Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tissue cholestasis is a histologic feature in some patients with alcoholic liver disease, but its significance is unknown. We studied prospectively the clinical, laboratory, and histologic findings of 306 chronic male alcoholics in whom liver tissue was available. Tissue cholestasis permitted identification of two groups: group I, absent or mild cholestasis (239 patients), and group II, moderate to severe cholestasis (67 patients). Statistical evaluation was performed by Student's t test and regression analyses. In patients with tissue cholestasis, 97% had elevated serum cholylglycine levels, while only 61% had significant jaundice (serum bilirubin greater than 5 mg/dl). In patients without tissue cholestasis, 66% had elevated serum cholylglycine and 13.5% jaundice. Highly significant statistical correlations (P less than 0.0001) were found between cholestasis and malnutrition, prothrombin time, AST, alkaline phosphatase, bilirubin, Maddrey's discriminant function, serum cholylglycine level, albumin, and histologic severity score. In group I, 54% survived 60 months versus 22% in group II (P less than 0.0001). Highly significant statistical correlations (P less than 0.0001) were noted between serum cholylglycine levels and the parameters enumerated earlier, but not with survival. We conclude that tissue cholestasis is a highly significant prognostic indicator of outcome in alcoholic hepatitis and is more consistently associated with bile salt retention than jaundice.
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PMID:Prognostic significance of cholestatic alcoholic hepatitis. VA Cooperative Study Group #119. 236 44

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

Forty six children suffering from Protein Energy Malnutrition (PEM) were classified according to the Wellcome classification. Their aspartate aminotransferase, alanine aminotransferase and gamma-glutamyl transferase were measured. Aspartate aminotransferase was raised in 20 patients (43.5%) and alanine aminotransferase was raised in 12 patients (26%). Y-glutamyl transferase was raised in only one patient suffering from marasmic kwashiorkor, who, in contrast to the rest of the patients had a marked rise in aminotransferases. The aminotransferase elevation correlated positively with a Severity Index calculated from height and weight retardation and serum albumin levels. It is suggested that the moderate rise in aminotransferases found in PEM is not due to damage to the liver. However, marked enzyme elevations can occur in a small minority of patients, suggestive of liver injury, probably caused by hepatotoxins.
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PMID:Serum aminotransferases and gamma-glutamyl transferase in protein energy malnutrition. 286 77

26 of 46 Nigerian children with protein-energy malnutrition (PEM) had elevated S-Ferritin levels; the geometric mean value in the entire group of children with PEM was 146 micrograms/l and the observed range 11-7000 micrograms/l. There was no statistically significant correlation between the logarithm of the S-Ferritin level and the amount of stainable iron in marrow fragments (r = 0.23; p greater than 0.2). A stepwise multiple linear regression analysis in which the logarithm of the S-Ferritin level was used as the dependent variable and a total of 17 clinical, biochemical and haematological parameters were used as the independent variables showed that 34.8% of the variability in S-Ferritin could be accounted for by variations in the percentage of lymphocytes in the bone marrow. We speculate that the latter parameter may be an index of previous infection and that the elevated S-Ferritin levels may, therefore, be at least partly caused by infections. Increased serum aspartate transaminase activities were also encountered in PEM, suggesting that hepatocellular damage may contribute to the high S-Ferritin levels in this condition. Our data indicate that S-Ferritin has a limited value as an indicator of iron status in subjects with PEM, presumably because of the frequency of infections and of hepatocellular damage in such subjects.
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PMID:Limited value of serum ferritin in evaluating iron status in children with protein-energy malnutrition. 393 5

