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)

Dimethadione (DMO)/trimethadione (TMO) ratios in serum after oral administration of TMO were investigated in 15 normal subjects and in 20 patients with cirrhosis and esophageal varices. Severe impairment of liver function was associated with a decrease in total cholesterol, total protein and plasma albumin, or an increase in total bilirubin, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, serum gamma-glutamyl transpeptidase and indocyanine green retention rate (ICG R15). Serum concentration ratios of DMO to TMO at 2 or 4 h after oral administration of TMO in patients were significantly decreased by 67 or 66%, respectively, compared to normal subjects. DMO/TMO ratios at 2 or 4 h following oral administration of TMO were well correlated with the liver function parameters (plasma albumin r = 0.758 at 2 h, r = 0.776 at 4 h; total protein r = 0.613 at 2 h, r = 0.619 at 4 h; ICG R15 r = -0.683 at 2 h, r = -0.746 at 4 h, in patients only; cholinesterase r = 0.873 at 2 h, r = 0.908 at 4 h) as well as with pharmacokinetic parameters (total body clearance r = 0.794 at 2 h, r = 0.786 at 4 h) in both the normal subjects and the patients. It suggests that the DMO/TMO ratio obtained in a single blood sample collected after oral administration of TMO might provide a useful measure for function hepatic reserve.
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PMID:Trimethadione tolerance test for evaluation of functional reserve of the liver in patients with liver cirrhosis and esophageal varices. 372 21

Changes in the amount of hippurate synthesized and excreted in the urine after 1.5 gm benzoate loading (intravenous hippuric acid test [HAT]) in patients with liver disease before surgery were studied in relation to arterial blood ketone body ratio (acetoacetate/beta-hydroxybutyrate) (BKBR), reflecting energy status of the liver. In these patients, the HAT values for 120 minutes were decreased significantly (1.088 +/- 0.129 gm, n = 9; 1.071 +/- 0.258 gm, n = 7; 1.258 +/- 0.126 gm, n = 10; in cirrhosis with liver tumor, cirrhosis with esophageal varix, and obstructive jaundice, respectively) as compared with the value in patients without liver disease (1.829 +/- 0.093 gm, n = 16, P less than 0.01). The correlation coefficient of the BKBR and the HAT value was 0.766, which was higher than that of the BKBR and albumin or the BKBR and choline esterase (r = 0.532 and r = 0.646, respectively). Serum levels of glutamic-oxaloacetic transaminase, glutamic pyruvic transaminase, alkaline phosphatase, gamma-glutamyl transpeptidase, leucine aminopeptidase, total and direct bilirubin, creatinine, and blood urea nitrogen were not correlated with the HAT values. Because hippurate is synthesized in liver mitochondria by the continuous supply of adenosine triphosphate through mitochondrial oxidative phosphorylation, HAT is considered to be a test that evaluates the energetic capacity of the liver to manage a metabolic load imposed on it.
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PMID:Clinical significance of hippurate-synthesizing capacity in surgical patients with liver disease: a metabolic tolerance test. 377 26

gamma-Glutamyl transpeptidase activity was measured in liver and serum from 110 patients undergoing diagnostic liver biopsy, including patients with alcoholic liver disease, fatty liver not due to alcohol, primary biliary cirrhosis, persistent hepatic disease, chronic active hepatitis and normal livers. Serum gamma-glutamyl transpeptidase was markedly elevated in patients with alcoholic liver disease and primary biliary cirrhosis while mean hepatic gamma-glutamyl transpeptidase activity was significantly increased only in the alcoholic liver disease group. There was considerable overlap of individual enzyme values among the different disease groups. There was no inhibitors or activators of liver gamma-glutamyl transpeptidase in any of these disorders. The increased liver activity was not related to the degree of hepatic fibrosis or cirrhosis. There was no correlation between hepatic and serum gamma-glutamyl transpeptidase activity. Hepatic and serum gamma activities were equally increased in individuals with alcoholic liver disease whether or not they were drinking at the time of the study. The data suggest that increased hepatic gamma-glutamyl transpeptidase activity is neither specific for alcoholic liver disease nor essential for serum GGTP to be elevated.
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PMID:gamma-Glutamyl transpeptidase activity in liver disease: serum elevation is independent of hepatic GGTP activity. 612 80

Out of 126 alcoholic patients treated in a hepatogastroenrology unit, 55 were lost sight of after discharge, mainly because they lived far from the hospital, and 71 (56.3%) were followed up for a mean period of 10 months. Among the patients followed up, 11% showed clinical evidence, and 43.5% clinical and biochemical evidence (return to normal of mean corpuscular volume and gamma-glutamyl transpeptidase levels) of having stopped taking alcohol. Forty-five p. cent resumed drinking habits. Is was found that those patients who were married, had a professional activity, social contacts and no serious mental disorders were more likely to be weaned. There were more patients with cirrhosis of the liver among those who discontinued alcohol than among those who kept drinking. The authors underline that these subjects are best treated by a team comprising clinicians, psychiatrists, psychologists, social workers and members of associations of former alcoholics.
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PMID:[Follow-up of alcoholic patients in a hepatogastroenterology unit. Preliminary results (author's transl)]. 722 Mar 3

