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)

Two hundred cases of various kinds of viral hepatitis and hepatocellular carcinoma were tested for serum anti-HCV. The positive rates of anti-HVC in patients with severe hepatitis and patients with cirrhosis were 42.86% and 46.15%, respectively. They were significantly higher than those in patients with other kinds of hepatitis (P < 0.05). The positive rate of anti-HCV was 67.5% in patients with posttransfusion hepatitis, 20.47% in healthy blood donors. In posttransfusion hepatitis B it was only 2.5%. Our results demonstrated that blood transfusion played an important role in transmitting HCV. Our findings also indicated that dual infection of HBV and HCV was important in the course of chronic hepatitis, cirrhosis and severe hepatitis. 50% of the anti-HCV positive patients with chronic hepatitis had slightly elevated serum alanine aminotransferase level. This showed that liver damage caused by HCV may be a chronic course.
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PMID:[The anti-HCV assay in viral hepatitis and hepatoma and the relationship between HCV infection and blood transfusion]. 753 55

Techniques of enzyme-linked immunosorbent assay based on synthetic multiple peptide fragments and second generation recombinant immunoblot assay (RIBA) were used to study the patterns of specific antibody response in 10 cases of posttransfusion hepatitis (PTH) during a period of 36-38 weeks after blood transfusion. Nine cases were positive with serum anti-HCV, including 8 cases positive with serum HCV-RNA. Antibodies to core protein of HCV showed a higher positive rate and were detected 1-3 weeks earlier than those to the putative nonstructural (NS) protein. Anti-HCV IgM to core protein were detected 1-4 weeks earlier than anti-HCV IgG and the detective absorbent values of anti-HCV IgM were positively correlated with the levels of serum ALT (P < 0.01). "Passive transfer" of anti-HCV were found in 3 cases. These facts suggest that HCV is the major causative agent of PTH cases in our district and anti-HCV IgM to core protein is a putative serological marker not only for early diagnosis of HCV infection but also for demonstration of active HCV infection.
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PMID:[A study on the patterns of early specific antibody response in patients with posttransfusion hepatitis C]. 753 48

Screening of blood donors by testing for antibody to HBcAg and antibody to hepatitis C virus is commonly done. However, the applicability of these screening tests may vary depending on the prevalence of hepatitis B virus and hepatitis C virus infection in various populations. We have therefore prospectively evaluated 158 adult patients who received blood or blood products during open-heart surgery in Hong Kong to compare the efficacy of various serological screening tests in the prevention of posttransfusion hepatitis. Serum from five (0.5%) donors was positive for antibody to hepatitis C virus by second-generation enzyme immunoassay; in two, optical-density readings in enzyme immunoassay were greater than 2.0, but only one was positive for hepatitis C virus RNA by reverse transcription-polymerase chain reaction. The latter donor was also positive for antibody to HBcAg and had elevated serum ALT activity. The recipient of a unit of this donor's blood was the only one in whom posttransfusion hepatitis C developed (0.1% per unit transfused). Screening with antibody to hepatitis C virus was more specific than that with antibody to HBcAg or ALT in excluding donors from transmitting hepatitis C (99.6%, 79.4% and 98.8%, respectively). Both the sensitivity and negative predictive value of screening for antibody to hepatitis C virus were 100%, but the positive predictive value was only 20%. Forty-five blood recipients were considered susceptible to hepatitis B virus infection because testing for hepatitis B serology in serum (HBsAg, antibody to HBsAg and antibody to HBcAg) was negative before being transfused. Asymptomatic hepatitis B seroconversion developed in three (6.7%) recipients (1.1% per unit transfused).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of posttransfusion hepatitis B and C by screening for antibody to hepatitis C virus and antibody to HBcAg. 769 69

Hepatitis C virus (HCV) represents a major cause of posttransfusion hepatitis worldwide. Posttransfusion hepatitis associated with hepatitis B virus (HBV) continues to occur. HBsAg-negative donor sera from the Rhode Island Blood Center between 1987 and 1988 were screened using more sensitive techniques to assess the prevalence of low level HBV infection. Group I consists of 866 healthy blood donors without HBV serologic markers, group II consists of 377 donors with ALT elevations (> 45 IU/L), group II consists of 148 donors positive for anti-HBc, and group IV consists of eight donors positive for both surrogate markers. A sensitive monoclonal immunoradiometric assay (M-IRMA) was employed for detection of HBsAg-associated epitopes (detection limit of 20 pg/ml) in serum. A subset of sera were analyzed for the presence of HBV DNA using the method of anti-HBs capture of HBV related virions in serum followed by polymerase chain reaction (PCR) amplification. Using these techniques, 0.8% and 1.7% of donors were positive for HBsAg and HBV DNA respectively in group I. In contrast, 0.9% and 9.5% in group II and 0.7% and 18.1% in group III were positive, respectively. There were eight donors with both ALT elevation and anti-HBc; and four (50%) of these were positive for HBV DNA. In the group with anti-HBc, the majority (80%) of donors with HBV DNA had either no or low (signal to noise ratio < 10) anti-HBs titer. Using anti-HCV testing and reverse transcription-PCR for detection of HCV genomes, we detected evidence of HCV infection in nine of the 49 donors with low level HBV DNA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Presence of hepatitis B and C viral genomes in US blood donors as detected by polymerase chain reaction amplification. 815 10

