Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe liver damage revealed by a sharp transaminase elevation may be seen in patients with leukemia. This may be due to several possible causes, including viral hepatitis, chemotherapy-induced hepatotoxicity and leukemic infiltration. HCV infection may be suspected to play a relevant role as these patients are often heavily transfused after the onset of their hematologic disorder. We have therefore examined the role of HCV in 15 children with leukemia who developed severe liver damage shortly after the diagnosis of leukemia. All patients were tested for HCV-RNA by the polymerase chain reaction at the time of peak SGPT elevation and for anti-HCV on serial serum samples taken thereafter. Only one patient (6.6%) showed hepatitis C viremia and none developed confirmed anti-HCV positivity during follow-up, suggesting that HCV had not played a major role in causing these severe episodes of liver necrosis. This is in agreement with observations made in non-immunocompromised patients in whom fulminant hepatitis is only exceptionally due to HCV.
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PMID:Evidence against the role of hepatitis C virus in severe liver damage occurring early in the course of acute leukemia in children. 751 43

Fourteen patients who developed acute post-transfusion hepatitis C after open-heart surgery were studied for seroconversion, viremia, and aminotransferase. Anti-HCV antibodies were measured by first and second generation ELISA and became positive between one week and more than 6 months after infection. Seroconversion in four patients and passively transfused antibodies were only found by the second generation assay, indicating its significantly higher sensitivity. Viremia was detected by reverse transcription and the polymerase chain reaction within the first 4 weeks of infection in 13 patients and persisted for more than 2 years in all of them. One patient died of cardiac cause. Viral strains were heterogeneous between the different patients, but showed no significant variation within one patient during the course of hepatitis deduced from the results with different sets of oligonucleotides. Viremia preceded hepatitis by 4 weeks, seroconversion determined by ELISA II followed after an 8 week interval, and anti-C-100 antibodies appeared 26 weeks later. Aminotransferase activities returned to normal values in 10 patients.
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PMID:Antibodies and viremia in acute post-transfusion hepatitis C: a prospective study. 751 52

A nested polymerase chain reaction was used to assess viraemia in blood transfusion recipients with no serological evidence of hepatitis C virus (HCV) infection (naive recipients) and in recipients with prior or existing HCV infection (infected recipients), who were transfused with HCV-positive blood. In 10 hepatitis cases in naive recipients, defined as primary infection, nine showed clinical hepatitis, and one was sub-clinical; the time between transfusion and elevation of alanine aminotransferase (ALT) levels was 15-60 days (37.9 +/- 13.9). All 10 naive recipients showed abnormal ALT, and 10/10 and 7/10 were persistently positive for anti-HCV and HCV-RNA, respectively, for more than 1 year. Similarly, in five cases in previously infected recipients, defined as re-infection, 4/5 showed clinical hepatitis, the time to elevation of ALT was 30-46 days (34.8 +/- 6.4), and 5/5 and 3/5 were persistently positive for anti-HCV and HCV-RNA, respectively, for more than 1 year. All five infected recipients showed abnormal ALT. In conclusion, there was no significant difference (P = 0.05) in the frequency of the markers of infection resulting from primary or re-infection with HCV, suggesting that primary infection fails to induce a protective immune response.
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PMID:A study of primary- and re-infection with hepatitis C virus in blood transfusion recipients. 751 93

Antibodies to hepatitis C virus (HCV), investigated by second- and third-generation assays, were detected in 74% of 43 children with chronic non-A, non-B hepatitis. The polymerase chain reaction identified HCV ribonucleic acid in 26 (93%) of 28 seropositive and in 1 of 10 seronegative cases. Intermittent HCV ribonucleic acid positivity, suggesting low and fluctuating viremia, was frequent in younger patients.
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PMID:Patterns of antibodies to hepatitis C virus and hepatitis C virus replication in children with chronic non-A, non-B hepatitis. 752 49

Persistent viremia after clinical or subclinical hepatitis C virus (HCV) infection is believed to occur in patients with chronic hepatitis C, but little is known about the duration of HCV replication in patients with acute hepatitis who have recovered or the relation of HCV viremia with the kinetics of antibodies to HCV (anti-HCV). We tested HCV-RNA and anti-HCV in serial serum samples from 41 patients with posttransfusion non-A, non-B hepatitis, followed for an average of 6 years after transfusion. Serum HCV-RNA was measured by nested polymerase chain reaction, which used primers from the 5' untranslated region of the HCV genome. Anti-HCV were tested with first- and second-generation enzyme-linked immunosorbent assays (ELISA 1 and ELISA 2), and with a second-generation recombinant immunoblot assay. Of the 41 patients, 10 recovered and 31 progressed to chronic liver disease. HCV-RNA was detected in serum before or simultaneously with the onset of hepatitis in all cases, and lasted between 2 and 6 weeks in 5 of the 10 patients who recovered, whereas it persisted for the entire follow-up period in every case with chronic hepatitis and in the remaining 5 patients with self-limiting hepatitis. Anti-HCV were detected with ELISA 2 in the first serum sample, with raised serum transaminases in 57% of patients, but in only 6% with ELISA 1. In the sample obtained 1 month after the onset of hepatitis, anti-HCV were detected with ELISA 2 in 94% of patients, but in 34% with the ELISA 1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistent hepatitis C viremia after acute self-limiting posttransfusion hepatitis C. 753 21

