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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was aimed to clarify the virologic status, liver histologies, and the results of follow-up liver tests in symptom-free individuals with anti-HCV antibodies and normal liver tests. Forty-nine individuals with normal liver tests and positive second generation anti-HCV antibody assay were entered into this study. Cases with hepatitis C viremia were evaluated for HCV genotype, amount of circulating HCV-RNA, and liver histology and were followed-up for more than one year. Of the forty-nine individuals, 36 had hepatitis C viremia, indicated by polymerase chain reaction (PCR) assay. Liver histology was as follows: 3 had non-specific changes, 25 had chronic persistent hepatitis (CPH), and 8 had chronic active hepatitis (CAH). Twenty-four cases with CPH and CAH developed an elevated AST and/or ALT concentration (> 30 IU/l) between 12 and 32 months of follow-up. The amount of circulating HCV-RNA ranged from 10(2) to 10(7) copies/50 microliters serum. The distribution of HCV genotypes was nearly the same as that for symptomatic CAH. These data suggest that the histological examination and follow-up examination are very important for following symptom-free individuals with hepatitis C viremia because there are some candidates for interferon therapy among them. There are few individuals who will remain healthy among asymptomatic HCV carriers.
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PMID:Circulating HCV-RNA, HCV genotype, and liver histology in asymptomatic individuals reactive for anti-HCV antibody and their follow-up study. 887 94

The correlation of serum hepatitis C virus (HCV) titers to the progression of type C chronic liver disease remains controversial. We have investigated the relationship between serum HCV titers and different histological stages of chronic liver disease, including chronic persistent hepatitis (CPH), chronic active hepatitis and/or liver cirrhosis (CAH/LC), and hepatocellular carcinoma (HCC) in 94 well-characterized Taiwanese patients. The mean age of patients in the HCC group was significantly older than those in the CPH and CAH/LC groups, whereas those in the CAH/LC group had the highest mean serum alanine aminotransferase level among the three groups. The prevalence of HCV type 1b increased with the progression of histological severity, and the mean serum titer of the HCC group was significantly higher than that of CPH group. The difference of virus titers between the HCC group and those of the other two groups became more significant when only type 1b virus-infected patients were analyzed. In conclusion, elevated serum HCV titers are more frequently observed among Taiwanese patients with advanced type C chronic liver disease, an association not related to the high prevalence of HCV type 1b infection in such patients.
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PMID:Serum hepatitis C virus titers in the progression of type C chronic liver disease. With special emphasis on patients with type 1b infection. 895 30

Approximately 50% of patients with chronic hepatitis C respond to treatment with interferon-alpha. The aim of this randomized controlled trial was to evaluate whether an increase in dose of interferon-alpha augments response rate. One hundred thirty-eight patients with newly diagnosed chronic hepatitis C received a three-month course of 3 MU IFN-alpha2b administered every two days. All patients were anti-HCV and HCV-RNA (PCR) positive. Prior to treatment, a liver biopsy was performed. Complete response was defined by normal serum ALT concentrations and disappearance of HCV-RNA. After three months, 60 nonresponders were randomized (stratified according to histology) either to continue 3 MU interferon-alpha2b every two days for another six months (group A, total dose: 410 MU) or to receive increasing doses of interferon-alpha2b (6 MU every two days for three months, followed by 10 MU every two days for three months) (group B, total dose: 870 MU). Serum ALT concentrations were measured monthly and HCV-RNA at three-month intervals. Liver biopsy was repeated six months after end of treatment. Pretreatment characteristics of the randomized patients were: group A: N = 30; male/female: 20/10; age: 54 +/- 10 years; CPH 9, CAH 8, cirrhosis 13; mean ALT 108 +/- 98 units/liter; group B: N = 30; male/female: 21/9; age: 57 +/- 15 years; CPH 10, CAH 9, cirrhosis 11; mean ALT 90 +/- 40 units/liter. At the end of treatment six patients in group B but none in group A became responders [P = 0.011 (Fisher's exact test), intent-to-treat analysis]. All six responders were noncirrhotics. High-dose interferon was not tolerated by six patients in group B. Noncompliance resulted in five dropouts in group A and one in group B. During the six-month follow-up, four of the six responders relapsed. A patient in group A with increased serum ALT concentration but negative HCV-RNA at the end of treatment became a full responder after six months. Of nonresponders to 3 MU interferon alpha2b every two days for three months, 20% responded to higher interferon doses, but none to continued standard dose. Prolonged treatment with interferon may be necessary to obtain a sustained response. However, treatment with higher-dose interferon was not tolerated in 20% of the patients.
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PMID:Dose increase augments response rate to interferon-alpha in chronic hepatitis C. 901 66

