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)

To investigate the association between GB virus C/hepatitis G virus (GBV-C/HGV) infection and the development of hepatocellular carcinoma (HCC) in H city, in the inshore area of the Yangtze River, where high prevalence of HCC has been reported, we determined hepatitis B virus (HBV) and hepatitis C virus (HCV) markers, GBV-C/HGV-RNA and GBV-C/HGV E2 antibody (anti-HG E2) among 114 HCC patients and the same number of age- and sex-matched controls. There were no significant differences in the clinical and demographic characteristics between them, except for serum alanine aminotransferase level and history of liver diseases. There was a significant difference of hepatitis B virus surface antigen (HBsAg) prevalence between the HCC patients (75.4%) and the controls (20.2%; P<0.01). Hepatitis C virus antibody was detected in 4.4% of the HCC patients, compared with 1.7% of the controls. GB virus-C/HGV-RNA and anti-HG E2 were detected in 14.9 and 1.7% of the HCC patients, respectively, compared with 7.0 and 1.7% of the controls, respectively. Nucleotide sequences and molecular evolutionary analysis showed the strains of GBV-C/HGV-RNA were classified into genotype 2 and 3 (HG and ASIA type). An effect analysis showed an odds ratio (OR) for developing HCC from GBV-C/HGV infection among HBsAg-positive subjects was 14.9, with a 95% CI of 4.9-45.4. HBsAg infection alone was 13.83 (95% CI 7.4-25.9) and GBV-C/HGV infection alone, 3.74 (95% CI 1.1-13.1), respectively. These data indicate that HBV infection is considered to be one of the major risk factors in patients with HCC and although GBV-C/HGV infection was observed in both the HCC and the control groups, it might not play an important role in the development of HCC in this area.
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PMID:GB virus C/hepatitis G virus infection among patients with hepatocellular carcinoma in the inshore area of the Yangtze River, China. 991 33

The clinical significance of GB virus C/hepatitis G virus (GBV-C/HGV) co-infection was studied retrospectively in 100 consecutive patients with hepatitis C virus (HCV) infection. All 100 patients had been treated with interferon-alpha (IFN-alpha). Co-infection with GBV-C/HGV and HCV was detected in 10 of the 100 patients (10%) and anti-envelope 2 region (anti-E2) antibody was detected in 25 patients. None of the patients with GBV-C/HGV RNA had anti-E2 antibody. Co-infected patients were younger (P < .005) and their serum transaminase levels were lower than HCV-only infected patients (P< .01). In 7 of the 10 co-infected patients, HCV RNA was eradicated from serum after IFN-alpha treatment and normal alanine transaminase (ALT) levels continued in 6 of these 7 patients. In one patient who was negative for HCV RNA but positive for GBV-C/HGV RNA, the ALT level relapsed transiently. The rate of clearance of HCV and normalization of the ALT level was significantly higher in co-infected patients than in HCV-only infected patients (P < .05). GBV-C/HGV RNA disappeared from 6 of the 10 co-infected patients (60%) upon cessation of IFN-alpha treatment. However, continuous clearance of GBV-C/HGV was observed in only two patients and anti-E2 antibody could not be detected in the serum of these patients. These results indicate that co-infected patients tend to be younger and more sensitive to IFN-alpha treatment. However, long-term clearance of GBV-C/HGV after IFN-alpha treatment may be difficult. Moreover, anti-E2 antibody may act to neutralize GBV-C/ HGV.
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PMID:Correlation of interferon treatment response with GBV-C/HGV genomic RNA and anti-envelope 2 protein antibody. 1008 49