Selenium deficiency has been implicated as a cause of hepatic injury, possibly from accentuated lipoperoxidation due to decreased activity of the selenoenzyme, glutathione peroxidase. Because of possible clinical and biochemical links between selenium and alcohol, we performed nutritional assessment and assayed red blood cell, plasma, and whole blood selenium by spectrofluorometry in 27 normals (group I), 30 asymptomatic alcoholics on admission to a detoxification unit, (group II) and 16 alcoholics with severe liver disease (group III). We found a mean (+/- SD) whole blood selenium of 0.109 micrograms/ml +/- 0.014 for group I vs 0.076 +/- 0.010 for group II (P less than 0.001), and 0.047 +/- 0.006 for group III (P less than 0.001 vs group I and II). For plasma, the mean (+/- SD) selenium was 0.095 micrograms/ml +/- 0.016 for group I versus 0.065 micrograms/ml +/- 0.012 in group II and 0.038 micrograms/ml +/- 0.007 in group III (All P less than 0.001). Calculated red blood selenium levels were also significantly reduced in alcoholics versus controls. Whole blood and plasma selenium correlated directly with serum albumin. For whole blood selenium versus albumin, r = 0.73 (P less than 0.01), and for plasma selenium versus albumin, r = 0.71 (P less than 0.01). A significant inverse correlation was noted between whole blood selenium and the height of the total serum bilirubin (r = -0.46), alkaline phosphatase (r = -0.50), and AST (r = -0.51) (P less than 0.01 for all). Among alcoholics admitted for detoxification, selenium was diminished despite the absence of severe malnutrition, as determined by standard nutrition assessment parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low blood selenium levels in alcoholics with and without advanced liver disease. Correlations with clinical and nutritional status. 402 13

Plasma, whole blood, and red blood cell selenium levels were determined by spectrofluorometry in 30 patients with chronic heavy ethanol ingestion (group I) and 20 normal controls (group II). Nutritional and general medical evaluations were also performed. The mean plasma selenium level was 0.065 microgram/ml +/- 0.012 (SD) for group I versus 0.100 +/- 0.016 for group II (p less than 0.0001). Whole blood levels were 0.076 microgram/ml +/- 0.011 versus 0.114 +/- 0.015 (p less than 0.0001), and red blood cell levels were 0.092 microgram/ml +/- 0.016 compared with 0.130 +/- 0.025 (p less than 0.0001), respectively. Mean triceps skin fold was 8.2 mm +/- 3.5 for group I males versus 12.3 mm +/- 5.0 (p less than 0.005) for group II males but was not well correlated with whole blood selenium status (r = 0.33). Nutritional parameters of percentage of ideal body weight, midarm muscle circumference, serum albumin, and total lymphocyte count revealed no differences. Mildly elevated serum aspartate aminotransferase and/or alkaline phosphatase values occurred in 53% of alcoholics, but selenium levels in these patients were no different from those with normal liver tests. We conclude that depressed blood selenium levels occur frequently in patients with chronic heavy ethanol ingestion even in the absence of overt malnutrition. Since selenium deficiency can produce a spectrum of organ injury which resembles that associated with chronic alcoholism, the relationship of selenium deficiency to alcohol-induced organ injury deserves further study.
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PMID:Diminished blood selenium levels in alcoholics. 639 3

Hepatic injury in alcoholics due to intake of acetaminophen (APAP or acetylparaaminophenol) with therapeutic intent has been reported, but the extent of the phenomenon is not clear, pertinent details of the association remain insufficiently clarified, and the importance of the phenomenon is not widely appreciated. The present report describes 67 patients who developed hepatic injury after ingestion of APAP with therapeutic intent. All were regular users of alcohol. Sixty-four percent of the patients were considered to be "alcoholic" or reported intakes greater than 80 g/d, 35% took 60 g/d or less, and the remainder were vague in their reporting. Doses of APAP were in the "nontoxic" range ( < 6 g/d) in 60% of the group, within the recommended range ( < 4 g/d) in 40%, and at 4.1 to 6 g/d in 20%. Characteristic feature was the towering level reached by aspartate transaminase (AST) with figures ranging from 3,000 to 48,000 IU in more than 90% of cases. Almost 20% of the patients died. The data on these patients were similar to 94 cases of injury from APAP taken with therapeutic intent reported in the literature. This study provides further evidence of hepatic injury in regular uses of alcohol, especially chronic alcoholics, who take APAP with therapeutic intent. Susceptibility is presumably caused by induction of cytochrome P-4502EI by ethanol and by depletion of glutathione (GSH) because of the effects of alcohol, the malnutrition often associated with alcoholism, and the depletion associated with chronic use of APAP and impaired glucuronidation caused by fasting perhaps as well. The syndrome of liver injury is distinctive, marked by uniquely elevated levels of AST, and poses a significant threat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acetaminophen (paracetamol) hepatotoxicity with regular intake of alcohol: analysis of instances of therapeutic misadventure. 765 81

