Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic coinfection with the hepatitis B (HBV) and hepatitis delta (HDV) viruses is known to cause severe liver disease, but the importance of coinfection with hepatitis C virus (HCV) and HBV has not been well documented. In the present study, the clinical and pathological severity of liver disease among patients with hepatitis resulting from multiple viruses was examined and an open trial of the efficacy of interferon-alpha 2b (IFN-alpha) treatment was conducted. Nineteen patients with chronic HBV and HCV infection and 17 with HBV, HCV and HDV infection were studied; 12 in each group underwent liver biopsy. For each coinfected patient, two patients infected with HCV alone were selected as controls, and these were matched for age and risk factor and were estimated to have been infected for a similar duration. Coinfection with HBV and HCV or HBV, HCV and HDV was associated with more severe liver disease than HCV alone (P < 0.01); total Scheuer score, portal and lobular inflammation and fibrosis were all worse in coinfected subjects. Eight patients with chronic HBV and HCV were treated with recombinant IFN-alpha 2b [3 million units (MU), thrice weekly for 6 months]. Liver function tests normalized in two patients and one lost hepatitis B surface antigen (HBsAg). Seven patients with hepatitis B, C and delta coinfection were treated with the same regimen and only one normalized serum alanine aminotransferase (ALT) during (and after) treatment. It is concluded that coinfection with multiple hepatitis viruses is associated with histologically more severe liver disease than HCV alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coinfection with hepatitis B and C or B, C and delta viruses results in severe chronic liver disease and responds poorly to interferon-alpha treatment. 749 93

Serum samples from 1,765 consecutive Sardinian blood donors, negative for hepatitis B surface antigen (HBsAg) and for antibodies to human immunodeficiency virus (HIV) (anti-HIV), were evaluated for the presence of antibodies to hepatitis C virus (anti-HCV) by second-generation ELISA. Anti-HCV was detected in 25 (1.45%) of the 1,765 donors examined. Anti-HCV was found in 15 of the 1,690 (0.9%) donors with normal alanine aminotransferase (ALT) and in 10 of the 75 (13%) donors with elevated ALT (P < 0.0001). Of the 15 anti-HCV-positive donors with normal ALT, only five (33%) were confirmed to be positive by second-generation RIBA, six (40%) were indeterminate, while four (27%) were RIBA negative. HCV RNA, as detected by polymerase chain reaction (PCR) using a set of primers from the 5'-noncoding region, was found in six of the 15 (40%) donors with normal ALT, including five RIBA positive and one indeterminant. Of the 10 anti-HCV-positive donors with elevated ALT, all were RIBA positive and eight (80%) had detectable HCV RNA. Thus, among ELISA-reactive donors, those with elevated ALT had a significantly higher probability of being positive for second-generation RIBA and HCV RNA compared to those with normal ALT levels (P = 0.028). None of the 65 donors with elevated ALT but negative for anti-HCV by ELISA had detectable serum HCV RNA, as compared to eight of 10 anti-HCV ELISA-positive donors (P < 0.0001). However, although negative for HBsAg, 12 of the 65 (18%) had serum HBV DNA by PCR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Markers of hepatitis C virus infection in Sardinian blood donors: relationship with alanine aminotransferase levels. 750 72

The clinical significance of a semi-quantitative microparticle enzyme immunoassay (IMx Core-M, Abbott) was evaluated for detection of IgM-class antibodies against the hepatitis B core antigen (IgM anti-HBc) in 136 hepatitis B surface antigen (HBsAg) positive individuals (96 chronic HBV carriers, 20 patients with chronic HBV-HDV infections and 20 patients with acute hepatitis B) and 50 HBV-negative controls. Baseline and follow-up sera (4-11 samples) were analysed from 79 carriers with chronic hepatitis B, 44 of whom were treated with interferon. IMx indexes above 3,000 were found in 95% of the acute hepatitis B patients and above 0.300 in 91.5% of patients with ongoing chronic hepatitis B. IMx indexes between 0.200 and 0.300 were observed in (a) patients with recent HBeAg to anti-HBe seronconversion (6-12 months) and normal serum ALT levels, (b) patients immuno-tolerant to HBV infection and without liver disease despite high levels of viremia, and (c) patients with anti-HBe-positive chronic hepatitis B during 7-13-month intervals of asymptomatic carriage between episodes of disease reactivation. IMx indexes below 0.200 were detected in all HBV-negative individuals and healthy HBV carriers, in 14 (70%) of 20 chronic hepatitis D patients and in all but 1 of 22 interferon-treated patients with histological remission of liver disease, 5-12 months after clearance of viremia and normalization of serum ALT levels. In contrast, IMx indexes remained above 0.200 in all patients with hepatitis B reactivation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monitoring the natural course and response to therapy of chronic hepatitis B with an automated semi-quantitative assay for IgM anti-HBc. 751 11