Serologic, biochemical, and molecular analyses were used to study hepatitis G virus (HGV), antibody to the HGV envelope protein (anti-E2), risk factors, clinical significance, and the impact of HGV on coexistent hepatitis C virus (HCV). Among 329 donors with confirmed HCV infection, 12% were HGV RNA-positive and 44% were anti-E2-positive (total exposure, 56%). HGV RNA and anti-E2 were mutually exclusive except in 9 donors (1.5%); 8 of 9 subsequently lost HGV RNA but anti-E2 persisted. HGV had little impact on alanine aminotransferase, aspartate aminotransferase, or gamma-glutamyl transpeptidase in donors with HGV infection alone or those coinfected with HCV. A multivariate analysis showed that intravenous drug abuse was the leading risk factor for HGV transmission, followed by blood transfusion, snorting cocaine, imprisonment, and a history of sexually transmitted diseases. In summary, HGV and HCV infections were frequently associated and shared common parenteral risk factors; HGV did not appear to cause hepatitis or to worsen the course of coexistent hepatitis C.
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PMID:Analysis of hepatitis G virus (HGV) RNA, antibody to HGV envelope protein, and risk factors for blood donors coinfected with HGV and hepatitis C virus. 1019 Dec 4

To study the prevalence and clinical significance of TT virus (TTV) infection in hemodialysis patients, we tested for TTV DNA in serum, using the nested polymerase chain reaction. The prevalence of TTV DNA in 352 hemodialysis patients was 32%, significantly higher than that in 50 healthy blood donors (12%). The prevalence increased with age (P = 0.0098): it was 20% (22/110) in patients aged less than 49 years, 37% (69/188) in those aged 50-69 years, and 41% (22/ 54) in those aged over 70 years. Other clinical features and the prevalence of other hepatitis viral markers tested did not differ between patients with TTV DNA and those without it. The detection rate of hepatitis C virus (HCV) and hepatitis G virus (HGV) viremias increased with duration of hemodialysis and with the number of blood transfusion units, but the prevalence of TTV viremia did not. Twenty-nine of 91 patients followed for 5 years were initially positive for TTV DNA. Of these 29 patients, 17 (59%) carried this viremia for at least 5 years. Fourteen of the 62 patients (23%) who were initially negative for TTV DNA acquired TTV viremia. Serum alanine aminotransferase (ALT) levels were elevated in patients with HCV viremia but not in patients with HGV or TTV viremia. However, the mean ALT level in patients with all three viremias (HCV, HGV, and TTV) was significantly higher than that in patients with one or two of the viremias. More than 30% of the hemodialysis patients had TTV viremia and the carrier state was maintained for years. The hemodialysis procedures, including blood transfusion, did not seem to be crucial for the transmission of TTV. The pathogenic effects of TTV on hepatitis appear to be limited.
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PMID:Transmission of and liver injury by TT virus in patients on maintenance hemodialysis. 1021 36

The aim of this study was to detect hepatitis G virus RNA (HGV RNA) and antibodies against the virus envelope protein E2 (anti-E2) in 107 patients either on maintenance haemodialysis (n = 78) or peritoneal dialysis (n = 29) to evaluate the prevalence of HGV infection and to establish its role in liver disease. The total prevalence of HGV infection was of 15.4% among haemodialysis patients, whereas it was 10.3% among peritoneal dialysis patients. HGV RNA was detected in 2 haemodialysis patients (2.6%) and in 3 peritoneal dialysis patients (10.3%). Anti-E2 was found in 10 haemodialysis patients (7.8%), whilst all peritoneal dialysis patients resulted negative. In only 1 patient the alanine aminotransferase level was elevated. This patient underwent liver biopsy that did not reveal evidence of chronic hepatitis. The lower HGV prevalence in haemodialysis patients, when compared with data reported by other European authors, should be related to the lower rate of polytransfused patients in our series (29.5%). Multiple blood transfusions should be considered as the main factor to explain the different prevalence of HGV infection among various European dialysis centres. Detection of both antibody and viraemia is important to establish the real rate of the infection.
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PMID:Hepatitis G virus infection in haemodialysis and in peritoneal dialysis patients. 1022 79

