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 hepatotoxicity from phenobarbital occurred in an infant boy who had a complicated illness with chronic bilateral subdural hematomas and sepsis. Skin rash began after 2 weeks of treatment, and signs of hepatocellular failure developed 3 weeks after phenobarbital had been started. Signs of severe liver disease included elevated aminotransferases, conjugated hyperbilirubinemia, significant coagulopathy, hepatosplenomegaly and ascites. Other features of this adverse drug reaction were unremitting fever, leukocytosis with eosinophilia and atypical lymphocytosis, and proteinuria. Sepsis, viral hepatitis, and metabolic liver disease were excluded. The child was on no other medication and had been previously well. In-vitro rechallenge of the patient's lymphocytes with cytochrome P-450 generated metabolites of phenobarbital showed extensive cytotoxicity compared to control. These data support the hypothesis that a defect in drug detoxification was responsible for the child's susceptibility to this drug hepatotoxicity.
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PMID:Phenobarbital hepatotoxicity in an 8-month-old infant. 233 96

In hepatitis B virus carriers who are anti-HBe positive despite ongoing viral replication (HBcAg in liver and HBV-DNA in serum) the natural course of hepatitis is severe and the response to interferon is low. We investigated whether a new hepatitis B virus (HBV) strain could be involved. A translational termination codon at the carboxyterminal end of the pre-C region responsible for the lack of HBeAg secretion was found in 18 of 19 HBV clones isolated from seven pedigreed patients with this clinical syndrome. The same findings were confirmed by direct sequencing. One of these patients underwent a liver transplant and HBV infection of the new liver resulted in high titered viremia and intrahepatic expression of HBcAg, without detectable HBeAg in serum. Another patient was superinfected by hepatitis delta virus (HDV) and developed high titres of total and IgM anti-HD. In spite of this, chronic hepatitis remained unchanged during 7 years of follow-up. These data strongly suggest that a viable precore minus mutant of hepatitis B virus is responsible for the lack of HBeAg in the serum of these patients. The HBV variant may explain the peculiar geographic distribution of anti-HBe positive hepatitis. The variations in the virus genome sequence may cause the more severe form of liver disease and modify the pathogenicity in the case of HDV superinfection.
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PMID:A new hepatitis B virus strain in patients with severe anti-HBe positive chronic hepatitis B. 233 98

We analysed the serum samples and the liver biopsies of six consecutive chronic HBsAg/anti-HBe carriers admitted to hospital because of an episode of acute hepatitis. The six patients became positive for IgM anti-HBc and negative for HBeAg, hepatitis Delta virus (HDV) markers, IgM anti-hepatitis A virus (HAV), anti-cytomegalovirus (CMV) and anti-Epstein-Barr virus (EBV). Two patients showed positivity for hepatitis B virus (HBV)-DNA in serum obtained on admission, with no positivity in the subsequent weeks; the results of the other four patients were always negative for seric HBV-DNA. The Southern-blot analysis of the DNA extracted from the liver tissue of four subjects showed the presence of HBV-DNA in the form of replicative intermediates; focal positivity of HBcAg was detected in the liver of only one. The liver biopsies of the last two patients were negative for HBV-DNA and for HBcAg. The analysis of HBV-DNA in the liver extracts and the demonstration of an increase of the IgM anti-HBc titre at the time of the abrupt elevation of the aminotransferase levels seem to be the most useful tools in revealing HBV activation as a cause of acute hepatitis in chronic HBsAg carriers, overall when the phase of viremia is transient.
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PMID:Hepatitis B virus (HBV) markers and HBV-DNA in serum and liver tissue of patients with acute exacerbation of chronic type B hepatitis. 236 78

