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)

A group of 18 chronic alcoholic patients who had sclerosing hyaline necrosis in noncirrhotic livers was compared with a group of 12 similar individuals with acute alcoholic hepatitis, but no centrilobular fibrosis. In cases with sclerosing hyaline necrosis, the most characteristic features were portal hypertension with very large, tender livers and unusually high glutamic-oxalacetic transaminase values; these were associated with centrilobular fibrosis and abundant alcoholic hyalin. Three of these patients died within two years and in two of these, early cirrhosis was found at necropsy. In the cases of acute alcoholic hepatitis, hepatomegaly was the most conspicuous finding, and only a single patient died; death here was unrelated to hepatic disease, the liver being unremarkable at necropsy. Patients who had sclerosing hyaline necrosis tended to remain ill for significantly longer periods. These observations, in conjunction with evidence gathered from the literature, seem to suggest that sclerosing hyaline necrosis is an obligatory step in the natural evolution of alcoholic hepatic disease, especially in cases that evolve into cirrhosis.
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PMID:Sclerosing hyaline necrosis in noncirrhotic chronic alcoholic hepatitis. 6 9

The determination of enzyme activity in serum for the diagnosis of chronic hepatitis has become increasingly popular. According to the author's experience serum aminotransferase is raised in about 100% of cases of chronic active hepatitis and also in active cirrhosis, but in only about 70--80% of persisting hepatitis or in moderately active chronic hepatitis. They are frequently normal in inactive cirrhosis. After aminotransferases the alkaline phosphatase is of great importance for the differential diagnosis of icterus. If aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase are determined at the same time, every cholestatic icterus can be diagnosed with certainty.
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PMID:[Clinical enzyme diagnosis in chronic hepatitis. Possibilities and limitations (author's transl)]. 10 40

The activities of glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT) and glutamate dehydrogenase (GLD) were determined in liver biopsy specimens and sera of patients with various liver diseases. Mitochondrial and cytosol isozymes of GOT were also separated for their assay. The activity ratio of GOT/GPT in serum was found to reflect the ratio in liver cytosol. The increased ratio in advanced or severe liver diseases, such as liver cirrhosis, was due to the greater decrease in liver cytosol GPT activity, this being pronounced in primary hepatoma. The activity of GLD decreased similarly but less markedly. The relatively greater decrease in GPT compared with GOT in advanced liver diseases was not mainly due to leakage of the enzyme from the liver, but to a specific mechanism associated with hepatic injury or its progression. Other pathological conditions of the liver such as those in obstructive jaundice and alcoholic liver injury also appeared to result in reduced liver GPT activity, which was reflected in the serum as an increased GOT/GPT ratio.
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PMID:The mechanism of release of hepatic enzymes in various liver diseases. II. Altered activity ratios of GOT to GPT in serum and liver of patients with liver diseases. 16 Jan 82

Serum mitochondrial glutamic-oxaloacetic transaminase activity was determined in 83 patients with various liver diseases and 10 healthy adults. 1) The average of mitochondrial glutamic-oxaloacetic transaminase value was 1.2 mU in healthy adults, 8.3 mU in patients with acute hepatitis, 13.7 mU in patients with post-transfusion hepatitis, 5.0 mU in patients with persistent hepatitis, 4.5 mU in patients with chronic inactive hepatitis, 9.6 mU in patients with chronic active hepatitis, 5.6 mU in liver cirrhosis, and 295 mU in a patient with fulminant hepatitis. 2) While one patient with acute hepatitis showed the highest value in the group of 29 mU, one patient with fulminant hepatitis showed an extremely high value of 295 mU, revealing an obvious difference between them. 3) One patient with fresh myocardial infarction also showed an extremely high value of 110 mU.
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PMID:Clinical significance of mitochondrial glutamic-oxaloacetic transaminase in serum of patients with liver disease. 21 85

