Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We postulated that three tests could be used to advantage in the prognosis of patients with alcoholic liver disease. Ninety-eight patients who entered the hospital in hepatic failure, and who survived that illness, were observed for an average of 3.5 years after discharge. At the time of entry, most had jaundice, ascites, edema, and hepatosplenomegaly. Biopsy of the liver disclosed both cirrhosis and hepatitis in 75-80%. Neither clinical features nor laboratory tests could differentiate these patients at the time of entry. However, as early as 3 months after hospitalization, the clinical course and laboratory tests served to distinguish two groups: group 1 comprised 46 patients in whom the serum bilirubin was less than 2 mg/dl; the aspartate aminotransferase less than 55 mU/ml; and the alkaline phosphatase less than 125 mU/ml. In 40 (87%) of these 46 patients, clinical findings improved concomitantly with laboratory tests. Group 2 comprised 52 patients in whom one or more of these three tests showed persistent abnormality; only 12 (23%) of the 52 patients in this group improved clinically and three subsequently died. Although the majority of patients (76%) in group 1 reported abstinence on follow-up, 44% of group 2 patients also claimed abstinence. Complications of liver disease, shunt surgery, and continuing alcoholism contributed to liver failure. Early identification of such patients should aid in the management of alcoholic liver disease.
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PMID:Predicting clinical recovery from alcoholic liver disease. 688 50

The two categories of anti-albumin antibodies (AAA), namely precipitins (AA-P) and agglutinins (AA-Aggl), were investigated in 260 patients with morphologically diagnosed chronic liver diseases (CLD). A parallelism was observed between AA-P titre and the severity of chronic hepatitis as revealed by clinical diagnosis. Thus, significant differences in AA-P titre were noticed between chronic persistent hepatitis (CPH) and chronic aggressive hepatitis (CAH) and between CAH and liver cirrhosis (LC). No correlation was found between AA-P positivity and either HBsAg presence or disease activity, maximum AA-P values being registered in decompensated, inactive LC. AA-P positivity was found associated with a higher degree of liver cell dysfunction. In every category of CLD a striking association was also observed between AA-P positivity and raised serum aspartate transaminase and bilirubin levels, thus suggesting a common pathogenic substrate, namely liver cell membrane damage. These correlations were also observed after immunosuppressive therapy which would argue for the maintenance of AA-P diagnostic value. AA-Aggl showed raised incidences and titres in CAH patients, the values decreasing in LC. Therefore, the main diagnostic value is attributed to AA-P.
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PMID:Anti-albumin antibodies in chronic liver diseases: diagnostic significance of these antibodies in patients with conventional or immunosuppressive therapy. 697 71

Extreme elevation of the serum aspartate aminotransferase level typically suggests acute hepatocellular necrosis and may militate against the diagnosis of chronic active hepatitis. However, we found that 26 of 160 patients (16%) with chronic active hepatitis had aminotransferase elevations of more than 1,000 IU/liter. These patients were younger and more often jaundiced than the others, but they exhibited signs of chronic liver disease as often. In only 2 of 26 patients with extreme aminotransferase abnormality were features of chronic disease absent. Patients with extreme enzyme elevation had histologic findings of confluent necrosis (P greater than 0.005) and features associated with acute viral infection (P greater than 0.005) more often than others, but they as often had cirrhosis on biopsy specimens. Virologic markers did not distinguish the patients or correlate with viral features in liver tissue. Corticosteroids improved immediate survival (P greater than 0.005) and the likelihood of remission (P greater than 0.005). Although chronic active hepatitis may present with extreme aminotransferase elevation and histologic features associated with acute viral infection, ancillary features of chronic disease facilitate the correct diagnosis and the initiation of appropriate therapy.
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PMID:Prognostic and therapeutic implications of extreme serum aminotransferase elevation in chronic active hepatitis. 704 6