The prevalence of HBV recurrence after liver transplantation is higher in patients with viral B cirrhosis than in patients with viral B-D cirrhosis or fulminant hepatitis B and is related to the presence of HBV replication prior to transplantation. Long-term passive anti-HBs immunoprophylaxis is the best current way for prevention of HBV reinfection and improved long-term survival. The rate of recurrence of HCV infection is high, reaching 85%, and the rate of HCV hepatitis in the graft is approximately 75%. In most cases, HCV hepatitis leads to chronic hepatitis. The severity of graft hepatitis is related to the level of viremia at the time of the hepatitis and to the genotype 1b. The methods of prevention of HCV infection after liver transplantation are yet to be found. The treatment of graft HCV infection with interferon should be well evaluated and given cautiously. Other antiviral treatments without an immunostimulating effect are needed. Finally, patients transplanted for hepatitis B without HBV replication, receiving posttransplant long-term anti-HBs immunoprophylaxis, and those transplanted for HCV cirrhosis have a 5-year survival similar to other groups of transplanted patients. Patients belonging to these groups can be considered as candidates for transplantation. Patients with active HBV replication should be included in specific trials for prevention of HBV reinfection.
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PMID:Liver transplantation for viral hepatitis: the experience of the hepatobiliary center at Hospital Paul Brousse. 754 34

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

We prepared a hepatotropic conjugate, suitable for intramuscular (IM) injection, of lactosaminated poly-L-lysine with adenine arabinoside monophosphate (ara-AMP), a drug active against hepatitis B virus (HBV). We studied its organ distribution in mice and its antiviral activity in woodchucks that are carriers of woodchuck hepatitis virus (WHV). In mice, after IM administration of a conjugate tritiated in the drug moiety (5.2 micrograms/g equal to 2 micrograms/g of ara-AMP) radioactivity in liver was three times greater than in kidney, spleen, and intestine. On the contrary, after IM injection of unconjugated, tritiated, ara-AMP (5 micrograms/g) the amounts of radioactivity in liver, spleen, and kidney were similar. Unconjugated ara-AMP and the conjugate were administered IM to woodchucks for 13 days. Unconjugated ara-AMP decreased viremia at the daily dose of 5 mg/kg but was ineffective at 2.5 mg/kg. The conjugate at the daily doses of 4.2 and 7 mg/kg (equal to 1.5 and 2.5 mg/kg of ara-AMP, respectively) markedly lowered the viremia, which decreased to undetectable levels in the animals treated with the higher dose. Assuming that in HBV-infected patients the same doses will be active, then the amount of conjugate (soluble at 200 mg/mL) required by a 70-kg patient will be contained in a volume of 1.5 to 2.5 mL, compatible with the IM route. Compared with a similar ara-AMP complex with lactosaminated human albumin, currently being studied in clinical trials for the treatment of chronic type B hepatitis, which must be infused intravenously, the present conjugate might provide more patient compliance because of IM administration.
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PMID:Inhibition of woodchuck hepatitis virus replication by adenine arabinoside monophosphate coupled to lactosaminated poly-L-lysine and administered by intramuscular route. 755 53

Hepatitis delta virus (HDV) encodes only a single protein, the hepatitis delta antigen (HDAg), which is expressed as two molecular forms (large and small) with different functions in viral replication. Compared with small antigen, large antigen has a 19 residue carboxyl terminal extension. Antibodies that recognize a large antigen-specific epitope within this carboxyl extension, or an epitope shared by both large and small antigens (total antigen), were used in immunohistochemical studies of liver sections from superinfected woodchuck carriers of woodchuck hepatitis virus. There were no differences in the subcellular distributions of large and total antigens, with both generally present only in nuclei of hepatocytes. Rare cells demonstrated cytoplasmic staining. Complete or partial granular nucleoplasmic staining with stained nucleoli was the most common pattern observed. Within 31 days of infection, 0.1% to 19% (mean = 7.4%) of all hepatocytes contained antigen. The proportion of these nuclei containing large antigen ranged from 0 to 100% (mean, 39%), and increased during the first month of infection. The number of antigen-positive nuclei and the proportion staining for large antigen were reduced with progression to chronicity, correlating with reductions in the level of viremia. Thus, the large hepatitis delta antigen shares a common subcellular distribution with small antigen and is found in an increasing proportion of the nuclei of infected cells during the course of acute infection.
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PMID:Subcellular distribution of large and small hepatitis delta antigen in hepatocytes of hepatitis delta virus superinfected woodchucks. 755 56

Precore/core genes from hepatitis B e antigen (HBeAg)-positive and antibody to HBeAg (anti-HBe) positive individuals with active hepatitis have been analyzed to search for correlations with response to interferon before and after treatment. Pretreatment, no precore stop codon mutants were detected, even at the 3% level, in HBeAg-positive responders or nonresponders. In anti-HBe-positive patients, precore mutants did not influence response. No significant core amino acid variability was observed in HBeAg-positive patients, irrespective of interferon response. However, anti-HBe-positive cases had multiple core protein substitutions, mostly in B- ant T-helper cell epitopes, but responders had fewer (P = .02 for responders versus nonresponders and reactivators). None of four responders, three of seven reactivators, and three of three nonresponders had mutations within the major T-helper epitope from aa50 to aa69 (P = .03). Precore mutants appeared in eight of nine natural seroconverters compared with 3 of 10 interferon-induced anti-HBe seroconverters (P = .01). Those in whom precore wild-type remained after treatment often tested negative in the last available sample using polymerase chain reaction (PCR), whereas emergence of mutants led to ongoing viremia in all cases. In anti-HBe-positive cases, precore sequences remained stable during therapy, except for 2 cases in whom a precore mutant appeared accompanied by reactivation. In the core protein, anti-HBe-positive cases selected a mean of 3.5, 1.6, and 1.7 amino acid substitutions in responders, nonresponders, and reactivators respectively (P = NS). In conclusion, core but not precore sequence before therapy may predict response. Appearance of precore mutants during therapy usually predicts failure to clear virus but substitution in core does not influence outcome.
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PMID:Hepatitis B virus precore/core variation and interferon therapy. 759 Jun 47


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