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)

Cloning and expression of hepatitis C virus have allowed the development of immunoassays to detect hepatitis C virus infection. However, currently available recombinant fusion protein C100-3 assays, based on a nonstructural protein of the virus, are limited in sensitivity, particularly for detecting acute infection. In this report seroconversion panels showed that an assay based on synthetic peptides, derived from immunodominant regions of both capsid and nonstructural proteins, accelerated hepatitis C virus antibody detection by 4-10 weeks. In screening, this enzyme immunoassay increased detection from 47% to 64% in plasmapheresis donors with elevated alanine aminotransferase levels (greater than 100 international units per liter), from 15% to 24% in anti-hepatitis B core antigen-positive blood donors, and from 28% to 42% in renal dialysis patients when compared with nonstructural peptide-based assays. The screening assay was repeatedly reactive for 27 of 2902 volunteer blood donor samples (0.93%); four sera reacted only with the capsid antigen. The peptide test distinguished true from false positive results in agreement with recombinant immunoblot assay in 96% of blood donor samples repeatably reactive on a recombinant hepatitis C virus enzyme immunoassay.
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PMID:Improved serodiagnosis of hepatitis C virus infection with synthetic peptide antigen from capsid protein. 185 Aug 34

We performed an epidemiological study of the hepatitis C infection on 112 patients of 3 urban hemodialysis units using a recently developed anti-HCV recombinant based assay. Eleven patients (9.8%) were positive for anti-HCV. Among them, 8 (72.7%) were positive for anti-HBc, one of whom was HBsAg positive and 6 of whom were also anti-HBs positive. Surprisingly, all of the anti-HCV (+) patients were normal alanine aminotransferase. The mean age of the anti-HCV (+) patients was 50.7 +/- 3.3 (mean +/- SE) and that of the anti-HCV (-) was 47.6 +/- 1.3. The mean duration (month) of hemodialysis of the anti-HCV (+) and anti-HCV (-)groups were 52.7 +/- 7.2 (mean +/- SE) and 60.9 +/- 9.7, respectively. The prevalence of anti-HCV among anti-HBc positive subjects was 9.5% and that among anti-HBc negative subjects was 17.6%. This didn't have any statistical significance according to the criteria of the study (p = 0.308). The prevalence of anti-HCV among the transfusion positive group was 11.0% and that of the transfusion negative group was 7.7%. This data showed the tendency for a higher prevalence of anti-HCV among the transfusion positive group, but this also didn't reach statistical significance (p = 0.424). Of the 40 normal controls, none were anti-HCV positive. The prevalence of HBsAg in our hemodialysis units was 12.5%. This rate was not so much higher than the average population in Korea. The prevalence of anti-HCV and previous hepatitis B virus infection also had no significant relationship.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatitis C infection in hemodialysis units. 196 82

Patients with severe Lassa fever have high serum levels of liver enzymes. Studies of the histology of the liver have shown only minor alterations, seemingly insufficient to account for death. Pichinde virus is an arenavirus which causes severe illness similar to Lassa fever in strain 13 guinea pigs, but does not cause severe illness in man. This can serve as a relatively safe model for studying the pathology and pathophysiology of fatal arenaviral infection. We used this infection to evaluate the effect of arenavirus on liver morphology and function. When guinea pigs were infected with Pichinde virus, all developed severe disease and died within 14 days of infection. The animals lost large amounts of weight. Higher levels of virus were detected in the liver than in serum. Aspartate aminotransferase and alanine aminotransferase were elevated late in the course of the disease; no elevations were seen in gamma glutamyl transpeptidase or bilirubin. Alkaline phosphatase, initially high in these growing animals, was markedly decreased early in infection. Prothrombin time and activated partial thromboplastin time were increased late in the disease, and decreased levels of Factors VIII and IX were seen relatively early. Fatty metamorphosis, indicating problems in lipid processing, occurred by day 11, but necrosis was minor and occurred late. Pichinde virus infection results in significant alterations in the metabolic and synthetic capacities of the hepatocytes early in infection in the absence of significant necrosis.
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PMID:The effect of an arenavirus infection on liver morphology and function. 197 92