Serum glycocholic acid (SGC) was measured by radioimmunoassay in 277 samples from 122 children with hepatobiliary disorders and from 23 healthy age-matched controls. In patients with hepatobiliary disease the SGC was more frequently abnormal (83%) than values for serum albumin (7%), prothrombin time (17%), bilirubin (22%), alkaline phosphatase (45%), aspartate transaminase (57%) and gammaglutamyl transpeptidase (63%). The cumulative frequency of abnormality of these six tests was equal to that of SGC alone. Serum glycocholic acid concentrations were raised in 13 patients in whom all other tests of liver function were normal. Two of these had clinical and histological evidence of liver disease, while four had biopsy-proven hepatic fibrosis or cirrhosis, and two of three with chronic active hepatitis in remission subsequently relapsed. Four patients have as yet, no other clinical or biochemical evidence of continuing liver disease. Serum glycocholic acid was normal in seven children with abnormal aspartate transaminase or gammaglutamyl transpeptidase in whom there is strong suspicion of significant hepatic disease. A wide range of values of SGC was found with marked overlap between the values found in the different disease entities studied. The SGC value was related to the serum concentration of aspartate transaminase and gammaglutamyl transpeptidase but not to other tests of liver function. Serum glycocholic acid concentration was considered in relation to the severity of histological abnormality in 25 percutaneous liver biopsies. The extent of the rise in SGC was related to the presence or degree of histological severity of oedema in the portal tracts, disruption of the limiting plate, parenchymal fibrosis and hepatocellular necrosis but not to other histological features. The very high incidence of abnormal SGC values found in this study does suggest that in an ordinary inpatient and outpatient service SGC determination is a practical and sensitive indicator of the presence of significant liver disease but for its comprehensive identification aspartate transaminase and gammaglutamyl transpeptidase must also be determined.
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PMID:Radioimmunoassay of serum glycocholic acid, standard laboratory tests of liver function and liver biopsy findings: comparative study of children with liver disease. 711 20

Quadratic multiple discriminant analysis of 25 commonly ordered laboratory tests resulted in correct classification of 100% of nonalcoholics without overt liver disease, 98% of alcoholism treatment program patients with presumed mild liver involvement, 96% of alcoholics with liver disease, and 89% of nonalcoholics with liver disease. Direct comparison of the biopsy-verified alcoholic and nonalcoholic liver disease groups resulted in 100% discrimination, and removal of traditionally evaluated liver tests from the battery of 25 tests did not substantially alter the original classification accuracy. Alcoholic and nonalcoholic liver disease was still 100% differentiable when equated for number of patients with cirrhosis, hepatitis, and hepatitis combined with cirrhosis or fibrosis. Additional utility of the quadratic discriminant approach was demonstrated when 83% alcoholic and 83% nonalcoholic liver disease cases were diagnosed correctly in a prospective manner. In contrast, use of aspartate aminotransferase to alanine aminotransferase ratios (ie, SGOT to SGPT) identified correctly 75% and 33% of patients, respectively.
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PMID:Biochemical and hematologic correlates of alcoholism and liver disease. 713 77

To evaluate factors predisposing to liver injury following jejunoileal bypass, 27 patients underwent clinical evaluation and liver biopsy prior to bypass and at 3, 6, 12, 18, and 24 months and yearly thereafter. Nineteen patients developed increased fatty infiltration of the liver, 1 developed cryptogenic cirrhosis, and 7 developed steatonecrosis, central hyaline sclerosis, or cirrhosis indistinguishable from alcoholic liver disease during the period of rapid weight loss. Two of these 7 patients developed clinical liver failure; inactive cirrhosis evolved after parenteral alimentation and reanastomosis in one, and after oral nutritional supplementation in the other. Four of 5 asymptomatic patients resolved to inactive cirrhosis as weight loss diminished. Each of the 7 patients had pericentral fibrosis on pre-bypass liver biopsies, suggesting a previous hepatic injury. These patients were older (p less than 0.02) and, 3 months following bypass, had greater cumulative per cent weight loss (p less than 0.05), higher levels of serum aspartate aminotransferase (p less than 0.005), and greater 45-min bromosulfophthalein retention (p less than 0.02). Histologic evidence of pericentral fibrosis identified patients at risk to develop steatonecrosis and cirrhosis; these lesions occurred in older patients who had greater weight loss following jejunoileal bypass.
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PMID:Prognostic indicators of hepatic injury following jejunoileal bypass performed for refractory obesity: a prospective study. 728 95

