholine. 71 Sep 73

C4b-binding protein (C4bp), a glycoprotein involved in regulating the classical pathway of the complement system, binds the activated form of C4b and accelerates the decay rate of the C4b, C2a complex. Recently, sequence analysis of the cDNA for proline-rich protein (PRP) demonstrated that PRP is identical with C4bp. We measured the concentration of C4bp in serum by single radial immunodiffusion in patients with various liver diseases. Concentration of C4bp was significantly lower in hepatic cirrhosis (P = 0.001) and higher in fatty liver (P = 0.0002) than the control values, after adjusting for age, sex, and concentration of total cholesterol, triglyceride, and C-reactive protein. Significant positive correlations were observed between the concentration of C4bp in serum and total protein, albumin, cholinesterase level, and lecithin-cholesterol acyltransferase activity. Immunohistochemical analysis of human liver with specific antiserum to human C4bp demonstrated reaction endproducts in the hepatocytes around the central veins. These observations provide evidence that C4bp is synthesized by hepatocytes.
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PMID:Evidence that C4b-binding protein (proline-rich protein) is synthesized by hepatocytes. 204 87

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

Dietary cholesterol induces a hemolytic anemia in guinea pigs, accompanied by changes in the lipid composition of red cells and of plasma lipoproteins. This report presents a characterization of the lipoprotein species present in each main density class in both control and cholesterol-fed guinea pigs. Traces of a typical high density lipoprotein (HDL) were detected in control plasma. HDL from cholesterol-fed, anemic guinea pigs differed from control HDL in electron microscopic appearance and lipid and peptide composition. Long stacks of discs were observed in the electron microscope in addition to smaller, spherical particles characteristic of control HDL. Low density lipoproteins (LDL) from cholesterol-fed, anemic guinea pigs had two main populations, which were separated by gel chromatography. One population appeared in the electron microscope as large transparent discs and contained mainly unesterified cholesterol and phospholipids in a 2:1 molar ratio. The other population resembled control LDL in size and composition except for its high unesterified cholesterol content. Dietary cholesterol also altered the composition and decreased the electrophoretic mobility of very low density lipoproteins. Gel electrophoretic and immunochemical evidence indicates that a peptide (mol wt 35,000) appears in lipoproteins from cholesterol-fed, anemic guinea pigs that is undetectable in those of controls. Similarities between the cholesterol-induced lipoprotein abnormalities in guinea pigs and those reported in patients with obstructive jaundice, biliary cirrhosis, type III hyperlipoproteinemia, or familial lecithin:cholesterol acyltransferase deficiency are discussed.
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PMID:Characterization of guinea pig plasma lipoproteins: the appearance of new lipoproteins in response to dietary cholesterol. 434 26

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

Serum lipids and lipoproteins were analyzed after an overnight fast, and following a fatty meal in 10 patients with cirrhosis, 5 with fatty liver, and 5 normal subjects. Cirrhotic patients were divided into two groups of five on the basis of serum lecithin-cholesterol acyltransferase activity. Fasting triglyceride levels were similar in all four groups. In all but cirrhotic patients with low lecithin-cholesterol acyltransferase activity, most fasting triglyceride was found in very low density lipoproteins; in the latter group, most of it was found in low density lipoproteins. We confirmed that patients with fatty liver have a higher serum triglyceride response to fat feeding than normal subjects, but we did not find higher levels in cirrhotic patients. Cirrhotic patients with "normal" lecithin-cholesterol acyltransferase activity had a normal triglyceride response to dietary fat. In patients with cirrhosis and low lecithin-cholesterol acyltransferase activity, the increase in triglyceride was less than in normal subjects. In this group, most of the extra triglyceride was carried in low density lipoprotein, and not in chylomicrons and very low density lipoprotein, as in the other groups.
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PMID:Plasma lipid and lipoprotein response to fat feeding in alcoholic liver disease. 684 Jun 80

