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)

Four cases of chronic active hepatitis with cholestasis resembling primary biliary cirrhosis are reported. Two patients were women and two were men; their age ranged from 18 to 52 years. They had recurrent jaundice with pruritus, and, in two cases, xanthelasma or xanthomas. All patients had hyperbilirubinemia, a moderate increase in serum aspartate aminotransferase activity, an increase in serum alkaline phosphatase activity and immunoglobulins G levels. Hepatitis B surface antigen was present in one patient. Histological examination of the liver revealed active chronic hepatitis with cholestasis. Moderate doses of prednisone had no effect on clinical or biochemical signs in any of the patients.
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PMID:[Ineffectiveness of corticosteroids in cholestatic forms of chronic active hepatitis]. 718 71

Hepatitis B virus associated DNA polymerase activity, hepatitis b surface antigen (HBsAg), and serum aspartate aminotransferase were followed in 21 patients with chronic active hepatitis while immunosuppressive therapy (prednisone +/- azathioprine) was being withdrawn. In every case, DNA polymerase activity fell within 6-10 wk of decreasing treatment and became undetectable in 8 patients. This was usually accompanied by a fall in HbsAg titer and a transient rise in serum aspartate aminotransferase activity. Four additional patients with previously untreated HbsAg positive chronic active hepatitis were placed on prednisone for 12 wk. There was a rise in DNA polymerase activity and HBsAg titer with a fall in serum aspartate aminotransferase values during treatment. Upon discontinuing therapy, DNa polymerase activity fell dramatically in all 3 patients who completed their course of prednisone and became undetectable in 1. These findings suggest that immunosuppressive therapy has a potentiating effect on hepatitis B viral replication in patients with chronic active hepatitis.
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PMID:Effects of immunosuppressive therapy on viral markers in chronic active hepatitis B. 728 93

Vinyl chloride monomer (VCM) is a suspected human carcinogen. Its metabolite, chloroethylene epoxide, is able to alkylate the DNA molecule and to produce single strand breakage (SSB). A total of 244 workers from 4 polyvinyl chloride (PVC) manufacturing factories were recruited to assess the SSB of their peripheral lymphocyte DNA. The method of alkaline unwinding and hydroxyapatite chromatography was used to detect and calculate frequencies of SSB. In addition, hepatitis B and C markers and the liver function of the workers were also examined. The worker's cumulative exposures to VCM were retrospectively constructed from the current monitoring data and each worker's job history. Multiple linear regression models were constructed to predict the worker's level of SSB and liver functions based on various exposure indices and variables, such as age, sex, smoking, drinking, and hepatitis markers. The results showed that current smoking and drinking status, and the presence of VCM exposures on the previous day were 3 major determinants of the level of SSB. Among the liver function tests, only gamma-glutamyl transpeptidase (GGT) was associated with current VCM exposures. In contrast, aspartate aminotransferase (AST), alkaline phosphatase (ALP) and alanine aminotransferase (ALT) were mainly affected by the presence of hepatitis B surface antigen (HBsAg) or anti-hepatitis C virus (anti-HCV). We conclude that GGT should be considered to be included in the regular health screening of VCM workers, and that the SSB method may not be suitable for long-term monitoring of cumulative exposure because of the quick DNA repair mechanism in humans.
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PMID:Changes in lymphocyte single strand breakage and liver function of workers exposed to vinyl chloride monomer. 761 65

The value of serum transaminases (ST) in evaluating hepatitis B (HBV) and C (HCV) infection was studied in 217 hemodialysis (HD) patients and 804 normal controls. Mean serum aspartate aminotransferase (AST) was 22.3 (22.0-22.7) and 22.6 (21.6-23.6) IU/l or 0.371 (0.366-0.378) and 0.376 (0.36-0.393) mu kat/l in controls and HD patients, respectively (nonsignificant), while mean serum alanine aminotransferase (ALT) was 20.3 (19.9-20.7) and 16.3 (15.3-17.3) IU/l or 0.338 (0.331-0.345) and 0.271 (0.255-0.288) mu kat/l in these two groups (p < 0.001). However, both AST and ALT became significantly depressed in HD patients after adjusting for age, gender, HBV surface antigen (HBsAg) and anti-HCV. The usual practice of regarding AST and ALT as being 'abnormal' in evaluating viral hepatitis when they exceeded the upper reference range (40 and 46 IU/l or 0.666 and 0.766 mu kat/l in our laboratory) was then critically assessed by the receiver operating characteristic (ROC) curve. ROC analysis showed that ST was useless in detecting HBsAg, while the best cutoff point for detecting the presence of anti-HCV was 18 IU/l (0.3 mu kat/l) for AST and 16 IU/l (0.266 mu kat/l) for ALT in HD patients, respectively. These are considerably lower than the conventional criteria for an 'abnormal' ST. We conclude that ST are decreased in HD patients and that the cutoff value of ST for detecting HCV should be set at lower levels to enhance their diagnostic yield.
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PMID:Impact of decreased serum transaminase levels on the evaluation of viral hepatitis in hemodialysis patients. 777 13