Thirty patients with cirrhosis were evaluated with the 2-hr [14C]aminopyrine breath test (score) and with conventional liver tests. Of the 30 patients, 24 also had current liver biopsies. There was a good correlation between necroinflammatory activity in the 24 cirrhotic liver biopsies and the 2-hr aminopyrine scores. All five patients who had at least grade 2 necroinflammatory activity on their biopsy had an abnormal prothrombin time (greater than 3.5 sec above control) and their aminopyrine score was less than 2%. The correlation was good between the 2-hr aminopyrine score and the prothrombin time (seconds over control). No correlation was found between the 2-hr aminopyrine score and either the serum aspartate aminotransferase (SGOT) or any other liver test except for the prothrombin time. It seems that the 2-hr aminopyrine score and prothrombin time are more likely to give a quantitative estimate of total functioning parenchymal mass which is left unaffected by hepatocellular disease in cirrhosis, than the other commonly used liver tests.
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PMID:The relationship between conventional liver tests, quantitative function tests, and histopathology in cirrhosis. 37 24

Insulin degradation was measured by the C-peptide/insulin ratio in 19 patients with portal vein block with extensive spontaneous portal-systemic shunting but minimal liver cell damage: 13 patients with biopsy-proved cirrhosis and 12 controls. Blood obtained fasting and for 3 hr after oral glucose was assayed for glucose, insulin, and C-peptide. Fasting C-peptide and insulin levels in patients with portal vein block and those in controls did not differ. Eight of 13 cirrhotic patients had fasting hyperinsulinemia with a significantly reduced C-peptide/insulin ratio. After glucose administration, the C-peptide/insulin ratio in portal vein block patients with normal aspartate transaminase levels did not differ from control values. In portal vein block patients with elevated asparatate transaminase levels, the C-peptide/insulin ratio was significantly reduced only from 60 min onwards. All the cirrhotic patients showed a significantly reduced C-peptide/insulin ratio after glucose administration. It is suggested that portal-systemic shunting of blood in the presence of a normal liver does not influence hepatic insulin metabolism and that the hyperinsulinemia of cirrhosis is a feature of parenchymal liver damage. In addition, insulin degradation was abnormal in all cirrhotic patients at high insulin secretion rates, even when fasting insulin levels were normal.
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PMID:Effects of spontaneous portal-systemic shunting on insulin metabolism. 42 95

The present study reported a group of 168 chronically alcoholic patients with a daily ingestion superior to 80 grams. Twenty of these patients (10 percent) did not have liver disease, and 148 (68.5 percent) had different forms of liver disease classified by histopathologic examination. Considering a 97 fi MCV as macrocytosis, we have found in the group of alcoholics without hepatopathy a 50 percent rate of macrocythemia with a mean value of 97.9 fl. In the group of chronic alcoholics with liver disease there was a 64.2 percent macrocytosis with a mean value of 100 fl. We have also studied 43 (21.5 percent) patients with cryptogenetic cirrhosis with a 32.6 percent macrocytosis and a mean value of 93.9 fl. With respect to the alcoholic hepatopathy subgroups, macrocytosis is more frequent in portal fibrosis and acute alcoholic hepatitis, the mean value being higher in the latter. We consider macrocytosis to be frequent among alcoholics, and a good persistence indicator of alcoholic ingestion, pathogenically linked to the now proven dyserythropoietic factor of the alcohol upon the bone marrow. There is no statistically significant correlation between anemia and reticulocytes. We consider macrocytosis to be a more precocious data, and believe that the positive correlation with certain intraerythrocitary enzymes in the juvenile population of red cells corroborates this fact. With respect to the rest of parameters studied there was a correlation with gammaglutamiltranspeptidase, glutamic-oxalacetic transaminase, and the value of prothrombin. The values of mean macrocytosis and elevations of gammaglutamiltranspeptidase and glutamic-oxalacetic transaminase are good persistence indicators of alcoholic ingestion.
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PMID:[Macrocytosis in chronic alcoholism (author's transl)]. 52 26