To examine bile acid synthesis in chronic liver diseases, serum total 7 alpha-hydroxycholesterol level was measured by gas-liquid chromatography-mass spectrometry in patients with cirrhosis (n = 23), patients with chronic hepatitis (n = 21), and control subjects (n = 18). The serum 7 alpha-hydroxycholesterol levels were significantly lower in patients with cirrhosis than the controls (78 +/- 59 pmol/mL vs. 237 +/- 97 pmol/mL; mean +/- SD). However, in patients with chronic hepatitis, the level was fully retained (262 +/- 102 pmol/mL). Serum 7 alpha-hydroxycholesterol levels of 17 patients with cirrhosis classified as Child B and C ranged from 33 to 69 pmol/mL, and all were less than the normal range (between 104 and 466 pmol/mL), however, those levels of some patients classified as Child A were within the normal range. Serum 7 alpha-hydroxycholesterol levels significantly correlated with serum albumin, cholinesterase, total bile acid, direct bilirubin, alkaline phosphatase, indocyanine green (ICG) retention rate, hepaplastin test, and lecithin-cholesterol acyltransferase activities. We conclude that bile acid synthesis is well preserved in patients with chronic hepatitis and that it is decreased in most patients with cirrhosis. Serum 7 alpha-hydroxycholesterol may be a new parameter of liver function testing to assess hepatic bile acid synthesis in patients with chronic liver diseases.
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PMID:Serum 7 alpha-hydroxycholesterol as a new parameter of liver function in patients with chronic liver diseases. 755 70

Lipid composition, fluidity, and Na+,K(+)-adenosine triphosphatase (ATPase), Mg(2+)-ATPase, and acetylcholinesterase (AChE) activities of erythrocyte membranes were examined in comparison to plasma lipid composition and lecithin:cholesterol acyltransferase (LCAT) activities in 39 patients with hepatic cirrhosis due to viral hepatitis (Child-Pugh class A, n = 12; class B, n = 13; and class C, n = 14). Plasma LCAT activities decreased and the plasma free-cholesterol to phospholipid molar ratio (C/PL) increased with progressive severity of hepatic cirrhosis. C/PL and fluorescence polarization (inverse of fluidity) of erythrocyte membranes also increased with disease progression (C/PL: Child-Pugh A, 0.911 +/- 0.010; B, 0.941 +/- 0.011; C, 0.979 +/- 0.028; and normal, 0.798 +/- 0.010; fluorescence polarization: Child-Pugh A, 0.348 +/- 0.002; B, 0.351 +/- 0.002; C, 0.355 +/- 0.002; and normal, 0.340 +/- 0.002). There was a correlation between C/PL and fluorescence polarization of erythrocyte membranes (r = .629, P < .001). Na+,K(+)-ATPase activity of erythrocyte membranes did not differ between cirrhotic patients and normal subjects. On the other hand, Mg(2+)-ATPase activity decreased in Child-Pugh C cirrhosis. AChE activity was decreased in Child-Pugh A cirrhosis, and decreased further in Child-Pugh B and C cirrhosis. AChE and Mg(2+)-ATPase activities correlated inversely with fluorescence polarization (r = -.652, P < .001 and r = -.381, P < .01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered lipid composition and differential changes in activities of membrane-bound enzymes of erythrocytes in hepatic cirrhosis. 761 39

The activities of lecithin-cholesterol acyltransferase (LCAT) and lipid transfer protein (LTP) were assayed using sensitive radioassay methods in controls (n = 113) and in patients with various liver diseases (n = 72). Plasma LCAT activity decreased with progression of hepatocellular damage. Plasma LTP activity in controls was 216 +/- 68 nmol/mL/h, and there were no significant differences between controls and patients with chronic hepatitis ([CH], 193 +/- 70), compensated liver cirrhosis (LC) with or without hepatocellular carcinoma ([HCC], 197 +/- 48 and 193 +/- 62, respectively), or decompensated liver cirrhosis ([dLC], 182 +/- 65). In acute viral hepatitis, LTP activity decreased significantly; however, the degree of reduction was not as dramatic as that for LCAT. There was no correlation between LCAT and LTP activity both in controls and patients with various liver diseases. LCAT activity was positively correlated with serum albumin (r = .52, P < 0.1) and cholinesterase (r = .37, P < .01) levels, and inversely correlated with serum bilirubin level (r = -.38, P < 0.1); there was no correlation between plasma LTP activity and these parameters of liver function. That plasma LTP activity did not change with hepatocellular damage may indicate that the liver in humans may not be the primary site of LTP production.
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PMID:Lecithin-cholesterol acyltransferase and lipid transfer protein activities in liver disease. 844 43


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