Hepatitis C virus (HCV) can infect peripheral blood mononuclear cells (PBMC) of patients with chronic HCV infection. No data are available on PBMC testing for HCV RNA in acute hepatitis C. This study investigated the presence of HCV RNA in PBMC of patients with acute posttransfusion hepatitis C, compared with those with chronic HCV infection. Nested polymerase chain reaction (PCR) was applied to detect HCV RNA in 111 and 48 paired samples of serum and PBMC of 11 patients with acute posttransfusion hepatitis C and 48 patients with chronic HCV infection, respectively. In patients with acute posttransfusion hepatitis C, HCV RNA was detected in 17 of 29 (59%) and 67 of 82 (82%) serum samples collected during the incubation period and acute phase, respectively. Meanwhile, of the 48 patients with chronic HCV infection, 41 had serum HCV RNA (85%). HCV RNA was not detected in PBMC samples from incubation period or from acute-phase hepatitis, although it was detected in 12 of the 48 PBMC samples of chronically infected patients (25%) P < .005). Of the 12 PBMC specimens positive for positive-stranded HCV RNA, 6 were also positive for negative-stranded HCV RNA. Among patients with chronic HCV infection, HCV infection of PBMC was not related to age, sex, blood transfusion, serum alanine transaminase (ALT) levels, or serum virus titers. In conclusion, HCV infection of PBMC rarely exists in patients with acute hepatitis C. As HCV infection persists, the incidence of HCV infection of PBMC becomes higher.
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PMID:Hepatitis C virus RNA in peripheral blood mononuclear cells: comparing acute and chronic hepatitis C virus infection. 862 Nov 78

To study the incidence and outcome of GB virus C (GBV-C) infection in blood recipients. Serum samples collected in a prospective study were examined for GBV-C RNA by a nested polymerase chain reaction assay. Among the 400 adults who underwent cardiac surgery, 40 were positive for GBV-C RNA, including six whose pretransfusion sera were already positive and seven coinfected with hepatitis C virus (HCV) during transfusion. The risk of transmission was estimated to be approximately 0.46% per donor. GBV-C viremia was detectable 1 week after transfusion and could persist for 8 years. However, no evident symptoms or signs were noted in the 25 patients infected by GBV-C alone, and the average peak serum alanine aminotransferase activity was 31 IU/L only (range, 12 to 123), with persistently normal levels in 20 patients. In the seven patients coinfected with HCV, the clinical courses of posttransfusion hepatitis were similar to those infected by HCV alone. In eight patients with posttransfusion non-A approximately E hepatitis, only one was positive for GBV-C RNA. Sixty samples were chosen to test hepatitis G virus (HGV) sequences, 26 of the 30 GBV-C positives were positive for HGV RNA in contrast to none of the 30 GBV-C negative samples. In conclusion, GBV-C can be transmitted by transfusion in approximately 9% of patients who underwent cardiac surgery. Nevertheless, this virus does not seem to cause classic hepatitis in most instances.
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PMID:A prospective study of transfusion-transmitted GB virus C infection: similar frequency but different clinical presentation compared with hepatitis C virus. 878 48

The distribution of genotypes of the hepatitis C virus (HCV) was studied in 24 children with chronic posttransfusion hepatitis C. Genotypes were determined by reverse transcription-nested polymerase chain reaction with type-specific primers. Twenty (83%) were infected by a single genotype: 14 by type II [1b], 3 by III [2a], and 3 IV [2b]. Four (17%) were coinfected by two genotypes. The amount of blood transfusion given to the patients infected by multiple genotypes was significantly larger than to those infected by a single genotype (mean +/- SD, 15.2 +/- 14.4 vs 78.6 +/- 42.0 U). Three of the four patients infected by multiple genotypes were considered to be immunocompromised by anticancer therapy for malignant disease. Eighteen patients showed a raised level of alanine aminotransferase throughout the follow-up, while the remaining six patients (three of type II [1b], two of IV [2b], and one of III [2a] + IV [2b]) achieved biochemical remission. Liver biopsy was performed on 19 patients. Compared to those with type III [2a] or IV [2b], those with type II [1b] appeared to show more severe histological changes with higher histological activity index scores, although there was no significant difference. The positive rates of antibody to C100-3 or 5-1-1 in patients with type III [2a] or IV [2b] were lower than in those with type II [1b] (33 and 33 vs 43 and 50%), whereas the antibody to C33C or C22-3 was detected in nearly all patients regardless of their genotypes. In the present study, we found a high incidence of multiple-genotype infection among children with chronic posttransfusion hepatitis C.
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PMID:Genotyping of hepatitis C virus: coinfection by multiple genotypes detected in children with chronic posttransfusion hepatitis C. 878 92

