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)

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

In a randomized controlled trial, 41 chronic hepatitis B virus carriers were allocated, by opening numbered computerized randomization envelopes, to receive recombinant interferon-alpha 2A at three different doses: 2.5; 5.0, and 10.0 mU per m2. Thirty-two patients received treatment (6 for 3 months, 26 for 6 months), and 9 patients were controls (received no treatment). Ninety-three per cent of our patients were homosexual, and 41% had anti-HTLV-III in their serum. None of the control patients lost HBeAg. In contrast, six of the anti-HTLV-III-negative patients (33%) responded to treatment (p less than 0.02): five of these responders were homosexual (p less than 0.05). The response rate was greatest (44%) in the anti-HTLV-III-negative patients who received 10 mU per m2 of recombinant interferon-alpha 2A. None of the anti-HTLV-III-positive patients responded to treatment. The percentage reduction of hepatitis B virus DNA was significantly less in the anti-HTLV-III-positive group in comparison to the anti-HTLV-III-negative group at 1 and 4 months of treatment and at 3 months after the end of treatment (p less than 0.05). These patients were younger (33 vs. 42 years, p less than 0.02), had lower mean baseline AST values (42 vs. 80 IU per liter, p less than 0.02) and tended to have milder histological disease. Homosexual men with HBeAg-positive chronic liver disease who are anti-HTLV-III-positive appear to be less responsive to the direct antiviral and immunomodulatory effects of recombinant interferon-alpha 2A. This may be due to the subclinical immunosuppressive effects of co-infection with HTLV-III.
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PMID:Diminished responsiveness of male homosexual chronic hepatitis B virus carriers with HTLV-III antibodies to recombinant alpha-interferon. 303 22

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

The ratio of the serum aspartate to alanine amino-transferase levels (AST/ALT) is often used as a clue to the etiology of the underlying liver disease. This ratio is usually greater than 2.0 in alcoholic liver disease and less than 1.0 in patients with chronic hepatitis and chronic cholestatic syndromes. We analyzed the AST/ALT ratio in 177 patients with various forms of nonalcoholic chronic liver disease who underwent medical evaluation and percutaneous liver biopsy. In the majority of cases of chronic viral hepatitis, the AST/ALT ratio was less than 1.0. However, there was a statistically significant correlation between the AST/ALT ratio and the presence of cirrhosis. Among 100 patients with chronic type B hepatitis, the mean AST/ALT ratio was 0.59 in those without cirrhosis and 1.02 in those with cirrhosis. Furthermore, the AST/ALT ratio often rose to greater than 1.0 when cirrhosis first became manifest. Thus, the finding of an AST/ALT ratio of greater than 1.0 in a patient with nonalcoholic liver disease should suggest the presence of cirrhosis. In addition, the use of the AST/ALT ratio as a means of separating alcoholic and nonalcoholic liver disease must be tempered with the knowledge that this ratio may be less helpful in the presence of cirrhosis.
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PMID:Ratio of serum aspartate to alanine aminotransferase in chronic hepatitis. Relationship to cirrhosis. 313 26

In 1964 a 42-year-old woman was hospitalized with clinical and laboratory signs of posttransfusion hepatitis five weeks after administration of six whole blood transfusions. During the following 17 years anicteric chronic liver disease was repeatedly documented by elevations of serum aspartate aminotransferase (SGOT) and alkaline phosphatase enzymes. In 1981 hepatomegaly, progressive jaundice, and a serum alphafetoprotein level of 516,000 ng/ml were observed. Percutaneous liver biopsy showed a primary hepatocellular carcinoma (PHC). Serologic examinations failed to reveal markers for hepatitis B virus including HBsAg, anti-HBs, and anti-HBc by radioimmunoassay; antibody to hepatitis A virus was also absent. This sequence of events demonstrates a presumptive association of PHC and the agent(s) of non-A, non-B viral hepatitis.
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PMID:Primary hepatocellular carcinoma following non-A, non-B posttransfusion hepatitis. 619 33