The advent of specific antiviral therapy for chronic hepatitis C has increased the importance of establishing the correct etiology of chronic hepatitis in patients, especially because interferon alfa (IFN-alpha) has been reported to exacerbate autoimmune hepatitis (AIH), whereas corticosteroids increase viral replication in chronic hepatitis C. In our medical center, we have treated many patients with apparent chronic hepatitis C and serological or clinical evidence of autoimmunity. Our aim was to estimate the prevalence of this association and to learn whether demographic or clinical features distinguished between patients with or without autoimmune markers. We performed a retrospective review of the records of 244 unselected patients seen at the Clinics and Hospital of the University of Massachusetts between May 1991 and November 1993, who had elevated serum aminotransferases. One hundred seventeen patients had chronic hepatitis C defined by elevations of serum alanine transaminase (ALT) for at least 6 months, positive serum antibodies to hepatitis C virus (HCV; second-generation enzyme immunoassay [EIA2] or recombinant immunoblot assay [RIBA]), and absence of hepatitis B surface antigen in the serum. Records were reviewed for results of autoimmune markers in sera, including anti-nuclear antibodies (ANAs), anti-smooth muscle antibodies (SMAs), rheumatoid factor (RF), antimitochondrial antibodies (AMAs), anti-liver and kidney microsomal (LKM) antibodies, and cryoglobulins. We found a high prevalence of positivity, particularly for anti-SMAs (66%) and RF (76%) in both men and women. Forty of 41 patients tested negative for anti-LKM antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High prevalence of serological markers of autoimmunity in patients with chronic hepatitis C. 753 20

The presence of hepatitis B virus (HBV) DNA in sera of 56 chronic carriers of hepatitis B surface antigen (HBsAg) was determined by three methods: the Abbott hybridization assay, the polymerase chain reaction (PCR) followed by gel electrophoresis and UV visualization (PCR-GE), and PCR followed by DNA enzyme immunoassay (PCR-DEIA). HBV DNA was detected in four samples positive for hepatitis Be antigen (HBeAg) by all methods used. Both PCR-GE and PCR-DEIA detected viraemia in two anti-HBe, anti-HBc IgM positive samples. In the group of 50 anti-HBe positive samples the sensitivity of the three methods was 10%, 24% and 32%, respectively. PCR-GE and PCR-DEIA results correlated well with the patients' clinical status; of 20 patients with elevated ALT levels, 12 (60%) were found to be positive in the PCR-GE and another 2 were found to be positive in the PCR-DEIA (70%). These data indicate that PCR-DEIA is the most sensitive method for detection of HBV DNA. This method can be relatively easily applied in the clinical laboratory for monitoring the progression of disease and/or interferon therapy in patients with chronic hepatitis B.
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PMID:Detection of hepatitis B virus DNA in chronic carriers of hepatitis B surface antigen in southwestern Greece. 755 41

The T helper (Th) cell response to hepatitis B core antigen (HBcAg) was analyzed in 76 chronic hepatitis B virus (HBV) carriers with varying degrees of hepatic inflammation and HBV replication. Fifty-five patients had active viral replication, 28 with minimal histological changes and normal alanine transaminase (ALT) and 27 with active hepatic inflammation and elevated ALT. The remaining 21 chronic hepatitis B surface antigen (HBsAg) carriers had undetectable HBV replication, minimal histological activity, and normal ALT. In addition, 34 chronic HBV carriers were studied prospectively during treatment with alpha-interferon. The HBcAg-specific Th cell response was evaluated by a proliferative assay using 3H-thymidine uptake and gamma-interferon production by peripheral blood mononuclear cells. The proliferative response and gamma-interferon production of patients with active hepatic inflammation were significantly higher than in patients with minimal histological changes and in controls. In the longitudinal analysis during alpha-interferon treatment, 22 of 34 patients sustained an ALT flare accompanied by a parallel, significant Th cell response, which preceded or coincided with the ALT flare. The elevation in the Th cell response and the ALT flare were followed by a significant rise in the serum immunoglobulin (Ig) M anti-HBc index. Ten of twenty-two patients with an enhanced Th cell response and an ALT flare seroconverted after alpha-interferon treatment. The Th cell activity in the 10 responders rapidly subsided after hepatitis B e antigen (HBeAg) to anti-HBe seroconversion, whereas in the 12 nonresponders it remained elevated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Induction of T-helper cell response to hepatitis B core antigen in chronic hepatitis B: a major factor in activation of the host immune response to the hepatitis B virus. 755 49

