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)

To determine if liver dysfunction in children affects energy and macronutrient homeostasis, we performed 13 metabolic studies in 11 patients (age, 17.8 +/- 5.9 months [mean +/- SEM]) with extrahepatic biliary atresia (EHBA). Nutritional balance, indirect calorimetry, anthropometry, and biochemical liver function tests were utilised. Sixty-four percent of the energy losses were in the form of stool fat. Energy expenditure (68 kcal/kg/d) was 29% higher than normal (P less than 0.0025). Only one third of the metabolisable energy intake (37 kcal/kg/d) was stored in the body for new tissue synthesis. In spite of the bountiful protein intake for age, the increased protein oxidation (2g/kg/d) resulted in a virtually zero mean nitrogen balance. In addition, four patients oxidised endogenous protein as well. The respiratory quotient was 0.96, and did not change significantly between pre- and post-meal measurements, suggesting a predominant utilisation of carbohydrate for energy metabolism. Net lipid oxidation was severely diminished. We found that the higher the serum aspartate aminotransferase level (previously named SGOT), the lower the net fat oxidation, and the higher the conversion of glucose to fat. These data suggest that markedly increased energy expenditure contributes to the malnutrition of patients with EHBA. We characterised for the first time how severe liver disease in infants and children affects carbohydrate, fat, and protein metabolism, thus inducing protein-energy malnutrition.
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PMID:Resting energy expenditure is increased in infants and children with extrahepatic biliary atresia. 273 18

The distal splenorenal shunt (DSRS) was performed in 125 consecutive variceal bleeders. To date, no patients have been lost to follow-up (mean of 79 +/- 20 months). Liver pathology was documented in 85 patients: 45 patients had schistosomal hepatic fibrosis, 17 had nonalcoholic cirrhosis, and 23 had mixed pattern (hepatic fibrosis and cirrhosis). The preoperative data base for these three groups was matched (p greater than 0.05), with a mean follow-up of 79 +/- 20, 70 +/- 14, and 77 +/- 22 months for each population, respectively. The results showed low operative mortality (4.8%), high cumulative patency rate (94.8%) and low recurrent variceal hemorrhage (5.6%). The biochemical data showed significant increase in serum bilirubin (p less than 0.001) and aspartate transaminase (AST) (p less than 0.05) in the nonschistosomal patients. Chronic hyperbilirubinemia was found in 33% of the schistosomal group. Prograde portal perfusion was detected in 94% of the patients, with development of collaterals in 91%. The angiographic pattern of these collaterals was 50% pancreatic, 45% gastric, and 26% colosplenic. Patients with mixed liver disease had a high incidence of Grade III portal perfusion (57%) and more common pancreatic and gastric collaterals (71%). The cumulative survival for all patients was 74.1%, with hepatic cell failure being the leading cause of death (13 patients, 50% of all deaths). The schistosomal patients had a 91.6% incidence, whereas the cirrhotic and mixed groups had survival rates of 75.6% and 65.2%, respectively. Also, of a 15% total incidence of encephalopathy, 4.4% was related to the schistosomal patients, 23.5% to the cirrhotics, and 21.7% to the mixed population. Statistically, the survival rate was significantly better (p less than 0.05) and encephalopathy was significantly lower (p less than 0.05) in the schistosomal population. In conclusion, this data shows that: 1) DSRS has a high patency rate and a low variceal hemorrhage recurrence rate; 2) it maintains some degree of portal perfusion in patients with different nonalcoholic liver diseases, despite development of collaterals; and 3) the schistosomal patients have a better survival rate, with a low incidence of encephalopathy after DSRS, compared with the cirrhotic and mixed populations.
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PMID:Schistosomal versus nonschistosomal variceal bleeders. Do they respond differently to selective shunt (DSRS)? 278 63

A cross-sectional study was performed to define patients at risk of developing liver disease due to long-term treatment with anticonvulsive drugs. The activities of gamma-glutamyltransferase, aspartate aminotransferase, and alanine aminotransferase and the concentrations of primidone, phenobarbital, phenytoin, and valproic acid in serum were estimated. Epileptic children before therapy were used as controls. The results indicated enzyme induction due to phenobarbital and both enzyme induction and liver cell damage or plasma membrane leakage due to phenytoin. Gamma-glutamyltransferase may be an early indicator of liver disease due to valproic acid.
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PMID:Effects of anticonvulsive drugs on the activity of gammaglutamyltransferase and aminotransferases in serum. 287 3