Soluble HLA-class I and CD8 molecules were determined by sandwich ELISA in patients with viral-induced hepatic disorders. As a whole, the patients with hepatic disorders (acute hepatitis: AH; chronic hepatitis: CH; liver cirrhosis: LC; hepatocellular carcinoma: HCC) showed higher sHLA-class I and sCD8 levels than normal controls (P < 0.001). AH patients had the highest sHLA-class I levels (mean, 3513 +/- 2112 ng/ml), followed by CH (2896 +/- 1290 ng/ml), LC (2293 +/- 1266 ng/ml), and HCC (2221 +/- 1212 ng/ml) sCD8 levels wer highest in AH, followed by HCC, LC, and CH, in that order. Among histologically defined C virus-positive patients, sHLA-I levels were higher in those with chronic active hepatitis (CAH) 2A (3802 +/- 1124 ng/ml) than in those with chronic persistent hepatitis (CPH; 2200 +/- 711 ng/ml; P < 0.01), the levels then decreased as the disease progressed (CAH2B, 3564 +/- 1783 ng/ml, LC, 2376 +/- 1265 ng/ml). In contrast, sCD8 values showed little difference among the disorders. sHLA-class I levels showed a positive correlation with sCD8 values both in whole patients and in patients with AH (P < 0.01), but no correlation was shown, in any patients, with biochemical parameters such as GPT and GOT. These findings, taken together, suggest that hepatic destruction is not the only cause of sHLA-class I production, but that sHLA-class I levels, together with sCD8 levels, may reflect immunological activity in hepatic disorders.
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PMID:Serum concentrations of soluble HLA-class I and CD8 forms in patients with viral hepatic disorders. 921 47

In this study we aimed to correlate liver histology and the presence of hepatitis C virus (HCV) viremia, genotype, and quantity of HCV genome in 19 positive and 11 RIBA II indeterminate patients presenting persistently normal ALT values over 24 months before biopsy. In addition, after biopsy serum ALT values were monitored monthly for a mean follow-up period of 24.8 months, after which patients were reevaluated for RIBA II and the presence of viremia. Sixteen patients (53%) were serum HCV-RNA-positive; 13 of them (68%) were confirmed positive and 3 (27%) indeterminate on RIBA II. Histology of the HCV-RNA-positive patients showed eight cases of CPH (one case of genotype 1a; four cases type 1b; three cases type 2), six cases of CAH (three cases type 1b, three cases type 2), one case of CLH (type not determined), and one case of normal liver (NL) (type 1b). Histology of the HCV-RNA-negative patients showed four cases of CPH, one case of CAH, two cases of CLH, and seven cases of NL. During the follow-up period nine patients (30%) presented slight increases in ALT values (< 2 x N), and in particular, flares of ALT were observed four times in the CAH and five times in the CPH patients, who were all viremic, but never in the NL subjects. These results indicate that subjects positive on RIBA II, but with persistently normal ALT values, had a high probability of being serum HCV-RNA-positive and that almost all these viremic subjects presented histologic signs of liver disease. In contrast, RIBA II indeterminate subjects had a moderate probability of being HCV-RNA-positive, but a number of these may present signs of liver disease. In both cases there was no association with genotype or HCV-RNA serum levels. The other nonviremic cases included subjects with hepatic changes going toward resolution or with normal liver in whom hepatic biopsy can be avoided. Only one case was a true carrier since he was viremic with normal liver and persistently normal ALT values.
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PMID:Serum HCV-RNA and liver histologic findings in patients with long-term normal transaminases. 928 37