Reference intervals for prothrombin time (PT) and activated partial thromboplastin time (APPT) of undiluted and serial dilutions of citrated platelet-poor plasma were determined for 30 healthy dogs. The PT and APTT were similarly determined for 32 dogs with naturally occurring hepatic disease. Hepatic disease was confirmed by histopathologic examination of hepatic biopsy materials and comprised degeneration (13 dogs), inflammation (11 dogs), cirrhosis (4 dogs), and neoplasia (4 dogs). Coagulation test values were compared with serum alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transpeptidase activities and Bromsulphalein retention for sensitivity in detecting hepatic disease in the dog. Coagulation test results were at variance with reference values in 66% of the 32 dogs with hepatic disease; serum alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transpeptidase were increased in 59%, 72%, and 75%, respectively and Bromsulphalein retention was increased in 22% of the 32 dogs. Thus, the PT and APTT were sensitive indicators of hepatic disease. However, the PT and APTT lacked specificity for any given hepatic disease. The sensitivity of the coagulation tests for detecting hepatic disease was enhanced by using dilutions of citrated platelet-poor plasma. Only 15% of dogs with hepatic disease showed variances from reference values in the coagulation tests done with undiluted plasma, but 66% showed variances in the tests with dilutions of plasma. Coagulation tests were also done in 13 dogs with normal hepatic function amd morphology, but with various extrahepatic diseases: chronic renal disease (5 dogs), dirofilariasis (4 dogs), encephalitis (1 dog), cutaneous disease (2 dogs), and femoral fracture (1 dog). Twelve of the 13 dogs had coagulation test values within the reference intervals.
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PMID:Alterations of prothrombin time and activated partial thromboplastin time in dogs with hepatic disease. 734 May 74

Elevated levels of secretory IgA in serum have been demonstrated in several liver dysfunctions such as hepatic cytolysis and cholestasis. However, these possible alterations at an early stage of liver diseases have not yet been investigated. We studied a cohort of chronic alcoholic patients without cirrhosis in order to assess the changes in serum secretory IgA and other forms of secretory component, the split product of the polymeric Ig-receptor of epithelial cells. The possible diagnostic value of these measurements in the assessment of alcoholic disease was compared to that of serum gamma-glutamyl transpeptidase activity. Serum levels of secretory IgA and IgM and free secretory component, were quantified by an enzyme-linked immunosorbent assay in 71 patients with chronic alcoholic liver disease without cirrhosis and in 45 healthy controls. Patients were divided into two groups according to the severity of the liver abnormalities. In addition, the reversibility of serum secretory IgA, IgM and free secretory component abnormalities after alcohol withdrawal was evaluated in 15 patients. Serum levels of the three molecular forms of secretory component were significantly higher than those measured in control subjects, both in the whole population of patients and in the two groups of alcoholic patients without cirrhosis. In all groups, serum secretory IgA levels were correlated to free secretory component but not to total IgA levels. Serum secretory IgA levels were as discriminative as gammaglutamyl transferase activity in distinguishing between chronic alcoholic patients without cirrhosis and non-alcoholic subjects. The abnormalities of serum secretory IgA concentrations were reversible after alcohol withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum secretory IgA and secretory component in patients with non-cirrhotic alcoholic liver diseases. 760 78

Alcoholic and, to a lesser extent, nonalcoholic patients with liver disease have serum antibodies to acetaldehyde-protein adducts produced in vitro. These antibodies presumably reflect the presence of adducts in the liver, but the protein that triggers this immune response has not been identified. To study this, we measured the reactivity of cytosolic proteins to rabbit IgG developed against a P-450 2E1-acetaldehyde adduct, isolated from alcohol-fed rats, that recognizes acetaldehyde-modified epitopes in proteins. Adducts were determined on Western blots by scanning densitometry of antibody-linked alkaline phosphatase activity in 4 normal livers and in needle biopsy specimens from subjects with liver disease, 17 alcoholic and 14 nonalcoholic. In all livers, except for a normal one, we found a reactive protein of at least 200 kD, similar to the collagen-acetaldehyde adduct we reported to be markedly increased in rats with experimentally induced cirrhosis. The immunostaining intensity in the alcoholic patients with liver disease was eightfold (p < 0.01) and that in nonalcoholic patients with liver disease was fourfold, greater (p < 0.02) than the weak staining in normal livers; it correlated with the degree of inflammation and serum AST or gamma-glutamyl transpeptidase activities. The adduct was reproduced on incubation of normal cytosolic proteins with 2.5 mmol/L acetaldehyde, whereas higher concentrations yielded many additional adducts; the adduct also reacted with IgG antibody to rat collagen type I and disappeared after digestion with collagenase, suggesting that the target protein is a form of collagen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Collagen-acetaldehyde adducts in alcoholic and nonalcoholic liver diseases. 791 86