Twenty horses of various ages had inadvertently ingested alfalfa hay contaminated with Senecio vulgaris. Among them, 4 died of liver disease. Blood was collected from affected horses at monthly intervals for 7 months and at the 9th and 14th months. The following serum enzymes and chemical items were assayed: aspartate aminotransferase, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyl transferase, sorbitol dehydrogenase, total bilirubin, BUN, glucose, cholesterol, inorganic phosphate, calcium, total protein, and albumin. Amino acid profiles, conjugated bile acids, sulfobromophthalein clearance times, and liver histopathologic changes via serial biopsies were also monitored. Liver histopathologic changes revealed lesions progressively increasing in severity. Aspartate aminotransferase and plasma amino acid ratios indicated chronic liver degeneration (0.05 level of significance). gamma-Glutamyl transferase and lactate dehydrogenase as well as BUN values fluctuated, but returned to within reference values. Horses appeared clinically normal 14 months after intoxication, but were unable to tolerate stress of exercise.
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PMID:Clinicopathologic study of horses surviving pyrrolizidine alkaloid (Senecio vulgaris) toxicosis. 287 83

Serum mitochondrial aspartate aminotransferase (mAST) level and the mitochondrial aspartate aminotransferase/total aspartate aminotransferase ratio (mAST/AST) have been proposed as sensitive markers of chronic alcoholism. Their specificity, however, remains poorly defined. The purpose of this study was to compare these markers in three groups of hospitalized patients: group I, 80 patients with chronic alcoholic liver disease; group II, 51 patients with chronic liver disease without alcoholism; group III, 44 patients with extrahepatic cholestasis (due to choledocholithiasis in 21 and malignant in 23). mAST was measured after immuno-precipitation of cytoplasmic aspartate aminotransferase. The normal values of mAST (less than or equal to 2 mu/l) and mAST/AST (less than or equal to 6 p. 100) were defined in a group of 59 non alcoholic subjects without liver disease (controls). mAST was increased as compared with controls in 91 p. 100 of the patients of group I, 20 p. 100 of group II, 61 p. 100 of group III. mAST was comparable in groups I (mean +/- SD: 10 +/- 10.8) and III (10.3 +/- 12.9), and higher than in group II (1.8 +/- 2.4). m/AST was increased in 59 p. 100 of the patients of group I, 6 p. 100 of group II and 36 p. 100 of group III. It was higher in group I (8 +/- 4 p. 100) than in group III (6 +/- 4 p. 100, p less than 0.02), and particularly higher in both these groups than in group II (2 +/- 1 p. 100, p less than 0.00001). mAST was correlated to AST in each of these three groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serum activity of mitochondrial aspartate aminotransferase and extrahepatic cholestasis]. 292 44

Fifty-one patients (16 with malignant extrahepatic biliary obstruction, ten with benign extrahepatic biliary obstruction, eight with alcoholic liver disease, five with viral hepatitis and 12 with liver metastases) and 19 adult healthy controls were studied with determinations of beta-N-acetyl hexosaminidase (a lysosomal enzyme which is cleared from the circulation by the Kupffer cells), carcinoembryonic antigen (CEA), serum bilirubin, alkaline-phosphatase and aspartate aminotransferase (AST). Both CEA and beta-NAH were elevated in each disease group. Elevated beta-NAH levels distinguished between benign and malignant extrahepatic biliary obstruction better than CEA levels. Beta-NAH levels for the malignant and the benign groups were 47.6 +/- 14.7 U/l and 23.0 +/- 4.7 U/l (mean +/- S.D.) respectively. The groups differed significantly (P less than 0.001). Plasma CEA levels for both groups were 18.7 +/- 38.9 and 7.2 +/- 3.3 ng/ml (mean +/- S.D.) respectively. Beta-NAH levels for the 19 normal controls were 15.8 +/- 3.5 U/l (mean +/- S.D.). Beta-NAH also was significantly elevated in patients with hepatic metastases (36.9 +/- 20.1 U/l). In 25 cancer patients with metastases other than in the liver beta-NAH levels (18.3 +/- 5.2) were not significantly elevated over the control group. It has potential value as a marker for non-CEA-producing liver metastases.
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PMID:Serum beta-N-acetyl hexosaminidase (beta-NAH) as a discriminant between malignant and benign extrahepatic biliary obstruction: comparison with carcinoembryonic antigen (CEA). 293 60

