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)

Alcoholic liver disease (ALD) in Japan was compared clinicopathologically with the occurrence in the U.S.A. ALD found in Japan was more frequently complicated by other hepatic diseases including non-A, non-B chronic hepatitis than ALD found in the U.S.A. (9.9% versus 21.9%). Patients with such complications were excluded from this study. The chief complaints of the total of 51 alcoholics studied in the U.S.A. were abdominal distension or jaundice and those of 98 alcoholics studied in Japan were non-specific: general fatigue, weakness or appetite loss. The U.S. patients exhibited more elevated levels of serum bilirubin (8.1 +/- 7.5 versus 1.9 +/- 2.4 mg/dl, mean +/- SD) and a higher incidence of leukocytosis (49.0% versus 5.1%). While the serum glutamic-oxalacetic transaminase (GOT) levels were not significantly different between the two groups (146.5 +/- 116.8 versus 140.8 +/- 147.7 IU/L), the serum glutamic-pyruvic transaminase (GPT) levels among Japanese alcoholics were higher (38.6 +/- 31.4 versus 87.4 +/- 99.1 IU/L) and in about one quarter of these patients, serum GPT was higher than serum GOT, a feature not seen in the patients in the U.S.A. Comparative histopathologic study of 337 U.S. patients and 210 Japanese patients disclosed a higher frequency of cirrhosis (46.9% versus 33.8%), the presence of Mallory bodies (58.5% versus 13.8%) and marked neutrophilic exudation (45.1% versus 6.2%). Thus, the majority of Japanese alcoholics exhibited progression of liver disease, eventually leading to cirrhosis, due to hepatocellular drop-out and fibrosis caused by a mechanism different from alcoholic hepatitis. In addition, ALD in the U.S.A. revealed more striking extension of fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The characteristics of alcoholic liver disease in Japan. Clinicopathologic comparison with alcoholic liver disease in the United States. 369 16

We measured the activity of carnosinase, a prominent hepatic peptidase, in sera from 69 patients with liver disorders. Mean values (and SDs) for those with liver cirrhosis (17 cases) and hepatoma (seven cases) were 0.51 (0.28) and 0.68 (0.21) mumol/mL per hour, respectively--clearly less than for normal adults: 4.19 (0.95) mumol/mL per hour. Samples from 17 cases of chronic hepatitis also showed moderately decreased activity, 1.41 (0.97) mumol/mL per hour. In contrast, 14 cases of acute hepatitis generally showed values falling within the normal limits: 3.41 (1.97) mumol/mL per hour. Our results for carnosinase correlated with those for cholinesterase (r = 0.70) and with the concentration of albumin in serum (r = 0.59), but not with the activity of either creatine kinase, aspartate aminotransferase, or alanine aminotransferase in serum. Carnosinase values differed more among groups of disorders than did the values for cholinesterase or albumin. Measurement of serum carnosinase activity may be of clinical value in assessing the severity of chronic liver-cell damage, but not in differentiating liver disease from nutritional, muscle, or endocrine disorders.
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PMID:Decreased activity of carnosinase in serum of patients with chronic liver disorders. 373 53

Serum mitochondrial aspartate aminotransferase activity was measured using an immunochemical method in 251 subjects, of whom 140 were chronic alcoholics. The alcoholic patients included 37 with normal liver routine tests (Group I), 61 with noncirrhotic alcoholic liver disease (Group II) and 42 with cirrhosis (Group III), of whom 21 had been abstainers for at least 2 months. All of the remaining 111 subjects were nonalcoholic: 61 had various types of liver disease (Group IV) and 50 were healthy controls. A second assay of serum mitochondrial aspartate aminotransferase activity was performed in 76 alcoholics after a period of abstinence of about 7 days. In addition, serial mitochondrial aspartate aminotransferase determinations were performed in four nonalcoholic volunteers prior to, during and following an alcohol bout. Mean mitochondrial aspartate aminotransferase and mitochondrial aspartate aminotransferase/total aspartate aminotransferase ratio were significantly increased in the alcoholics whatever their liver status, with a sensitivity of the ratio of 81, 85 and 66% for Group I, Group II and the 21 drinkers of Group III, respectively. Only 1 of the 21 cirrhotic abstainers had an increased ratio. Among the 61 nonalcoholic patients with liver disease, 11 had an increased mitochondrial aspartate aminotransferase/total aspartate aminotransferase ratio, specificity of which was 82%. After drinking had been stopped for about 1 week, mitochondrial aspartate aminotransferase decreased by more than 50% and therefore appears as a reliable tool to assess abstinence. In the four cases of alcohol bouts, no significant modifications in mitochondrial aspartate aminotransferase serum values were observed, thus suggesting that mitochondrial aspartate aminotransferase is indeed a marker of chronic, but not of acute, alcohol intake.
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PMID:Serum mitochondrial aspartate aminotransferase as a marker of chronic alcoholism: diagnostic value and interpretation in a liver unit. 373 96