The concept of chronic hepatitis induced by alcohol (AL-CH) has not been widely accepted, because AL-CH may be due to non-A-E hepatitis virus in heavy drinkers. Recently, hepatitis G virus (HGV) was identified as a positive-strand RNA virus related to members of the Flaviviridae family. In this study, we determined serum HGV in patients with AL-CH and analyzed the clinicopathological changes after abstinence to evaluate whether AL-CH is caused by alcohol or not. Serum samples were obtained from 16 patients with AL-CH who had neither hepatitis B nor C virus. The diagnosis was confirmed histologically. In eight patients, liver biopsy was performed twice, within 3 days and 4 to 8 weeks after abstinence. The NS3 region of the HGV genome was detected using an reverse transcriptase-polymerase chain reaction method. Serum levels of AST, ALT and gamma-glutamyltranspeptidase were measured once a week sequentially after admission. Serum HGV-RNA was detected in only one patient with AL-CH (6.3%). In all patients, including one patient with HGV, serum levels of AST, ALT and gamma-glutamyltranspeptidase clearly decreased to normal levels after abstinence. Inflammatory activity in the periportal area of patients with actively drinking decreased or disappeared after abstinence for 4 to 8 weeks. These results suggest that HGV may not play an important role for development of AL-CH, and that AL-CH may be caused by alcohol itself, although a more larger number of patients with AL-CH are needed to obtain definitive conclusions.
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PMID:Clinicopathological study of chronic hepatitis induced by alcohol with or without hepatitis G virus. 1023 75

In a 4-year follow-up study, patients with acute sporadic non-A, non-B (NANB) hepatitis were evaluated to determine the etiology and natural history of the disease. Acute hepatitis C virus (HCV) was detected in 13 of 43 (30%) of patients, anti-hepatitis E virus (HEV) IgG in 5 (12%), and 25 (58%) were considered non-A-E. The HCV RNA was detected in all HCV patients but none of the non-A-E cases. The initial clinical and biochemical presentation of the HCV and non-A-E cases was quite similar, although 2 of the non-A-E patients had severe disease. The 5 patients who were found to be anti-HEV IgG-reactive recovered within 6 months of follow-up. Of the 13 HCV cases, alanine transaminase (ALT) levels returned to normal in 7 (53. 8%), while 6 (46.2%) continued to show abnormal ALT after 6 months of follow-up. However, 9 (69.2%) of them remained HCV-RNA-positive, denoting virological/biochemical dissociation. Long-term follow-up showed a reappearance of HCV RNA in 2 of the 4 patients who were in virological remission performing 84% of chronicity rate. Acute non-A-E hepatitis patients were less likely to evolve toward chronicity, as compared with acute HCV cases (16% vs. 84%; P =.0001). Only 4 (16%) of the non-A-E patients were hepatitis G virus (HGV)-RNA-positive. Concerning risk factors for acquiring parenterally transmitted viruses, tattooing was the only one that could be associated with HCV transmission (P =.002). No risk factors could be identified for putative non-A-E virus transmission. Liver biopsies performed for chronic HCV patients showed a variable degree of inflammation, while the non-A-E patients presented less severe histological disease.
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PMID:Acute sporadic non-A, non-B hepatitis in Northeastern Brazil: etiology and natural history. 1038 69

The aim of the present study was to investigate the prevalence of hepatitis G virus (HGV) and also hepatitis C virus (HCV) infections in maintenance haemodialysis patients, and to identify extrahepatic sites as HGV reservoirs. HGV RNA was detected in the serum of 6/61 (10%) patients and in the peripheral blood mononuclear cells of 2/61 (3%) patients (one of whom was serum negative). These findings suggest that lymphoid cells constitute an extrahepatic HGV reservoir. HCV RNA was detected in 7/61 (11%) patients. Five of these patients (71%) were identified as carrying HCV genotype 1b. Co-infection with HCV and HGV was detected only in one patient. Haemodialysis patients are at risk for HGV infection, by nosocomial routes or via transfusions. HGV itself does not seem to be an important cause of hepatitis since all six HGV RNA positive patients not co-infected by HCV or HBV showed normal ALT values.
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PMID:Detection of HGV in serum and peripheral blood mononuclear cells of maintenance haemodialysis patients. 1038 66