A 51-year-old woman who had been treated for primary biliary cirrhosis (PBC) was admitted to our hospital for evaluation of unexplained, isolated, persistently increased aspartate aminotransferase (AST) activity. Results of laboratory tests on admission showed: AST 171 KU, alanine aminotransferase 28 KU, and anti-mitochondrial titer 1/1280. Results of hepatitis B surface antigen (HBs Ag) and hepatitis C virus antibody (HCV Ab; C100-3) assays were negative. Histology of a liver biopsy specimen was compatible with a diagnosis of PBC (stage III of Scheuer's classification). The molecular size of serum AST was estimated to be more than 500,000 by high-performance size-exclusion liquid chromatography. Electrophoretic analysis showed an abnormal band of AST between supernatant AST (sAST) and mitochondrial AST (mAST), which band was characteristic of AST-immunoglobulin complexes (AST-Ig). Ouchterlony double-diffusion and immunoprecipitation tests identified the immunoglobulin component as IgM. The presence of AST-Ig appeared to be responsible for the elevated serum AST.
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PMID:Aspartate aminotransferase-linked immunoglobulin complexes in serum of a patient with primary biliary cirrhosis. 801 13

With ages between 14-17 years, none of the 2157 subjects studied in the central Taiwan area had ever been inoculated with the hepatitis B vaccine. Whether a hepatitis B virus surface variable, either the hepatitis B surface antigen (HBsAg) or its antibody (anti-HBs), was an interpretation factor in reading laboratory data for a common serum biochemical test was analyzed by two-way analysis of variance (ANOVA). The two independent variables were gender and the hepatitis B surface variable. Either HBsAg or paired HBsAg/anti-HBs was a necessary factor for the seven items:total protein, albumin, total cholesterol, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. Anti-HBs alone was not an effective agent for the above seven tests and four additional tests, blood urea nitrogen, uric acid, creatinine, and total bilirubin. The analyses yielded no interaction between gender and either hepatitis B surface variable for all tests except uric acid.
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PMID:Hepatitis B virus surface antigen as an interpretation factor for serum biochemical tests in young adults. 817 Nov 66

Eighteen patients with presumed childhood acquisition of chronic hepatitis B virus infection were initially entered into this randomized controlled trial. Twelve were treated with prednisolone for 4 weeks followed, after a 2-week gap, by thrice weekly lymphoblastoid alpha-interferon for 12 weeks. Two of these had previously acted as untreated controls. Three of the 12 patients (25%) [who were initially hepatitis B virus (HBV) surface antigen (HBsAg), 'e' antigen (HBeAg) and HBV-DNA positive] became HBeAg and HBV-DNA negative during therapy and remained so after 12 months post-therapy follow-up. One of these also lost HBsAg. A further two patients lost HBeAg and HBV-DNA during therapy but relapsed 6 and 9 months later. Two additional patients were HBV-DNA negative but HBeAg positive at the end of follow-up. None of the eight untreated control patients seroconverted during an identical follow-up period. Two further patients were HBsAg and HBeAg positive but HBV-DNA negative at the start of therapy. These were omitted from the final analysis: both subsequently lost HBeAg. The treatment response was associated with a rise in aspartate aminotransferase, peaking 2-6 weeks after prednisolone withdrawal, loss of HBV-DNA 0-8 weeks later and subsequent normalization of liver function tests. Treatment was well tolerated.
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PMID:Short report: prednisolone withdrawal followed by lymphoblastoid interferon in the therapy of adult patients with presumed childhood-acquired chronic hepatitis B virus infection. 836 39