We have used a new hybridization assay for the detection of the genome of hepatitis delta virus (HDV) in serum using a strand-specific RNA probe obtained by transcription of a recombinant riboprobe. This assay was tested on a panel of 30 sera from HBsAg carriers with hepatitis delta antigen (HDAg) in the liver. The riboprobe assay detected HDV RNA in the serum of 83% of the patients, while 63% were positive using the DNA hybridization assay. HDAg was detected in 73% of the same sera by immunoblotting. The riboprobe assay was also compared to other assays on serial samples from an experimentally infected chimpanzee. These results demonstrate that the Northern blot assay using the RNA probe is more sensitive than the homologous DNA probe for the detection of HDV in serum and is also more sensitive than the immunoblot assay for HDAg. The riboprobe assay is the most sensitive of currently available methods to measure HD viremia.
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PMID:Riboprobe assay for HDV RNA: a sensitive method for the detection of the HDV genome in clinical serum samples. 240 72

Vidarabine (ara A) produces severe dose-dependent side-effects. To examine whether its monophosphate ester (ara-AMP) can be effective in the treatment of chronic hepatitis B when given in reduced dosage as a conjugate with lactosaminated human serum albumin (L-HSA), which selectively enters hepatocytes, five patients with chronic type B hepatitis (HBsAg/HBV-DNA positive for at least 2 years) were treated with the conjugate. The daily dose of conjugate given (35 mg/kg) contains 1.5 mg ara-AMP, whereas the usual daily dose of free ara-AMP is 5-10 mg/kg. In three patients HBV-DNA fell to undetectable levels and remained negative in two; in one of them anti-HBe developed. In the other two patients HBV-DNA decreased but was detectable during treatment--one received three cycles of therapy, and became HBV-DNA negative and anti-HBe positive 45 days after the end of treatment; the other remained HBeAg/HBV-DNA positive. No adverse effects were observed, and biochemical variables (including aminotransferases) remained unchanged or decreased with viraemia. No antibodies (IgM and IgG classes) that bound the conjugate were detected. Thus L-HSA-ara-AMP inhibits HBV replication as well as free ara-AMP but at a third to a sixth of the dose.
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PMID:Inhibition of hepatitis B virus replication by vidarabine monophosphate conjugated with lactosaminated serum albumin. 245 4

Ninety-three consecutive orthotopic liver transplantations in 78 patients were followed prospectively to study the incidence of cytomegalovirus (CMV) hepatitis. CMV hepatitis occurred in 13 (17%). The diagnosis was established by both histology and culture in 5, only by histology in 6, and only by culture in 2. All 13 patients had CMV viruria and 9 had viremia at diagnosis. CMV hepatitis developed in 64% of CMV-seronegative (pretransplantation) patients who received a liver from a CMV-seropositive donor, compared with 3% or 6% of CMV-seropositive patients who received a liver from a CMV-seronegative or CMV-seropositive donor, respectively (P less than .001). CMV hepatitis was not a cause of fulminant or irreversible liver dysfunction in any of the 13 cases. Ganciclovir was administered to 6 of the 13 patients and was associated with clinical and virologic cure in 5. CMV hepatitis was self-limited in patients not treated with ganciclovir (illness less severe). The presence of inclusions within the liver tissue correlated with active disease.
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PMID:Cytomegalovirus hepatitis in liver transplantation: prospective analysis of 93 consecutive orthotopic liver transplantations. 255 24

The small and the middle surface proteins of hepatitis virus form either the virion or the 22 nm particle both of which are secreted. The large surface protein by itself remains cell bound in artificially transfected cell culture unless it is accompanied by an excess of the smaller protens. Its behavior in vivo is not yet well studied. Using specific monoclonal antibodies for immunoblotting, we found an abundance of small surface protein in the serum of chronic virus carriers and moderate amounts in the liver irrespective of viremia. The large surface protein was present in the serum and the liver of viremic carriers. In nonviremic carriers, the large protein was absent from serum, but in the liver a shorter form of the large protein was readily detectable. These findings suggest a complex regulatory mechanism of the viral surface protein depending on the expression of other viral gene products.
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PMID:Immune blot analysis of viral surface proteins in serum and liver of patients with chronic hepatitis B virus infection. 262 52