Eight women with chronic hepatitis C virus (HCV) infection during pregnancy gave birth to 11 children. Five of these children had elevated ALT, but only two had increased levels in more than one sample. All children tested before 6 months of age were positive for anti-HCV at most up to 7 months of age and then became negative. One child with a maximum ALT level of 8.4 mukat/l however, regained anti-HCV positivity at 12 months of age, and a liver biopsy at 21 months of age showed resolving hepatitis. Passively acquired HCV antibodies are obviously found in newborns of anti-HCV-positive mothers with chronic hepatitis. In 1 of 11 children, active anti-HCV production and concomitant liver disease suggested mother to infant transmission of hepatitis C virus infection.
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PMID:Mother to infant transmission of hepatitis C virus infection. 211 72

During the last week of December 1989, an outbreak of respiratory system infection involved 32 hospital personnel and 2 patients was detected in Gazi University Medical Faculty Hospital. White blood cells count of the patients were either normal or there were a slight leucopenia. Throat cultures of the most patients were normal. Serum ASO, CRP, bilirubin, AST and ALT were usually within normal limits. According to symptoms, signs and laboratory data we considered a viral disease, especially influenza. All patients recovered without any sequelae. Of 34 in-patients, 8 paired sera, 2 acute phase sera, and 10 convalescent phase sera were tested for the presence of Hemagglutination Inhibition (HI) antibody to three influenza virus strains recommended by WHO in the 1989-1990 season: Influenza A/Taiwan/1/86 (H1 N1), Influenza A/Shanghai/11/87 (H3 N2), Influenza B/Victoria/2/87. All of the sera were negative for Influenza B/Victoria/2/87. There were no significant rises in HT antibody titer for Influenza A/Taiwan/1/86 (H1 N1). The sera for 4 of 8 patients examined both acute and convalescent phase sera had fourfold or greater rise in HI antibody for Influenza A/Shanghai/11/87 (H3 N2). Four patients examined only convalescent sera had 1/40 or greater rises in HI antibody for this influenza subtype. It was considered that this influenza outbreak was probably caused by Influenza A/Shanghai/11/87 (H3 N2).
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PMID:[An outbreak of influenza in hospital personnel]. 228 92

The aim of this study was to evaluate the long-term outcome of chronic hepatitis B in 27 children who had increased alanine aminotransferase activity and antibody to hepatitis B e antigen in serum from the time of their first clinical observation. Initial histologic changes were consistent with chronic active hepatitis in 13 cases (three with associated cirrhosis) and with persistent or lobular hepatitis in the remaining cases. On the basis of virologic testing, three groups of patients were identified: (1) two children had hepatitis delta antigen in the liver and anti-delta antibody in serum, and both had severe hepatitis; (2) 10 children had hepatitis B virus DNA in serum, and 60% of them had active hepatitis; (3) 15 patients had no hepatitis B virus DNA, and 33% of them had active hepatitis. During a follow-up period of 12 months to 12 years (mean +/- SD: 6.1 +/- 2.4 years), the disease remained active in both children with anti-delta antibody, but they had no major complaints. In all eight patients who could be followed in group 2, test results became negative for hepatitis B virus DNA and alanine aminotransferase activity normalized within 4 years; biochemical remission was delayed in three patients with higher hepatitis B virus DNA levels on entry, and one of these patients had a severe exacerbation of disease activity before remission. In group 3, a total of 10 patients (71%) achieved biochemical remission within 1 year, and two within 26 months; only two patients, who were transfused at birth, had long-lasting liver damage. These results indicate a trend to early remission of liver disease in children with chronic hepatitis B with antibody to hepatitis B e antigen without delta virus infection. Antiviral therapy aimed at accelerating the termination of hepatitis B virus replication may be indicated only in those with higher levels of hepatitis B virus DNA.
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PMID:Long-term evolution of chronic hepatitis B in children with antibody to hepatitis B e antigen. 231 1