Eight subjects with HBsAg-positive chronic liver disease received levamisole therapy continuously for 6 to 8 weeks. Depressed T-lymphocyte concentrations, found in all patients before therapy, transiently returned towards normal. All of the three patients who had normal delayed hypersensitivity responses before treatment showed an acute hepatitic reaction manifested by elevation of serum aspartate transaminase (AsT) and HBsAg levels, with transient cell-mediated immunity to HBsAg. This was interpreted as indicating increased lysis of infected hepatocytes. All of the five anergic patients showed no change in AsT or HBsAg levels. The clinical features and hepatic histology were unchanged. In patients with the capacity to mount normal delayed hypersensitivity responses, levamisole enhanced the cell-mediated response to HBsAg, and there was increased lysis of infected cells. Nevertheless, this treatment failed to eradicate the virus, as all patients remained HBsAg-positive.
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PMID:Levamisole therapy for HBsAg-positive chronic liver disease. 697 83

A controlled trial has been undertaken to evaluate adenine arabinoside in the treatment of hepatitis B surface antigen-positive chronic liver disease. Thirteen patients (7 hepatitis B virus DNA polymerase and hepatitis B e antigen-positive, 6 DNA polymerase negative and hepatitis B e antibody-positive) were treated with adenine arabinoside. Eleven comparable patients served as controls, and follow-up was for 6 mo. In the 7 hepatitis B e antigen-positive patients, adenine arabinoside produced a fall in DNA polymerase activity during treatment. When this effect was sustained, it was followed by a loss of e antigen (3 patients). Hepatitis B surface antigen concentrations and aspartate transaminase levels fell significantly at 6 mo (p less than 0.05) in the treated group compared with controls. In the hepatitis B e antibody-positive patients, adenine arabinoside treatment produced no significant change in hepatitis B surface antigen concentrations or aspartate transaminase levels at 6 mo as compared with controls. Adenine arabinoside would appear to reduce either transiently or permanently, hepatitis B virus replication, and it may therefore be useful in reducing the infectivity of some carriers of this virus. In the dose used, adenine arabinoside was ineffective in clearing hepatitis B surface antigen from the serum and eradicating hepatitis B virus from the liver, but combination with other antiviral or immunostimulant agents may enhance its therapeutic effectiveness.
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PMID:Adenine arabinoside therapy in HBsAg-positive chronic liver disease: a controlled study. 700 10

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

Changes in markers of hepatitis B viral replication and standard liver function tests were studied in 30 patients with HBsAg positive chronic liver disease starting or stopping prednisolone/azathioprine therapy, and compared with those occurring in 15 patients who did not receive therapy. On stopping prednisolone/azathioprine, 10 out of 11 HBeAg positive patients and one out of three patients negative for HBeAg and anti-HBe, lost HBV-DNA polymerase activity (p less than 0.01), five lost HBeAg, three developed anti-HBe and HBsAg concentration decreased (p less than 0.01). Only one out of seven untreated HBeAg positive patients lost HBeAg and there were no significant changes in DNA polymerase activity. In the anti-HBe positive patients, 14 starting therapy and eight untreated, there were no significant changes in the markers of viral replication - although two patients developed DNA polymerase activity on high maintenance doses of prednisolone - but a significant decrease (p less than 0.05) in aspartate transaminase in the treated group. It is concluded that the cessation of prednisolone/azathioprine therapy in HBeAg positive patients will result in a reduction in viral replication. In anti-HBe positive patients such therapy may be beneficial.
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PMID:Effects of prednisolone/azathioprine in chronic hepatitis B viral infection. 709 59

To identify the route of hepatitis C virus (HCV) transmission, we investigated the sexual transmission of HCV by examining HCV markers among spouses of patients with chronic liver disease (CLD) due to HCV. Of 83 spouses, 14 (16.9%) had elevated serum aspartate aminotransferase or alanine aminotransferase, 20 (24.1%) had detectable anti-HCV antibodies, and 17 (20.5%) had measurable HCV-RNA in serum. However, the seropositivity rate of anti-HCV antibodies (24.1%) of patients' spouses was not significantly higher than that (15.4-27.5%) of an unselected population in the same district. Ten patient-spouse pairs underwent nucleotide sequence analysis of the HCV core and envelope genes. Overall the sequence homology of 10 couples (91.1%) was not significantly higher than that of 10 randomly chosen unrelated pairs (88.2%). As reported earlier, in an age and sex matched case-control study of HCV transmission, a history of surgery is a prominent HCV risk factor. These results suggest that sexual transmission of HCV is rare.
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PMID:Analysis of nucleotide sequences of hepatitis C virus isolates from husband-wife pairs. 753 61


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