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

Common bile duct ligation (CBDL) in rats was used to induce liver disease and secondary kidney damage. The biochemical changes in the liver, kidney and plasma were studied at 3, 6, 10 and 21 days post CBDL. The observed alterations climaxed at the 6th day following ligation. Renal, activities of aldolase (ALD), lactic dehydrogenase (LDH), isocitric dehydrogenase (ICDH), sorbitol dehydrogenase (SDH), and alkaline phosphatase (ALP), were lowered in CBDL rats. Further, microsomal Na,K-ATPase and Mg-ATPase and mitochondrial oxidative-phosphorylation were inhibited. In the liver from CBDL rats the activities of aspartate aminotransferase (AST), Mg-ATPase and ALP were elevated, while SDH, ALD, malic dehydrogenase (MDH), LDH, malic enzyme (ME) and Na,K-ATPase were lowered. Plasma enzymes, AST, ALP, MDH, LDH, ALD, acid phosphatase (ACP) and ICDH and the metabolites bile acids, bilirubin, creatinine and urea were elevated. Addition of bile acids or bilirubin at concentrations comparable to those found in the plasma of CBDL rats, to the reaction mixture of the various enzymes strongly inhibited most, particularly mitochondrial oxidative phosphorylation. High concentrations of these substances in the blood may explain the development of renal failure during liver disease and its reversibility when liver function returns to normal.
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PMID:Biochemical changes in liver, kidney and blood associated with common bile duct ligation. 378 11

To assess the spectrum of hepatic abnormalities in acquired immune deficiency syndrome (AIDS), we reviewed clinical, biochemical, and pathological material in 32 patients with AIDS. Eight-four percent of AIDS cases had a history of intravenous drug abuse. Ninety percent of AIDS patients has some liver biochemical abnormality at the first presentation of illness. During the course of AIDS, significant (p less than 0.05, paired Student's t test) rises in alkaline phosphatase and bilirubin occurred, without rises in aminotransferases. Mean abnormalities were mild, reflecting approximately 2-fold increases over baseline. Liver failure was not believed to contribute to the death of any AIDS patient. Pathological findings in AIDS included specific infectious diagnosis in 26%, granulomas in 16%, hemosiderosis in 26%, nonspecific abnormalities in 39%, cirrhosis in 23%, and chronic active hepatitis in 3%. AIDS cases were also compared to 10 selected age, sex, and epidemiologically similar non-AIDS patients. Although granulomas or infections were not seen in our comparison group, only the incidence of chronic active hepatitis was significantly different between the groups. If only those with intravenous drug abuse were studied, then none of 24 AIDS patients versus four of eight non-AIDS cases (p less than 0.005) had chronic active hepatitis. AIDS patients with specific hepatic infections tended to have a higher alkaline phosphatase and aspartate aminotransferase (p less than 0.05) than noninfected cases. However, substantial overlap existed, and no difference in hepatomegaly was noted. Ninety percent of AIDS patients were ingesting at least one potentially hepatotoxic drug. We conclude that AIDS patients have a high incidence of underlying hepatic abnormalities. However, clinical and biochemical abnormalities are similar in our selected liver biopsy patients with intravenous drug abuse with or without AIDS. As expected, AIDS patients have a higher incidence of hepatic granulomas and infections, but these patients were not clearly distinguishable from other AIDS cases. Histological examination showed a wide array of changes by light microscopy, but no specific lesion of AIDS was noted. The low incidence of chronic active hepatitis in this AIDS population may imply that the altered T lymphocyte function in AIDS could influence the course of liver disease in these patients.
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PMID:The liver in acquired immune deficiency syndrome: emphasis on patients with intravenous drug abuse. 382 29

