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)

Insulin-like growth factor II is secreted primarily by the liver and is reported to be transcribed in many primary hepatocellular carcinoma (PHC) cell lines. We have studied diagnostic significance of serum IGF-II in chronic liver diseases using specific enzyme immunoassay. Serum IGF-II levels (mean +/- SE) were decreased in chronic hepatitis (538 +/- 51 ng/ml; N = 29), liver cirrhosis (427 +/- 45; 50) and PHC (260 +/- 41; 17) compared to controls (830 +/- 49; 57). Serum IGF-II was not different from controls in any of nonhepatic diseases such as diabetes (1032 +/- 97; 19) pancreatic cancer (1413 +/- 282; 8), chronic pancreatitis (999 +/- 126; 17), peptic ulcer (1186 +/- 43; 11), irritable bowel syndrome (1002 +/- 109; 12), gastrointestinal tract cancer (1250 +/- 216; 21) and chronic renal failure (733 +/- 135; 14). In liver diseases serum IGF-II showed a significant correlation with liver function test (negative with retention of indocyanine green and total bile acids; positive with albumin, thrombo-test, and cholinesterase). These results suggest that serum IGF-II reflects a reduced production of IGF-II in the liver and that it can be an index for the residual capacity of liver function.
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PMID:Serum insulin-like growth factor II in chronic liver disease. 253 15

The high angiotensin-converting activity, in 13 of the 17 patients afflicted with hepatic cirrhosis, has been put in relation to the hypoxia influence. The insufficient cession of O2 seems to stimulate the enzyme activity, especially for the patients who simultaneously present low values of blood pseudo-cholinesterase. The AA think that this behaviour is to be ascribed to a deficiency of the hepatic proteic synthesis of vasoactive substances, such as the angiotensins.
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PMID:[Effects of hypoxia on the production of angiotensin converting enzyme in decompensated liver cirrhosis]. 255 20

Hepatic cirrhosis was induced in guinea pigs by ligation of the common bile duct and innervation of the liver was studied by fluorescence histochemistry (glyoxylic acid method), acetylcholinesterase (AChE) neurohistochemistry (modified Karnovsky and Roots method), and transmission electron microscopy. In control animals the adrenergic terminals showed connections with endothelial cells, hepatocytes and fat-storing cells, but no cholinergic terminals were evident. Cirrhosis was present 6 weeks after the bile duct ligation and marked fibrosis, accompanied by bile duct proliferation, was evident in the portal areas. Numerous AChE-positive nerve fibers traversed the collagenous bundles in the fibrotic areas, and cholinergic terminals formed close contacts with fibroblasts. Each axon terminal was found to contain numerous small coreless vesicles and AChE-reaction products were confirmed in the space between a nerve terminal and a fibroblast. In contrast, fluorescence adrenergic nerve fibers and their terminals remained unchanged. This study demonstrates that parasympathetic cholinergic innervation participates in some stages in the development of hepatic cirrhosis.
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PMID:Ultrastructure of cholinergic innervation in the cirrhotic liver in guinea pigs. Neurohistochemical and ultrastructural study. 256 52

To examine the pathogenesis of thrombocytopenia associated with liver cirrhosis, the platelet count, spleen size and serum cholinesterase levels were measured together with plasma concentration of beta-thromboglobulin, fibrinopeptide A and serum albumin in 38 patients with histologically proven, severe but stable liver cirrhosis. The spleen size contributed most significantly to thrombocytopenia in this disorder and the serum cholinesterase level also correlated with the platelet count, both in decompensated and compensated liver cirrhosis. Plasma beta-thromboglobulin, serum fibrinopeptide A levels and serum albumin did not correlate with the platelet count. These findings indicate that disseminated intravascular coagulation is not likely to be the cause of thrombocytopenia in liver cirrhosis. Splenomegaly as well as the diminished protein synthetic activity of the liver participates in the pathogenesis of the thrombocytopenia in this disease.
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PMID:Thrombocytopenia in liver cirrhosis. 261 53

The plasma fatty acid composition of cirrhotic patients and their dietary intake of fatty acids were determined. Significantly lower plasma arachidonic, docosahexaenoic, dihomo-gamma-linolenic and eicosapentaenoic acid levels were observed in cirrhotic patients than in healthy controls. A remarkably low dietary intake of polyunsaturated fatty acids supplied from fish, vegetable oil and pulses was shown in cirrhotic patients. Positive correlations were observed between plasma arachidonic acid concentrations and clearance rate of indocyanine green (KICG) (r = 0.826, p less than 0.05) and between dihomo-gamma-linolenic acid levels and cholinesterase activities (r = 0.841, p less than 0.05). From these results, we conclude that a supply of polyunsaturated fatty acids is necessary for the nutritional treatment of patients with liver cirrhosis.
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PMID:Lipid malnutrition of patients with liver cirrhosis: effect of low intake of dietary lipid on plasma fatty acid composition. 271 70

Serum dimethadione (DMO)/trimethadione (TMO) ratios after oral administration of TMO have been investigated in 10 patients with normal livers, 8 patients with hepatoma and 8 patients with hepatoma and cirrhosis. Serum concentration ratios of DMO to TMO at 4 h after oral administration of TMO in patients with chronic liver disease were significantly decreased by 27% for those with hepatoma and 52% for those with hepatoma and cirrhosis. Serum DMO/TMO ratios at 4 h correlated well with liver function characteristics (total protein r = 0.741, plasma albumin r = 0.826, total bilirubin r = -0.725, cholinesterase r = 0.853) as well as with pharmacokinetic parameters (total body clearance r = 0.852, half-life r = -0.636) in both patients with normal livers and patients with chronic liver disease. This study suggests that serum DMO/TMO ratios in a blood sample obtained by a single collection after an oral administration of TMO might provide a clinically useful index of the hepatic drug-oxidizing capacity in an individual patient with chronic liver disease without determining the liver function characteristics or the pharmacokinetic parameters.
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PMID:Trimethadione metabolism in patients with normal liver and in patients with chronic liver disease. 283 Mar 97