Hepatitis B core antibody (anti-HBc) has recently been recognized as a paradoxical (surrogate) marker for non-A, non-B hepatitis agents in donated blood. We studied prospectively the hepatitis B virus antigen and antibody status and liver functions in 63 uremic patients admitted consecutively to our dialysis program. Nineteen percent of uremic patients, negative for hepatitis B surface antigen (HBsAg), hepatitis B virus surface antibody (anti-HBs), hepatitis B virus DNA, and antibody to delta agents, had anti-HBc in their sera at the time of admission to maintenance dialysis. This prevalence was significantly higher than that of the medical personnel working in the dialysis unit (P = 0.043) and healthy controls (P = 0.027). The prevalence of persistent presence of isolated anti-HBc increased to 31% in these uremic patients on long-term maintenance dialysis. Four patients had developed anti-HBc alone during their course of maintenance dialysis, and the appearance of anti-HBc was preceded by blood transfusion within 4 to 8 weeks. Transient or recurrent hepatic dysfunction occurred in three of these four patients. Patients with isolated anti-HBc were characterized by a higher incidence of repeated liver dysfunction (P less than 0.005), elevated alanine transaminase levels (P less than 0.005), and a higher transfusion requirement (P less than 0.01). Our data strongly suggest that these patients with isolated anti-HBc may have acquired either hepatitis B virus infection or non-A, non-B hepatitis through repeated blood transfusions despite careful screening of the donated blood to exclude transmission of hepatitis B virus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isolated presence of antibody to hepatitis B core antigen in dialysis patients: occurrence of subclinical hepatitis? 249 42

The laboratory data from 136 patients suffering from a mass outbreak of rubella were serially examined. Alteration of thrombocytopenia (38.7%), leukopenia (26.4%), increased LDH (94.3%), and increased GOT (32.4%) were observed during the early days of disease. Slightly later, increased GPT was noted in 48.5%. LDH isozymes may be grouped into two specific patterns: 1) an LDH3 dominant pattern appeared (90.4%) during the beginning days of the disease. 2) an LDH3 dominant pattern with LDH5 greater than LDH4 was detected one week later. It was concluded that the increase of LDH3 may have been induced by thrombocytopenia due to viral infection. The increase of LDH5 appears to result from liver damage. In conclusion, LDH isozyme findings are significant in the early diagnosis of liver damage in rubella.
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PMID:[Significance of LDH isozyme pattern in rubella]. 258 78

Humoral and cell-mediated immune response to antigens of hepatitis B (HBsAg and HBeAg), delta-virus, rubella, and measles viruses was studied. Detection in a number of patients with rheumatoid arthritis of HBsAg and HBeAg in blood sera permits a conclusion that productive virus infection is formed in such patients. At the same time in patients with rheumatoid arthritis areactivity of immunocytes to HBsAg and HBeAg was found while marked sensitization of lymphocytes to rubella virus antigens was demonstrated. The patients with rheumatoid arthritis, however, do not develop mere long-term carrier state of hepatitis B virus but form primary chronic hepatitis as a consequence of virus infection. This is indicated by an increase in the level of alanine aminotransferase (1.6 +/- 0.8 mmol/l) and detection of antibody to delta-virus in such patients (28.6%).
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PMID:[Persistence of viruses in rheumatoid arthritis]. 272 9

NANB hepatitis was initially recognized in 1975 and 13 years later, the exact etiology of this presumed viral disease remains uncertain. The acute illness is relatively mild with only about 25% of patients becoming icteric. Nevertheless, at least one half of the patients have evidence of chronic infection, and, as recently recognized, 10% to 20% develop severe liver disease. Because approximately 2% of patients who receive transfusions and whose underlying medical condition permits long term follow-up develop posttransfusion hepatitis, procedures for reducing this risk are considered prudent. Unfortunately specific tests for detecting NANB hepatitis are not available, and it is unlikely that such tests will be available in the near future. Hence, testing by surrogate or nonspecific tests (ALT and anti-HBc) were recommended because evidence from two studies conducted during the 1970s showed these tests identify some donors thought to transmit the infection. However, randomized, controlled prospective studies to determine whether these tests will, in fact, reduce NANB posttransfusion hepatitis were not performed. By the mid-1980s it was apparent these studies would not be performed nor were studies to determine the incidence of NANB posttransfusion hepatitis in the post-AIDS screening era likely to be initiated. Therefore, surrogate testing, as the best available method for reducing posttransfusion hepatitis, was implemented in the United States in 1986-87.
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PMID:Rationale for surrogate testing to detect non-A, non-B hepatitis. 298 81


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