Liver injury produced by CCl4 depends on its metabolism by the liver cytochrome P450 enzyme system to a highly reactive intermediate (CCl3.). Cimetidine impairs cytochrome P450 and stimulates regenerative processes acting on DNA synthesis. This work was performed to investigate whether cimetidine may prevent CCl4-induced liver cirrhosis. Male Wistar rats were used: animals in group 1 received CCl4 (0.04 g per 100 g, i.p.) three times a week for 8 weeks; group 2 was treated with CCl4 plus cimetidine (120 mg kg-1, p.o.) three times a week for 8 weeks; group 3 received CCl4 for 8 weeks and then cimetidine for 4 weeks. Alkaline phosphatase, gamma-glutamyl transpeptidase (gamma-GTP) and alanine aminotransferase (ALT) activities, as well as protein and bilirubin, were measured in serum; collagen and lipoperoxidation were quantified in liver. Intoxication with CCl4 increased (P < 0.05) serum activities of alkaline phosphatase, gamma-GTP and ALT, and bilirubin concentration; liver collagen and lipoperoxidation were also increased. Cimetidine treatment prevented or reverted the increases in the three enzyme activities and in bilirubin content and the fall in proteins. It is worth noting that cimetidine co-treatment completely prevented both the increase in collagen content and the lipid peroxidation. The protective effect of cimetidine can be attributed to a reduction in cytochrome P450. However, it could also stimulate regenerative processes.
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PMID:Cimetidine prevents and partially reverses CCl4-induced liver cirrhosis. 791 3

In human and experimental CCl4-liver damage, S-adenosyl-l-methionine-synthetase and/or the intrahepatic content of S-adenosyl-l-methionine, are diminished and in human cirrhosis phospholipid methyltransferase is markedly reduced. Therefore the aim of this study was to investigate the effect of S-adenosyl-l-methionine administration on liver damage induced by 15-day bile duct ligation. Liver damage was analyzed by histological, ultrastructural and biochemical techniques. Biliary obstruction produced an increase in collagen content, dilation of the bile canaliculi and disorganization of mitochondria. These effects were not observed in the bile-duct-ligated group receiving S-adenosyl-l-methionine. Biochemical results showed that bile duct ligation increased serum bilirubins, and alkaline phosphatase and gamma-glutamyl transpeptidase activities. These effects were prevented significantly by S-adenosyl-l-methionine. On the other hand, glycogen content in the liver was depleted while lipid peroxidation was increased by biliary obstruction, S-adenosyl-l-methionine administration prevented these effects. In the bile-duct-ligated group, hepatocyte and erythrocyte plasma membrane Na+/K+ and Ca(2+)-ATPase were lower than in the control group (p < 0.05). Administration of S-adenosyl-l-methionine preserved ATPase activities. The exogenous S-adenosyl-l-methionine supply is probably responsible for restoring transmethylation lost in liver diseases.
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PMID:Protective effect of S-adenosyl-l-methionine on liver damage induced by biliary obstruction in rats: a histological, ultrastructural and biochemical approach. 796 28

This work details the histologic findings in 84 liver biopsy specimens from 28 patients with progressive familial intrahepatic cholestasis (PFIC), who met the clinical criteria of early onset of chronic unremitting cholestasis, exclusion of any known metabolic or anatomic etiology, and low serum gamma-glutamyl transpeptidase (GGTP) values. Hepato-canalicular cholestasis and disruption of the liver cell plate arrangement were early, uniform findings, and giant cell transformation was found in 56% of initial biopsies. Duct loss was a prominent finding; 70% of patients had ductal paucity, and many had abnormal bile duct epithelium, suggesting degeneration. Fibrosis was seen in the samples from 16 patients, including bridging fibrosis in specimens obtained from six patients during the first 2 years of life. Proliferating ductules at the margins of portal tracts increased as fibrosis progressed and were especially prominent in end-stage histology. Cirrhosis developed in nine of these patients and had a characteristic histologic pattern, consisting of biliary cirrhosis with diffuse stellate lobular fibrosis associated with severe cholestasis and pseudoacinar transformation. Mallory hyalin and hepatocellular carcinoma were observed in materials from some patients with advanced cirrhosis. The constellation of histologic findings in PFIC forms a recognizable pattern, and the liver histology appears to have a predictable progression.
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PMID:Histologic pathology of the liver in progressive familial intrahepatic cholestasis. 801 59


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