In rats that received a low protein isocaloric diet (protein content of the diet: 8 instead of 20%) during fetal life and thereafter up to the time of sacrifice at 12-13 weeks of age, a low plasma insulin concentration, a decreased insulin content of isolated pancreatic islets, and an impaired secretory response of the islets to either D-glucose or the association of L-leucine and L-glutamine coincided, in islet homogenates, with a low activity of the mitochondrial glycerophosphate dehydrogenase and an abnormally high ratio between glutamate-alanine and glutamate-aspartate transaminase activities. Opposite enzymatic changes were found in liver extracts of the same rats. No obvious change in these hormonal, secretory, and enzymatic variables were observed when the period of protein deficiency was restricted to fetal life. These findings support the view that, in protein malnutrition, an impaired activity of pancreatic B-cell mitochondrial glycerophosphate dehydrogenase contributes, possibly in association with other enzymatic anomalies, to the perturbation of islet function.
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PMID:Impaired activity of rat pancreatic islet mitochondrial glycerophosphate dehydrogenase in protein malnutrition. 775 Apr 86

Six serum enzymes, alkaline phosphatase, cholinesterase, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase and gamma-glutamyl transpeptidase were studied in 30 cases of protein energy malnutrition (PEM). The mean serum values of alkaline phosphatase, cholinesterase and lactate dehydrogenase in cases of PEM were significantly lower than the controls, lowering being maximum in PEM Grade IV. The mean serum values of aspartate aminotransferase and alanine aminotransferase in patients with PEM were significantly higher than the controls. The mean serum values of gamma-glutamyl transpeptidase showed similar significant rise in all but PEM Grade IV. The degree of increase in the serum values of these three enzymes were maximum in cases with PEM Grade I. These findings suggest that abnormalities in blood levels of these enzymes occur in any form of PEM and these are related to the severity of the disease.
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PMID:Serum enzyme abnormalities in protein energy malnutrition. 828 27

Clinical and biochemical parameters associated with the removal of the peritoneal catheter and death following continuous ambulatory peritoneal dialysis (CAPD) peritonitis were analyzed in 120 episodes of peritonitis. Episodes resulting in catheter removal (n = 24, 20%) and those ending in patient death (n = 12, 10%) were respectively compared with episodes in which peritoneal catheters were saved and from which the patients survived. Variables associated with catheter removal included advanced age, long duration of peritonitis, coexisting exit-site/tunnel infection, infection caused by pseudomonas or fungi, elevated aspartate aminotransferase (AST) and malnutrition at presentation with peritonitis (serum albumin 29.5 +/- 7.6 g/L vs 33.8 +/- 4.8 g/L in episodes in which the catheters were saved, p = 0.014), and worsening malnutrition during peritonitis. Variables associated with death from peritonitis included diabetes mellitus, persistence of the infection, removal of the peritoneal catheter, infection with pseudomonas, malnutrition prior to the infection (serum albumin 29.5 +/- 3.2 g/L vs 34.7 +/- 4.2 g/L in survivors, p < 0.001), presentation with elevated AST and worsening malnutrition, and the development of pronounced malnutrition during infection (serum albumin 18.1 +/- 4.1 g/L vs 28.9 +/- 5.8 g/L in survivors, p < 0.001). Deaths were caused primarily by cardiovascular events. Both removal of the peritoneal catheter and death as consequences of CAPD peritonitis are associated with malnutrition and pseudomonas infection. In addition, death is more frequent in diabetic patients.
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PMID:Peritoneal catheter loss and death in continuous ambulatory peritoneal dialysis peritonitis: correlation with clinical and biochemical parameters. 839 4


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