Serum activity of angiotensin converting enzyme (ACE) was serially measured in 47 hospitalized chronic alcoholics with liver disease. Compared to healthy controls, ACE activity, on admission, in the serum of alcoholics was significantly elevated (42.5 +/- 16.6 U/ml vs. 32.4 +/- 9.6 U/ml; p less than 0.005). About 36% of the patients had an elevated ACE level exceeding an upper normal value of 42 U/ml (mean +/- SD). In contrast to the rapid normalization of such enzymes as aspartate transaminase (AST), alanine transaminase (ALT) and lactic dehydrogenase (LDH) which represent parenchymal liver cell injury, the activity of ACE remained elevated over a period of 4 weeks even with abstinence. The serum level of ACE was significantly correlated with levels of alkaline phosphatase, gamma-glutamyltranspeptidase and monoamine oxidase, but not with those of AST, ALT and LDH. These data suggest increased ACE activity in alcoholics may be related to the influence of chronic consumption of alcohol on hepatic nonparenchymal systems.
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PMID:Mild but prolonged elevation of serum angiotensin converting enzyme (ACE) activity in alcoholics. 302 46

Data on 15 laboratory analytes obtained in 145 prospectively investigated cholestatic patients with viral hepatitis, chronic intrahepatic cholestasis and extrahepatic biliary obstruction were submitted to a computer-based graphical evaluation using probabilistic test analysis. This revealed a marginal utility for alkaline phosphatase, gamma-glutamyltransferase and the direct/total bilirubin ratio at specific cut-off points for the exclusion of extrahepatic cholestasis (PVneg 90%-100%). Aspartate aminotransferase and alanine aminotransferase values with cut-off points at 200 U/l and 300 U/l, respectively, were powerful discriminators between acute viral hepatitis and the other disease categories, while lactate dehydrogenase, erythrocyte sedimentation rate and the ratios gamma-glutamyltransferase/alanine aminotransferase as well as total bilirubin/gamma-glutamyltransferase were useful at specific cut-off points indicating the absence of this diagnosis (PVneg 92%-100%). An aspartate aminotransferase/alanine aminotransferase ratio above 1.5 and serum gamma-globulin concentrations above 20 g/l strongly suggested cholestasis due to chronic parenchymal liver disease (PVpos 92% and 90%, respectively). This graphical approach to laboratory data analysis enhances the understanding of the interrelations between cut-off points and sensitivity, specificity and predictive values and also of the influence of disease prevalence on disease prediction. It also adds to present knowledge by demonstrating the clinical relevance of several readily available, albeit rarely utilized diagnostic analytes.
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PMID:Graphical analysis of laboratory data in the differential diagnosis of cholestasis: a computer-assisted prospective study. 306 41

Because it remains debatable whether all patients with a clinical diagnosis of alcoholic liver disease should have a liver biopsy to help confirm the diagnosis, we evaluated the diagnostic value of liver biopsy in alcoholic liver disease. Studied were 108 consecutive patients who had a percutaneous liver biopsy for the first time. In all cases the patient's clinical diagnosis recorded before biopsy was compared with the histological diagnosis of an experienced histopathologist. Prebiopsy clinical data (reported alcohol intake, signs of chronic liver disease) and laboratory data (liver function tests, mean corpuscular volume, ferritin, hepatitis B serology) were reviewed. We found that a prebiopsy clinical diagnosis of alcoholic liver disease (n = 35) was confirmed by biopsy in all but one case. The prebiopsy diagnosis of alcoholic liver disease was significantly associated with a histological diagnosis of alcoholic liver disease (specificity 98%, sensitivity 79%). Individually, alcohol intake, signs of chronic liver disease, the alanine aminotransferase (ALT), the aspartate aminotransferase to ALT ratio, and the mean corpuscular volume were significantly associated with a histological diagnosis of alcoholic liver disease. When clinical and laboratory parameters were considered jointly using stepwise logistic regression, only reported alcohol intake and mean corpuscular volume were significant. Liver biopsy may not always be necessary for the identification of that broad group of patients with alcoholic liver disease.
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PMID:Diagnostic value of liver biopsy in alcoholic liver disease. 306 3

We studied unselected, hepatitis B surface antigen (HBsAg)-positive parenteral drug abusers for antibody to hepatitis D virus (anti-HD) and antibody to human immunodeficiency virus (HIV). The prevalences of anti-HD and antibody to HIV were 67% and 58%, respectively, and there was no association between positivity for these two markers. In a logistic regression model, anti-HD was associated with older age (P = .001), longer duration of drug abuse (P = .045), and the presence of liver disease (P = .002). Antibody to HIV was associated with a younger age (P = .003) and increased serum globulin levels (P less than .001). In patients infected with HIV, the severity of hepatic dysfunction remained correlated with anti-HD. In anti-HD-positive patients, most indices of hepatic dysfunction were similar whether or not antibody to HIV was present, but serum aspartate aminotransferase levels were significantly higher in patients with both anti-HD and antibody to HIV. (124 +/- 16 vs. 74 +/- 11, P less than .05).
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PMID:Hepatitis D virus and human immunodeficiency virus antibodies in parenteral drug abusers who are hepatitis B surface antigen positive. 317 Dec 27


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