The risk of hepatitis virus transmission from tranfusions has declined dramatically from that of the 1940s when posttransfusion hepatitis (PTH) was first appreciated. Introduction of hepatitis B surface antigen screening and conversion to volunteer donors for whole-blood donations in the late 1960s and early 1970s led to substantial reduction in PTH cases. However, up to 10% of the recipients continued to develop PTH, most cases of which were attributed to an unknown non-A, non-B viral agent. Implementation of surrogate marker testing (i.e., alanine aminotransferase and anti-hepatitis B virus core antigen) for residual non-A, non-B hepatitis in the late 1980s reduced the per unit risk of PTH from 1 in 200 to about 1 in 400. Hepatitis C virus was discovered in 1989 and quickly was established as the causative agent of > 90% of non-A, non-B PTH. Introduction of progressively improved antibody assays in the early 1990s reduced the risk of PTH due to hepatitis C virus to about 1 in 100000. Although additional hepatitis viruses exist (e.g., hepatitis G virus), these appear to be minor contributors to clinical PTH, which has been virtually eradicated.
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PMID:History of posttransfusion hepatitis. 926 99

A recently identified RNA virus, hepatitis G virus (HGV), has been investigated for its role in causing non-A-E hepatitis. The frequency and clinical outcome of HGV infection in children was studied. Two hundred apparently healthy children aged 6 mo to 12 y, and 90 children who had undergone open heart surgery in a prospective study for posttransfusion hepatitis were included in this study. The serum samples were tested for HGV RNA by nested reverse transcription-PCR with primers from the 5'-untranslated region. The HGV RNA viremic rate was found to be 1% (2/200) in apparently healthy children, 30% in children after open heart surgery. Among the 90 children, three were HGV-infected before the surgery. Twenty-four (28%) of the remaining 87 children tested positive for HGV RNA within 6 mo after the surgery. Sixty-five percents of these viremic children eventually became persistently infected at 1 y after surgery. No HGV RNA-positive children exhibited elevated alanine aminotransferase levels during the follow-up period. No coinfections of HGV with the hepatitis C virus or hepatitis B virus were found. Patients of younger age appeared more likely to become chronic carriers. Anti-HCV screening did not reduce the prevalence of HGV infection. In conclusion, in children with open heart surgery, the risk of transfusion-transmitted HGV infection and the chronicity rate have been found to be high. Young age is a risk factor of persistent infection.
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PMID:Hepatitis G virus infection in normal and prospectively followed posttransfusion children. 939 58

GB virus-C/hepatitis G virus (GBV-C/HGV) is an RNA virus that can be transmitted by transfusion with the diagnosis based on the detection of serum GBV-C/HGV RNA by reverse transcription-polymerase chain reaction. In order to evaluate the role of antibodies to the E2 protein (anti-E2) of GBV-C/HGV in patients with acute posttransfusion hepatitis, anti-E2 was measured in one patient with acute GBV-C/HGV infection, five patients with acute GBV-C/HGV and hepatitis C virus (HCV) coinfection, and four patients with positive pretransfusion GBV-C/HGV RNA who were superinfected with HCV after transfusion. One patient with acute GBV-C/HGV infection remained GBV-C/HGV RNA-positive 18 months after transfusion and did not develop anti-E2. Among five patients with acute GBV-C/HGV and HCV coinfection, one lost GBV-C/HGV RNA 28 months after transfusion and developed anti-E2 independent of serum alanine aminotransferase levels. The other four patients remained GBV-C/HGV RNA-positive and anti-E2-negative at the end of follow-up. Among four patients with positive pretransfusion GBV-C/HGV RNA and super-infected with HCV, one lost GBV-C/HGV RNA 2 months and one 10 months after superinfection and subsequently developed anti-E2. The other two patients remained GBV-C/HGV RNA-positive without anti-E2 at the end of follow-up. Sixty-five samples tested were mutually and exclusively positive for either GBV-C/HGV RNA or anti-E2; only one sample was positive for both GBV-C/HGV RNA and anti-E2. In conclusion, the development of anti-E2 of GBV-C/HGV usually indicates the clearance of serum GBV-C/HGV RNA in patients with acute posttransfusion hepatitis.
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PMID:Detection of antibodies to E2-protein of GB virus-C/hepatitis G virus in patients with acute posttransfusion hepatitis. 989 Apr 27


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