No experience has been reported to date in treating chronic hepatitis C virus (HCV) infection with interferon (IFN) therapy after BMT, mainly due to concerns related to the impact of an immunomodulatory drug in patients who are immunologic and haematologic chimeras. However, chronic inflammatory activity related to HCV infection results in a chronic fibrogenous mechanism potentially leading to liver cirrhosis and hepatocellular carcinoma. Moreover, patients transplanted for beta-thalassemia could be at greater risk because of concomitant iron overload and pre-existing fibrous liver damage. Eleven patients with serological, biochemical, histological and molecular biological evidence of HCV infection were included in the study and treated for 6-12 months with recombinant IFN 24-65 months following BMT. The serum alanine aminotransferase (ALT) was persistently elevated (range 85-1242 U/l; mean 416) for at least 1 year prior to IFN treatment. Ten patients completed the protocol; five were considered as responders to treatment. In these five patients the liver histology showed an overall reduction of inflammation and necrosis: histological inflammatory activity improved from chronic active hepatitis (CAH) to chronic persistent hepatitis (three patients) or minimal residual inflammatory activity (two patients). The Knodell total activity score varied from 5.4 (range 3-9) to 1.4 (range 1-2; P = 0.05). All responding patients revealed negativization of serum HCV-RNA, that has been persistent in four (follow-up 1-3 years). ALT level fell to 15-80 U/l (mean 52; P = 0.0027). No major complications occurred during the therapy and no influence on marrow engraftment parameters were noted. We conclude that IFN therapy does not adversely interfere with engraftment and that it is a feasible therapy for treatment of chronic hepatitis C virus after BMT.
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PMID:Alpha-interferon treatment of chronic hepatitis C after bone marrow transplantation for homozygous beta-thalassemia. 938 79

A rare case of "wild-type" HBV cirrhosis (CHIL A/HBeAG+/HBV-DNA+) with complete response to IFN treatment after 3 successive series based on different types of IFN is reported. In this patient, HBeAg and HBV-DNA negativization after the second treatment with r-alpha-2b-IFN was observed and after the third treatment with lymphoblastoid-IFN HBcAb,-IgM negativization simultaneously with ALT persistent normalization. Over one year after the interruption of the last treatment, HBV clearance with HBsAg elimination and HBsAb, seroconversion was observed. The effectiveness of IFN was histologically confirmed with decrease of the piecemeal necrosis in the liver and presence of light fibrosis whereas the results of 3 previous histological evaluations showed: 1) CPH (1985); 2) CAH lightly active with initial signs of cirrhotic evolution (1988); 3) CAH with presence of nodular cirrhosis in the liver (1991). In particularly selected cases the possibility of a favourable response to the series of IFN treatment is stresses even in more advanced chronic "wild" HBV forms in which there is not evidence of mutants in the viral population.
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PMID:[Complete response to IFN in a case of typical HBV cirrhosis]. 941 37

In the present study, intrahepatic CD8+ lymphocyte infiltrates as well as HLA class I and CD54 (ICAM-1) antigen expression at both tissue and serum levels were evaluated in 54 untreated patients with chronic hepatitis C stratified on the basis of histological diagnosis (Chronic Persistent Hepatitis/Chronic Lobular Hepatitis -CPH/CLH- and Chronic Active Hepatitis -CAH-: 22 and 32 subjects, respectively). The relationships between soluble HLA-I (sHLA-I) and ICAM-1 (sICAM-1) serum levels and their membrane-bound counterparts, CD8+ liver infiltration and serum alanine aminotransferase (ALT) were also studied. A strong HLA-I and CD54 tissue expression, associated to the presence of CD8+ cell infiltrates in necro-inflammatory areas, and elevated sHLA-I and sICAM-1 serum amounts were observed in all patients. At the same time, no difference was found at tissue level between the two groups of patients with respect to the mean scores of HLA-I and CD54 expression, while CAH subjects displayed a significantly higher CD8 periportal and lobular reactivity in comparison to the other subset. Serological assays outlined higher values of circulating HLA-I molecules in CPH/CLH patients and higher sICAM-1 levels in the CAH group. Finally, a negative correlation was found between sHLA-I and ALT in CAH subjects while, in all patients, sICAM-1 positively correlated with both CD8 tissue infiltration and ALT. Our findings confirm the occurrence of an immune activation status during chronic hepatitis C and suggest that sHLA-I molecules might play a down-modulating role on immunoresponsiveness of these patients.
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PMID:Immunoresponsiveness in chronic hepatitis C patients: correlation between tissue and serum findings. 973 40