Using a monoclonal antibody to bromodeoxyuridine, we studied the cell kinetics of human hepatocellular carcinoma, liver cirrhosis, chronic active hepatitis and alcoholic liver fibrosis. Specimens were taken either by biopsy or surgery and immediately incubated with 0.1% bromodeoxyuridine solution at 37 degrees C for 45 min. After in vitro labeling, the bromodeoxyuridine taken up by the nuclei of S-phase cells was determined by the avidin-biotin-peroxidase complex method, using an anti-bromodeoxyuridine monoclonal antibody as the first antibody. The number of positive nuclei in 1,000 hepatic cells was counted, and the bromodeoxyuridine labeling index was expressed per thousand. The mean bromodeoxyuridine labeling index +/- S.D. of the cancerous portion of hepatocellular carcinoma, the noncancerous portion of hepatocellular carcinoma, liver cirrhosis, chronic active hepatitis and alcoholic liver fibrosis were 64.1 +/- 31.3, 33.6 +/- 14.4, 23.2 +/- 20.8, 9.1 +/- 6.1 and 21.6 +/- 13.0, respectively. The mean bromodeoxyuridine labeling index of the hepatocellular carcinoma cancerous portion was statistically higher than that of any other group. There was no statistical difference by the t test or the Wilcoxon test between the noncancerous portion of hepatocellular carcinoma and liver cirrhosis, and these two groups were proved interdependent by chi 2 test (Fisher's exact test), whether they were subdivided by bromodeoxyuridine labeling index greater than or equal to 10 or not. Bromodeoxyuridine labeling index was not significantly correlated with the usual biochemical parameters such as serum AST, ALT, gamma-GTP, alkaline phosphatase, lactate dehydrogenase, cholinesterase, albumin, and alpha-fetoprotein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:S-phase cells in diseased human liver determined by an in vitro BrdU-anti-BrdU method. 284 68

The correlation between the amount of asialoglycoproteins and results of conventional liver function tests was studied in patients with chronic liver diseases, with or without hepatocellular carcinoma. The objective was to determine the clinical significance of the measurement of levels of serum asialoglycoproteins. The levels were elevated in accordance with the progress of liver diseases, and correlated with the decrease in albumin content, cholinesterase activity, the ratio of esterified cholesterol to total cholesterol and to the increase of indocyanine green retention at 15 min (p less than 0.001). There was no correlation with values of glutamic oxaloacetic and pyruvic transaminases. The amount of serum asialoglycoproteins also correlated with survival time in fatal cases of cirrhosis and/or hepatocellular carcinoma. Bilirubin and bile acids did not interfere with the measurement of serum asialoglycoproteins in cases of hyperbilirubinemia. Serum asialoglycoprotein levels are a good indicator of hepatic functional reserve in patients with chronic liver diseases, with or without hepatocellular carcinoma.
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PMID:Clinical application of the measurement of serum asialoglycoproteins to estimate residual liver function in patients with chronic liver diseases with or without hepatocellular carcinoma. 299 87

In a prospective study involving 25 consecutive adult orthotopic liver transplantation (OLT) patients, of whom 23 had cirrhosis, we have related pretransplantation recipient parameters to blood loss during transplantation. In phase 1 (explantation of diseased liver) blood loss was 0.1-7.2 1, in phase 3 (following restoration of the portal blood flow after implantation) 0.1-39.7 1, and total blood loss was 1.6-47.2, median 9.2 1. Five patients (20%) died from causes directly related to defective haemostasis during the operation. Pretransplantation cholinesterase, antithrombin III and albumin correlated most strongly with blood loss in phase 1; a history of ascites, antithrombin III and cholinesterase levels correlated with blood loss in phase 3, and a history of ascites, urinary sodium and antithrombin III with total blood loss. Cholestasis did not influence blood loss. Portal hypertension per se presumably played only a restricted role. A pretransplant 24-h urinary sodium excretion of 10 mmol or less and a serum sodium of 132 mmol/l or less were highly predictive of blood loss exceeding 10 1 during OLT. Urinary sodium determination under test conditions and serum sodium measurement should already be part of the assessment of potential OLT candidates by the referring hospital.
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PMID:Liver disease and its effect on haemostasis during liver transplantation. 299 51

Six-year survival of cirrhosis was assessed in a series of 1155 consecutive patients (751 men, 404 women). Among the men, 33% were alcoholics and 18% were HBsAg positive; corresponding figures for the women were 15% and 6% respectively. Features of decompensation at first presentation were observed in 63% of the patients. Six-year survival was 54% in compensated and 21% in decompensated patients. No significant differences in survival were found between alcoholics and nonalcoholics. Leading causes of death were liver failure (49%), hepatocellular carcinoma (22%), and bleeding (13%). The prognostic role of 21 variables was evaluated separately in compensated and decompensated patients by the Cox's regression model. The following variables were found to be significant predictors of death risk in compensated patients: male sex, HBsAg positivity, age, prothrombin time prolongation, and esophageal varices. In decompensated disease the significant indicators of death risk were: hepatocellular carcinoma, encephalopathy, hemorrhage, SGOT, esophageal varices, gamma globulins, prothrombin time prolongation, continued abuse of alcohol, HBsAg positivity, gamma glutamyl transpeptidase, and cholinesterase. A simple prognostic index based upon the relative risk coefficient of the significant variables is suggested.
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PMID:Survival and prognostic indicators in compensated and decompensated cirrhosis. 300 9


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