Serum activity of glutathione reductase (GR), glucose phosphate isomerase (GPI), aspartate aminotransferase (AST), alanine aminotransferase (ALT) phosphate alkaline (PAL), and gamma-glutamyl transferase (GGT) was studied in 142 patients, in all serum bilirubin was more than 2 mg/dl. Distribution was as follows; 68 cirrhosis of the liver; 27 acute hepatitis; 31 benign extra-hepatic biliary obstruction; and 16 neoplastic obstruction of the biliary tract without liver metastasis. Fifty-three healthy volunteer blood donors were used as the control group. Mean values for GR activity in our patients were significantly higher than those for the control group, although less so in benign obstruction (p less than 0.01) than in those with acute hepatitis (p less than 0.001), cirrhosis (p less than 0.01) and neoplasic biliary obstruction (p less than 0.001). The GPI values were higher than the control groups in patients with acute hepatitis (p less than 0.001) and obstructive neoplastic jaundice (p less than 0.02). In cases with cirrhosis, 87% presented slightly higher values of GR, while GPI was within normal levels in 93 % of all cases. In patients with acute hepatitis, 92% showed a definite increase in GPI and GR values. In 71% of those with benign biliary obstruction levels for both enzymes were normal, as they were in only 6% of those with obstructive neoplastic jaundice. These findings are statistically significant in all cases and of diagnostic value in establishing a differential enzymatic diagnosis in patients presenting with clinical and biological patterns of cholestasis.
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PMID:[Determination of serum activity of glucose phosphate isomerase and glutathione reductase in intra and extra hepatic cholestasis.(author's transl)]. 732 37

Plasma glucagon and growth hormone concentrations were measured fasting and after oral glucose in 19 patients with portal vein block with extensive portal-systemic shunting but minimal liver cell damage, 11 cirrhotic patients and 12 matched control subjects. Portal vein block patients and controls had similar fasting glucose and glucagon levels (glucose 3.8 +/- 0.1 mmol/l VS control 3.4 +/- 0.1 mmol/l (mean +/- SEM); glucagon 57.5 +/- 9.1 pg/ml VS control 51.3 +/- 7.8 pg/ml). Cirrhotic patients were hyperglycaemic (cirrhosis 4.3 +/- 0.2 mmol/l VS control 3.4 +/- 0.1 mmol/l, p < 0.01) with significantly elevated glucagon levels (167.3 +/- 61.1 pg/ml VS control 51.3 +/- 7.8 pg/ml, p < 0.05), which suppressed towards control values after oral glucose. There was no correlation between fasting plasma glucagon levels and the degree of portal-systemic shunting in cirrhotic patients. There was a strong correlation between fasting plasma glucagon concentrations and aspartate transaminase levels (r = 0.68; p < 0.01) in cirrhotic and portal vein block patients. Significant elevations of growth hormone were seen only in cirrhotic patients. It is concluded that hyperglucagonaemia is a feature of hepatocellular damage rather than portal-systemic shunting but the relationship between elevated glucagon and growth hormone concentrations and carbohydrate intolerance in cirrhosis remains unclear.
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PMID:Hyperglucagonaemia in cirrhosis. Relationship to hepatocellular damage. 741 64

Differential diagnosis of acute viral hepatitis, persistent chronic hepatitis, aggressive chronic hepatitis, and post-necrotic cirrhosis can reasonably be achieved on the basis of three well-known liver-function tests: aspartate aminotransferase, alanine aminotransferase, and glutamate dehydrogenase. With use of principal-component analysis, these four liver diseases can be characterized by two criteria: a "cytolytic" criterion, correlated particularly with a membrane-permeability test--namely, alanine aminotransferase activity--and a "mitochondrial damage" criterion, which is associated with above-normal ornithine carbamyltransferase and glutamate dehydrogenase activities.
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PMID:Multivariate analysis of an enzymic profile for the differential diagnosis of viral hepatitis. 743 42

Pseudoisocytidine (psi ICyd) is a C-nucleoside with enhanced stability and resistance to enzymatic deamination when compared to 5-azacytidine and 1-beta-D-arabinofuranosylcytosine. Elimination kinetics in plasma using [14C]psi ICyd showed a beta-phase for t1/2 for 14C of 2 hr and a beta-phase t1/2 of unchanged psi ICyd of 1.5 hr. Net recovery of radioactivity in urine over 24 hr varied between 40 and 80% of the administered dose; 50 to 90% was unchanged drug and the rest was pseudouridine. Human leukemic cells in vitro deaminated psi ICyd very slowly, formed appreciable quantities of pseudoisocytidine triphosphate, and incorporated small amounts into RNA and DNA. Clinical trials were done using a daily i.v. injection for 5 consecutive days. Hematological or intestine toxicities were not seen, nor was depression of white blood cell count observed in leukemic patients. Hepatic toxicity proved to be dose limiting; this was characterized by an early phase with elevation of prothrombin time and aspartate aminotransferase. A later phase with cirrhosis was observed in two patients. Autopsy showed massive hepatic necrosis in patients dying of acute toxicity and micronodular cirrhosis in one patient dying with the chronic form.
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PMID:Biochemical, pharmacological, and phase I clinical evaluation of pseudoisocytidine. 747 Oct 64


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