An 82-year-old male patient was admitted for liver dysfunction. Laboratory test showed the following data; aspartate aminotransferase (AST) 79 IU/l, alanine aminotransferase (ALT) 28 IU/l, total bilirubin (T. Bil) 0.9 U, zinc sulfate turbidity test (ZTT) 48.9 U, gamma-globulin 4.9 g/dl, immunoglobulin G (IgG) 5,046 mg/dl, anti-nuclear antibodies x 320, anti-mitochondrial antibodies (-), hepatitis B virus surface antigen (HBsAg) (-), HBcAb (-), anti-hepatitis C virus (anti-HCV) (-), hepatitis C virus (HCV-RNA) (-), anti-hepatitis G virus (anti-HGV) (-), alpha-fetoprotein 306.8 ng/ml, carcinoembryonic antigen (CEA) 2.3 ng/ml, carbohydrate antigen (CA) 19-9 77.2 U/ml. Abdominal ultrasonography and computed tomography showed a large mass occupying most of the right lobe and portal thrombosis in the liver. Liver biopsy revealed cirrhosis with inactive hepatitis in the nontumorous lesion and well-differentiated hepatocellular carcinoma in the tumorous lesion. We report a rare case of an aged male patient with autoimmune hepatitis complicated by hepatocellular carcinoma.
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PMID:An aged male patient with autoimmune hepatitis complicated by hepatocellular carcinoma. 1039 80

The objectives of this retrospective study were to determine the prevalence of hepatitis G virus (HGV) infection in hepatitis C virus positive (HCV+ve) renal transplant (RT) patients and to evaluate the impact of HGV both on liver function tests, liver histology tests and renal parameters such as the prevalence of acute rejection and renal function. Seventy-one HCV+ve renal transplant patients with a functioning graft for whom a post renal transplant liver biopsy was available, were included. Serum HGV RNA was assessed by reverse transcription polymerase chain reaction before, at the time of, and after renal transplantation. A total of 21 (30%) of the HCV+ve RT patients had a positive HGV RNA (Group 1); seventeen of these patients (81%) were already HGV RNA+ve when the most recent renal transplantation was performed. The other 4 patients became HGV RNA+ve following renal transplantation. The mean duration of HGV infection was at least 119 +/- 64 months (18-240). Patients in group 1 did not statistically differ from the 50 HGV RNA-ve/HCV+ve RT patients (Group 2) according to sex ratio; time on dialysis; number of blood transfusions; HLA matching; the duration of HCV infection; duration and type of immunosuppression or levels of liver enzymes i.e. aspartate aminotransferase, alanine aminotransferase and gamma glutamyl transpeptidase; serum HCV RNA concentration; or frequency of genotype 1b. However, Group 1 patients were statistically younger (41 +/- 10 y compared to 47 +/- 10 y; p = 0.016) than Group 2 patients. Liver histology showed a significantly lower degree of fibrosis in Group 1 (0.4 +/- 0.5) than in Group 2 (1 +/- 1.2; p = 0.02); two patients from Group 2 but none of Group 1 had overt cirrhosis. Conversely, the extent of hepatic inflammation and hepatocellular necrosis was not statistically different between the two groups. The number of patients who experienced at least one acute rejection episode was significantly higher in Group 1 (76.2%) than in Group 2 (46%; p = 0.02), although the difference was no longer significant in the multivariate analysis. In conclusion, this study shows that: i) HGV infection was often present when the patients seroconverted for HCV; ii) HGV RNA+ve/HCV+ve RT patients experience acute rejection more frequently than HGV RNA-ve/HCV+ve RT patients; iii) HGV infection seems to have no detrimental effect upon liver enzymes or liver histology in HCV+ve RT patients.
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PMID:[Long-term consequences of co-infection by hepatitis G virus in hepatitis c virus infected kidney transplant patients]. 1041 7


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