One hundred and thirteen patients with histologically confirmed oral lichen planus, from three stomatology clinics, were examined for evidence of liver disease. No patient had clinical evidence of liver disease. Nine patients (7.9%) had a raised serum concentration of a single enzyme; 6 patients had raised gamma-glutamyl transpeptidase, 2 had raised alkaline phosphatase, and 1 had raised aspartate transaminase levels. No patient had serum auto-antibodies suggestive of primary biliary cirrhosis or chronic active hepatitis. Most patients presenting with oral lichen planus are unlikely to have liver disease.
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PMID:Lichen planus and liver disease: how strong is the association? 392 77

Serum aminoterminal procollagen III peptide (PIIIP) was measured in 36 alcoholic subjects. There was a significant elevation of PIIIP in subjects with proven liver disease (median 17.5 ng/ml, n = 24) compared to those without liver disease (median 4.7 ng/ml, n = 12). Those subjects with raised serum transaminase values (AST) had elevated PIIIP values (median 13.7 ng/ml, n = 22) compared to those with normal transaminase values (median 3.7 ng/ml, n = 14). In those alcoholic subjects who were deficient in both selenium and vitamin E there was a significant elevation (p less than 0.01) of PIIIP values (median 26.4 ng/ml, n = 7) compared to subjects with normal levels (median 7 ng/ml, n = 11). Subjects deficient in selenium alone had PIIIP values in an intermediate range. Selenium and vitamin E, as important free radical scavengers, may protect the liver in alcoholic subjects from oxidative damage leading to hepatic fibrosis.
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PMID:Aminoterminal procollagen III peptide elevation in alcoholics who are selenium and vitamin E deficient. 395 42

Five enzymes were measured in 50 liver specimens (18 normal liver, 20 Reye liver, 12 diverse liver disorders other than Reye syndrome). The enzymes were: glutamic dehydrogenase (E.C. 1.4.1.3), monoamine oxidase (E.C. 1.4.3.4), lactate dehydrogenase (E.C. 1.1.1.27), D-glucose-6-phosphate dehydrogenase (E.C. 1.1.1.49), catalase (E.C. 1.11.1.6). The Reye syndrome group showed significant decreases in glutamic dehydrogenase (56%) and monoamine oxidase (70%) compared to normal control tissue and these changes were not characteristic of the non-Reye liver disorder group as a whole. Neither catalase nor lactate dehydrogenase appeared to be altered significantly in the Reye or in the abnormal control group compared with normal controls. Thus, only the prominent decreases in the mitochondrial enzyme activities appeared to be highly characteristic of Reye syndrome. Paradoxically, the means of the five hepatic enzymes and the admission levels of two serum enzymes indicative of liver damage (alanine and aspartate aminotransferase) were remarkably similar for both survivors and nonsurvivors of Reye syndrome.
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PMID:Quantitative evaluation of the extent of hepatic enzyme changes in Reye syndrome compared with normal liver or with non-Reye liver disorders: objective criteria for animal models. 396 10

A total of 159 hemophiliacs (149 treated) from our geographical area were screened in 1983 for serological evidence of HBV infection and biochemical evidence of liver disease. All were asymptomatic. HBsAg was detected in 16 cases (10%); anti-HBs and anti-HBc in 106 (67%); 19 (12%) subjects were susceptible to HBV. The HBV infection rate evaluated in 70 patients followed-up from 1980 to 1983 was 28% per year. The cumulative risk of HBV infection as well as the rate of seroconversion to HBV increased with increasing age and with increasing frequency of treatment given during the last 12 months. Anti-delta was detected in the serum of 5 (28%) out of 13 HBsAg-positive cases. Follow-up data showed that in 61% of subjects with liver dysfunction, hepatic damage could not be accounted for by HBV infection. AST and/or gamma-globulin increase was detected in 80% of patients. Abnormalities were more pronounced in HBsAg-positive cases and among them in subjects carrying anti-delta. Further follow-up studies are needed to clarify the long-term prognosis of liver disease in hemophiliacs.
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PMID:Liver disease in hemophiliacs: etiological and biochemical data on 159 cases from our geographical area. 400 63


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