Cherry valley ducks were infected by intravenous injection of DHBV positive serum in order to study the intrahepatic distribution of DHBsAg and the relation of the degree of hepatic lesions to viremia and humoral immunologic deficiency after surgical removal of Bursa of Fabricius. The anti-DHBsAg serum prepared in our laboratory showed high specificity. There was no cross reaction with HBsAg and DHBsAg was found to be located in the cytoplasm of hepatocytes as well as bile duct epithelial cells which usually showed stronger staining quality. The histopathology of liver revealed normal/mild hepatitis in the control group, moderate/severe hepatitis in the infected group. In comparison, hepatitis in the infected group was more severe in the older ducks than the ducklings, in those viremia-positive ones than in the negative ones, and in the bursectomized than in the non-bursectomized ducks. Evidently, the hepatic lesions were mostly due to DHBV infection in this series, although some other environmental factors could not be ruled out entirely. The present investigation shows that Cherry valley ducks are one of the best spices for experimental DHBV infection, and bursectomized ducks with humoral immunodeficiency might provide a reliable and useful model for the study of pathogenesis of hepatitis B virus infection.
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PMID:[Experimental duck hepatitis B virus infection]. 277 49

The authors report 16 cases of cytomegalovirus (CMV) disease in previously healthy adults. Constant features included pyrexia lasting 3 to 8 weeks and mononucleosis occurring 2-3 weeks after the onset of fever. Moderate hepatomegaly without jaundice, splenomegaly and morbilliform or petechial rush were observed in 30 to 50 p. 100 of cases. None had pharyngitis. Mild increase in serum transaminase activity (2 to 5 N) was present in 13 of the 16 patients, but increased alkaline phosphatase activity was observed in only 3 of them. Liver biopsy was obtained in 10 patients. Liver lesions were characterised by the association of intra lobular granuloma, abundant mononuclear cells in the sinusoids and hepatic peri-venous inflammation but hepatocellular necrosis was not prominent. Typical intracellular inclusions were not seen, either in hepatocytes or in cells of biliary ducts. The diagnosis was ascertained by positive viremia and or viruria and presence of IgM antibodies. The outcome was favourable although clinical and biological signs lasted for about 8 weeks. The authors conclude that adults with chronic pyrexia, no pharyngitis and sub-clinical hepatitis with mild increases in transaminase activity and histologic mononucleosis hepatitis showing mononuclear infiltrates and granuloma formation are likely to have CMV disease.
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PMID:[Granulomatous hepatitis in cytomegalovirus infection in healthy adults]. 282 62

The efficacy and safety of ganciclovir were evaluated for the treatment of 39 life-threatening or sight-threatening cytomegalovirus (CMV) infections in recipients of bone marrow transplants (15 patients), recipients of liver or renal transplants (8 patients), patients with AIDS (11 patients), and one patient each with lymphoma or systemic lupus erythematosus. Twenty-eight (72%) of 39 CMV infections improved during ganciclovir therapy, which was associated with elimination of CMV from cultures. Improvement occurred more frequently in patients with viremia, fever, and wasting (8 of 8), hepatitis (3 of 4), retinitis (5 of 5), or colitis (1 of 1), than in patients with pneumonia (11 of 21). Only two of nine marrow transplant recipients with CMV pneumonia survived, as compared with nine of 12 other immunosuppressed patients with pneumonia. However, all six marrow transplant recipients who were treated for CMV viremia, fever, and wasting without pneumonia survived. Neutropenia was the only adverse reaction associated with ganciclovir therapy and was more frequent in patients with AIDS (6 [55%] of 11) than in transplant recipients (5 [20%] of 25). These results suggest that ganciclovir is of clinical benefit for immunosuppressed patients with serious CMV infections. For bone marrow transplant recipients, ganciclovir may be more effective when used prophylactically or earlier in the course of CMV infection before the development of pneumonia.
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PMID:Ganciclovir therapy for cytomegalovirus infections in recipients of bone marrow transplants and other immunosuppressed patients. 284 92


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