The effect of alcoholic patient sera on in vitro lymphocyte transformation was studied using mitogen-induced uptake of (3)H-thymidine to measure blastogenesis. With pokeweed mitogen as the stimulus, transformation of normal lymphocytes in sera of alcoholics with either normal or fatty livers was not significantly different from that obtained in pooled human serum (PHS). However, in sera of patients with either alcoholic hepatitis or inactive cirrhosis mean transformation was significantly reduced (P <0.001, <0.02 respectively). With phytohaemagglutinin-P or concanavalin A as mitogens, suppression of transformation was not as marked but followed the same pattern. A significant negative correlation was observed between the magnitude of transformation and serum bilirubin and aspartate aminotransferase levels. An intra-patient comparison of the effects on transformation of normal lymphocytes by simultaneously collected peripheral and portal venous sera, and of peripheral sera obtained before and after portasystemic shunt surgery, indicated that the factor(s) responsible did not originate in the splanchnic circulation nor did it accumulate in the serum because of failed hepatic clearance. By performing transformation experiments in the presence of inhibitory patient sera diluted with PHS it was possible to show that these sera caused true inhibition of transformation rather than suppression due to failure to sustain cell culture because of nutritional deficiencies. Inhibitory sera did not contain high levels of the enzyme thymidine phosphorylase and did not significantly inhibit binding of (125)I-labelled mitogens to the lymphocyte surface. These findings indicate that the inhibitory effect of sera from alcoholics is of potential in vivo importance, that the effect increases with the degree of heptocyte damage, and that it is unrelated to the nonhepatic metabolic affects of chronic alcoholism.
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PMID:Suppressive effect of alcoholic liver disease sera on lymphocyte transformation. 53 94

The value of serum bile acids (SBA) in the diagnosis of hepatobiliary disease has been investigated. A modified GLC method was used, with an overall coefficient of variation of +/- 11% in the control range. Serum was obtained after a 12 hour fast, and two hours after a fatty meal from 73 patients and 14 control subjects. In controls the total fasting SBA of 2.17 +/- 0.86 mumol/l increased significantly (p less than 0.001) to 3.81 +/- 1.14 mumol/l after a meal. All icteric patients had raised SBA, but in 23 anicteric patients there was no significant difference in the detection of chronic liver disease by fasting SBA, postprandial SBA, AST, or gamma GTP. Compared with controls, serum in patients contained proportionately less deoxycholic acid (p less than 0.001), there was proportionately more cholic acid in extrahepatic obstruction (p less than 0.001), and proportionately more chenodeoxycholic acid in patients with cirrhosis, viral hepatitis, and neoplasia (p less than 0.001). In control subjects, the fasting cholic:chenodeoxycholic acid ratio ranged from 0.5-1.0, and differed significantly (p less than 0.001) from patients with extrahepatic obstruction 0.96-3.6, and cirrhosis 0.1-0.5. It is concluded that serum bile acids measured by sensitive methods can provide useful diagnostic information.
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PMID:Serum bile acids in the diagnosis of hepatobiliary disease. 59 Aug 51

The frequent occurrence of abnormal fibrin polymerisation in patients with liver disease has recently been reported. To investigate this further, fibrin polymerisation was studied in 68 patients with cirrhosis or chronic active liver disease. Thirty-three of these patients demonstrated impairment of this phase of blood coagulation. When other tests of liver function were compared in patients demonstrating this abnormality and those in whom fibrin polymerisation was normal, it was found that the former group demonstrated significantly reduced albumin concentrations (p less than 0.0002), raised bilirubin and aspartate aminotransferase levels (p less than 0.0006 and less than 0.003 respectively), and greater prolongation of the one-stage prothrombin time (p less than 0.001) with more marked reduction in factor VII levels (p less than 0.002) compared with the latter patients. It is concluded that defective fibrin polymerisation occurring in patients with liver disease indicates the presence of severely impaired hepatocellular function. This might account for the grave prognosis reported in cirrhotic patients with abnormal fibrin polymerisation who also suffer bleeding from gastro-oesophageal varices.
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PMID:Association of abnormal fibrin polymerisation with severe liver disease. 59 Aug 52


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