To investigate the significance of spontaneous hepatitis B e antigen (HBeAg) seroconversion during childhood, 415 hepatitis B surface antigen (HBsAg) carrier children (ages 0 to 15 years) were prospectively followed for 7.1 +/- 2.9 years. Hepatitis B virus (HBV) markers and liver function profiles of each child were tested at least once every 6 months. Among them, 50 were initially anti-HBe positive and 140 seroconverted from HBeAg to anti-HBe during follow-up. Before HBeAg seroconversion, jaundice occurred in 9 and alanine transaminase (ALT) activities elevated in 99 of the 140 seroconverters. Serum ALT returned to normal in all patients within 1 to 5 years of seroconversion. Six had reelevated ALT later after seroconversion. Only 7 (9.7%) of the 72 carrier infants seroconverted before 3 years of age. The peak ALT levels in five of them exceeded 100 IU/L, and two had jaundice before HBeAg seroconversion. One of the early seroconverters developed hepatocellular carcinoma (HCC) at 11 years of age, although his liver function profiles remained normal after HBeAg seroconversion. Liver biopsy specimens from 30 children during the anti-HBe-positive stag e showed inactive cirrhosis in 2 (including one with HCC), chronic hepatitis with marked fibrosis in 1, mild activity and moderate fibrosis in 2, mild activity and mild fibrosis in 9, and minimal histologic changes in the remaining 16. Although most will achieve a normalization of ALT and inactive liver histologic changes, the seroconversion of HBsAg carrier children from HBeAg to anti-HBe is not necessarily an indicator of favorable prognosis; a small proportion of children will develop cirrhosis or even HCC.
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PMID:The significance of spontaneous hepatitis B e antigen seroconversion in childhood: with special emphasis on the clearance of hepatitis B e antigen before 3 years of age. 759 Jun 52

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

Serum samples from 116 patients with hepatitis B surface antigen (HBsAg), from 7 patients without detectable HBsAg and from 71 healthy blood donors were tested by a branched DNA signal amplification (bDNA) method. Hepatitis B virus (HBV) DNA was detected in 39 (34%) of the 116 samples with HBsAg, including 19 (70%) of the 27 patients who were also positive for hepatitis B e antigen (HBeAg). In contrast, one of the 7 patients without HBsAg and none of the 71 blood donors were positive for HBV DNA. The titers of serum HBV DNA did not correlate with the serum alanine aminotransferase levels. All the samples positive by the bDNA assay were positive by the polymerase chain reaction (PCR). However, 59% of the PCR-positive samples were bDNA-negative. None of the PCR-negative samples was positive by the bDNA method. Although the sensitivity of bDNA method is not entirely satisfactory, it showed excellent specificity and reproducibility. Thus it may be considered as an alternative for quantitative detection of HBV DNA in serum samples of patients with relatively high titers of HBV viremia.
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PMID:Quantitative detection of hepatitis B virus DNA in human sera by branched-DNA signal amplification. 763 22

Acute hepatitis B virus (HBV) infection is typically distinguished from chronic disease by a positive IgM anti-hepatitis B core antigen (anti-HBc) test. Patients with chronic hepatitis B remain hepatitis B surface antigen (HBsAg) positive, often with raised serum alanine aminotransferase (ALT) activities, for more than six months. The presence of hepatitis B e antigen (HBeAg) and HBV-DNA correlates with infectivity (although patients infected with the pre-core mutated virus may be HBeAg negative). Immunity after HBV infection is characterised by the presence of anti-HBs and anti-HBc antibodies. Patients who respond to interferon alfa treatment lose HBV-DNA and HBeAg from serum and their ALT values return to normal; some also lose HBsAg and acquire anti-HBs. Diagnosis of acute hepatitis C virus (HCV) infection remains largely dependent on history and exclusion, as anti-HCV antibodies may appear late or never at all, although HCV-RNA may be detectable on polymerase chain reaction (PCR) within days of infection. Second generation ELISAs detect a range of anti-HCV antibodies in chronic infections, and confirmatory RIBAs have reduced the incidence of false-positive results. Direct tests for HCV antigens in serum are not yet available, although PCR testing for HCV-RNA can be used to confirm viraemia. Patients who respond to interferon alfa treatment show continuous normalisation of serum ALT values, and some lose HCV-RNA. Relapse occurs in about half of all those who respond.
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PMID:Viral markers in the treatment of hepatitis B and C. 768 14


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