We evaluated the impact of concomitant infection with Hepatitis B virus (HBV) and Hepatitis C virus (HCV) on the clinical course after renal transplantation (Tx). In 335 patients (pts) transplanted between 1991 and 1993 we found 30 (9%) recipients who were positive for Hepatitis B surface antigen (HBsAg) (ELISA, Organon) and anti-HCV antibodies (immunoblot assay Lia Tek) preTx. Chronic liver disease (CLD) (two-fold or greater increase in serum ALT and AST levels for at least six months) developed in 40.7% coinfected pts as compared to 24.4% and 25.7% pts infected only with HCV or HBV, respectively. Maintenance immunosuppression consisted of P + Aza + CsA, mean follow-up time was 28 +/- 15 months. The mean time of the onset of CLD was 3.0 months (range: 1-18 months) after Tx. Percutaneous liver biopsy performed in 5 CLD pts revealed chronic active hepatitis (CAH) in 4 and chronic persistent hepatitis (CPH) in 1 pt. Four pts who had CAH and were positive for HCV RNA (RT PCR) in serum and for HBcAg in liver tissue, received interferon-alpha therapy for 6 months. Clinical improvement of liver function was observed in all of them, but none cleared HBsAg or HCV RNA. One pt lost his graft due to acute rejection. Concomitant infection with HBV and HCV is associated with the high risk of development of CLD early after Tx. We recommend that pretransplant evaluation of both anti-HCV and HBsAg positive pts should include liver biopsy to exclude potential recipients with CAH.
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PMID:Clinical course of concomitant Hbv and Hcv infection in renal allograft recipients. 986 22

Due to the limited efficacy of alpha-interferon for chronic hepatitis C amantadine has been proposed as a possible alternative method of treatment. However, few studies about efficacy of amantadine in chronic hepatitis C are available with controversial results. Stimulated by recent data in the literature, we studied the effect of 100 mg of amantadine HCL (alone) PO bid, for a four month period on alanine aminotransferase serum levels and viral load in a cohort of 18 patients (14 males and 4 females) with chronic hepatitis C, non-responders to alpha-interferon. Inclusion criteria were: detectable serum HCV-RNA, alanine aminotransferase above the upper limit of normal, chronic inflammation on liver biopsy, no other associated chronic liver disease and written informed consent. Available biopsies showed initially four cases of cirrhosis, six of chronic persistent hepatitis and eight of chronic active hepatitis. The most prevalent HCV genotypes were 3a (n = 9, 52.94%) and 1b (n = 6, 32.29%). Viral load (Amplicor HCV Monitor, Roche, USA) and alanine aminotransferase levels were obtained at baseline and after four months of treatment. All patients enrolled into the study but one completed the treatment. One patient discontinued amantadine due to severe depression. No significant reduction was observed between baseline and final values of alanine aminotransferase (139.118 +/- 79.789 vs. 99.588 +/- 62.583 U/L, P = 0.059) and viral load (7.154 +/- 1.596 vs. 6.574 +/- 1.584 log copies/mL, P = 0.147). Amantadine alone was not effective neither eradicating viremia nor normalizing alanine aminotransferase levels in chronic hepatitis C non-responders to alpha-interferon patients. It is suggested that only a study with amantadine alone in-patients without previous treatments could determine its efficacy in comparison with alpha-interferon.
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PMID:[Amantadine-HCL in the treatment of chronic hepatitis C in non-responders to alpha-interferon. Effect on ALT serum levels and viral load]. 1051 83


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