Since 1980, at North London Blood Transfusion Centre 61 (14%) of a total of 442 hepatitis B surface antigen (HBsAg) positive carriers have been hepatitis B e antigen (HBeAg) positive by radioimmunoassay at the time of detection, with 353 (80%) anti-HBe positive. We have undertaken long-term follow-up of infectivity markers in 285 of these 442 HBsAg carriers detected by routine screening. Donors undergoing acute HBV infection were excluded from the analysis. The donor follow-up times ranged from 1.2 to 13.5 years. Regular follow-up samples were obtained and examined for HBsAg, HBeAg, anti-HBe, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Thirty-five (12.3%) of the 285 carriers were HBeAg-positive when first detected. Eight of these 35 developed anti-HBe during follow-up. At no time did any carrier revert from anti-HBe to HBeAg. When these data were subjected to a Kaplan--Meier analysis an estimated lower quartile time to seroconversion of 3.83 years, and a median seroconversion time of 8.25 years were predicted. This corresponds to a mean rate of 6.5% per annum for the first 25% to seroconvert, and 5.7 for the next 25%.
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PMID:Spontaneous loss of HBeAg and development of anti-HBe during long-term follow-up of blood donors found to be HBsAg-positive. 852 Feb 47

To determine the most prevalent forms of hepatitis in intravenous heroin addicts, 389 addicts consecutively admitted to outpatient treatment clinics throughout California were tested for antibodies to hepatitis A (anti-HAV), B core (anti-HBc), B surface (anti-HBs), C (anti-HCV), D (anti-HDV), and B surface antigen (HBsAg). The majority were also tested for serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, lactic dehydrogenase, total bilirubin, globulins, albumin, and platelet count. The seroprevalence of each marker was: anti-HAV (40.7%); anti-Hbc (73.6%); anti-HBs (46.7%); anti-HCV (93.6%); anti-HDV (9.6%), and HBsAg (3.5%). No single case was positive for IgM, anti-HAV, or for both HBsAg and anti-HDV, indicating the presence of recent hepatitis A or hepatitis D infection. Abnormal liver enzymes, serum proteins, total bilirubin, and platelet count were found to be normal in 5.3 to 44.8% of anti-HCV cases indicating persistent infection. Among anti-HCV cases, elevated total bilirubin or a low platelet count was invariably associated with one or more liver enzyme and protein abnormalities. We conclude that while acute hepatitis may be frequent and caused by various viral types, hepatitis C is the primary form of chronic hepatitis found in intravenous heroin addicts. Almost half of hepatitis C cases demonstrate liver function abnormalities indicating persistent infection that has the potential to be contagious and progress to cirrhosis, liver failure, and hepatocellular carcinoma.
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PMID:Seroprevalence of hepatitis A, B, C, and D markers and liver function abnormalities in intravenous heroin addicts. 855 78

Viral hepatitis and alcoholism prevail in four major Taiwanese aboriginal groups. To study the relative importance of the acquisition of hepatitis B virus or hepatitis C virus infection and alcoholism to the presence of impaired liver function in these groups, the authors conducted a semistructured clinical interview for alcoholism and test for seromarkers for viral hepatitis among 993 cohort members enrolled in 1990-1992 in an ongoing prospective study (Taiwan Aboriginal Study Project). The subjects' blood specimens were tested for serum alanine aminotransferase/aspartate aminotransferase levels and for the presence of hepatitis B surface antigen and anti-hepatitis C virus antibody. The prevalence of a combination of an alanine aminotransferase level of > 35 IU/liter and an aspartate aminotransferase level of > 40 IU/liter, implying impaired liver function or advanced liver disease, was 4.3% overall. Univariate and multiple logistic regression analysis showed that, rather than chronic hepatitis B virus infection, hepatitis C virus infection and alcoholism were the two dominant risk factors that signalled the risk of liver damage among these Taiwanese aborigines. In addition, these two contributing factors were able to act synergistically to cause impaired liver function.
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PMID:Alcoholism, hepatitis B and C viral infections, and impaired liver function among Taiwanese aboriginal groups. 861 Jul 7


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