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)

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

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 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 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

Different methods of performing the (14C) aminopyrine breath test have been assessed. A tracer dose of 2 muCi without a loading dose and with a single breath collection at two hours was the method selected, since it gave the best discrimination between patients with hepatocellular diseases and normal subjects (5.2 +/- 0.2%, mean +/- SEM). Reduced values occurred in patients with chronic active hepatitis (with and without cirrhosis) (1.5 +/- 0.2%), alcoholic cirrhosis (1.7 +/- 0.4%) and hepatitis (2.5 +/- 0.3%), and late primary biliary cirrhosis suggesting defective microsomal function with respect to demethylation. Normal results were common in early primary biliary cirrhosis. Two weeks of prednisolone therapy caused some improvement in the breath test in nine of 10 patients with chronic active hepatitis. It is concluded that the (14C) aminopyrine breath test is a simple test for detecting hepatocellular dysfunction, but has no obvious diagnostic advantage over the determination of serum aspartate transaminase and two hour post-prandial bile-acids.
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PMID:Assessment of the (14C) aminopyrine breath test in liver disease. 62 4

The total activity and activity of the cytoplasmic and mitochondrial isoenzyme of aspartate aminotransferase was examined in blood plasma of 56 patients with chronic liver diseases (chronic hepatitis in 27, liver cirrhosis in 23, secondary neoplastic effection of the liver in 6). All the patients with biochemically active forms of liver disease manifested increased the total as well as cytoplasmic enzyme activity, as compared with control group, 57% of the patients manifested simultaneously also increased activity of the mitochondrial isoenzyme. In 13% of the patients with stabilised forms of liver diseases manifested isolated increase of the mitochondrial isoenzyme activity. This might be of importance for the evaluation of the course of the disease. In patients with tumorous metastases in the liver a strikingly high share and activity of mitochondrial isoenzyme was shown.
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PMID:Isoenzymes of aspartate aminotransferase in chronic liver diseases. 65 44

Serum aspartate aminotransferase (AST) concentrations are commonly determined to detect hepatocellular damage. However, discrepancies between serum AST values and histological signs of active liver damage sometimes occur in patients with cirrhosis. The enzyme AST requires pyridoxal-5-phosphate (PLP) (active vitamin B6) as a co-enzyme to express its activity. Since approximately 90% of patients with severe cirrhosis are vitamin B6-deficient, it has been suggested that vitamin B6 supplements given to these patients might cause an elevation of falsely low serum AST concentrations. Treatment of 8 vitamin B6-deficient cirrhotic patients with pyridoxine hydrochloride (50 mg intravenously twice daily for 1 week) increased their serum AST concentrations from 121 +/- 18 (mean +/- SEM) to 136 +/- 26 lU/l, while treatment of a second group of 9 patients with the active co-enzyme PLP increased AST concentrations from 118 +/- 17 to 146 +/- 20 lU/l. Neither of these increases was statistically significant. Plasma PLP increased from 2,4 +/- 0,7 to 18,5 +/- 7,6 ng/ml after pyridoxine, and from 3,3 +/- 0,7 to 27,0 +/- 6,2 ng/ml after PLP supplementation. It is concluded that B6 deficiency is unlikely to be an important determinant of serum AST concentrations in patients with chronic liver disease.
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PMID:Vitamin B6 and aspartate aminotransferase activity in chronic liver disease. 67 85

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

The urinary excretion of D-glucaric acid, a catabolite of glucuronic acid, is considered to be a reliable index of the state of hepatic microsomal enzyme activity. Because enzyme activity may be altered in liver disease, we examined the effect of liver disease on the excretion of this metabolite and its correlation with liver function tests. We studied 89 patients with nonhemolytic jaundice, 39 with viral hepatitis, 33 with obstructive jaundice, six with cirrhosis, and 11 patients with jaundice of mixed etiology. Glucaric acid excretion was significantly increased in all these patients as compared to controls, most pronounced in the obstructive jaundice group. No correlation was found between glucaric acid excretion and concentrations of bilirubin, albumin, globulin, aspartate aminotransferase, alkaline phosphatase, cholesterol, or gamma-glutamyltransferase in serum, even though the concentrations of these analytes did vary with the type of liver disease. We suggest that this increase in glucaric acid excretion is an indication of normal or even increased glucuronidation (UDP-glucuronosyltransferase activity), which occurs in liver disease.
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PMID:Increased D-glucaric acid excretion by jaundiced patients. 69 85


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