Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cases of hepatitis virus infection in Japanese recipients of blood transfusions were serologically and clinically analyzed after the introduction of laboratory screening of donor blood for hepatitis B surface antigen by counter immunoelectrophoresis. Non-A, non-B hepatitis occurred in 116 (10.7%) and hepatitis type B in nine (0.9%) of the 1,082 recipients. The incubation period of the post-transfusion non-A, non-B hepatitis cases varied from two to 33 weeks, but most occurred within 15 weeks. In 97 (83.6%) of the 116 cases of non-A, non-B hepatitis studied, the duration of abnormal elevation of the level of serum alanine aminotransferase (glutamic-pyruvic transaminase [SGPT]) was 16 weeks. The cases of non-A, non-B hepatitis could be divided into three groups according to the pattern of elevation of SGPT levels. These findings may suggest either a multiple etiology for non-A, non-B hepatitis or a variety of clinical symptoms with a single etiology for the infection.
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PMID:Non-B hepatitis in Japanese recipients of blood transfusions: clinical and serologic studies after the introduction of laboratory screening of donor blood for hepatitis B surface antigen. 43 50

Serum DNA polymerase activity (DNA-P) was detected in 27.6 per cent of non-A, non-B (NANB) hepatitis patients, 8.7 per cent of patients with alcoholic liver disease (ALD), 8.6 per cent of hepatitis B surface antigen (HBsAg)-positive patients and 19.0 per cent of HBsAg-negative blood donors with elevated serum glutamic-pyruvic transaminase (SGPT) concentrations. In contrast, none of the patients with hepatitis A, drug-induced liver injury or non-alcoholic fatty liver had DNA-P in their sera in the acute phase of the illness. All HBsAg-positive samples with detectable DNA-P were strongly positive for hepatitis B virus (HBV) DNA, but the samples from patients with NANB hepatitis and ALD and HBsAg-negative blood donors had no HBV DNA. Sensitivity to actinomycin D showed the heterogeneity of DNA-Ps in HBsAg-negative blood donors; the enzyme activity of one type was inhibited by 100 micrograms/ml of actinomycin D, whereas the other was not. The preference for exogenous template primers of these DNA-Ps was different to those of HBV and human retroviruses. The results reveal the prevalence of serum DNA-P in NANB hepatitis patients and suggest that two distinct agents are relevant to the aetiology of NANB hepatitis.
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PMID:Prevalence and heterogeneity of serum DNA polymerase activity in patients with non-A, non-B hepatitis and HBsAg-negative blood donors with elevated SGPT. 212 73

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of polymyositis associated with chronic active hepatitis]. 218 64

Seven children with chronic active hepatitis (CAH) and one child with persistently abnormal results of liver function test due to hepatitis B virus (HBV) infection were treated with human leukocyte interferon (Hu-alpha-IFN). Five of them were positive for eAg and two of the three who were measured for DNA polymerase (DNAP) activity in sera showed moderate elevations of its levels. Hu-alpha-IFN was injected intramuscularly daily or once weekly at doses of 0.05-1 X 10(6) IU. The total dose per patient varied from 10.5-54 X 10(6) IU. After administration of Hu-alpha-IFN, rapid loss of eAg was observed in two of the five eAg patients, and DNAP activity reverted to normal ranges in the two patients with moderate elevations of its levels. One of the patients who lost eAg has retained normal serum glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase levels for more than 2 years after therapy with Hu-alpha-IFN. Serial hepatic biopsies were performed in only one patient. In the second biopsy, 3 months after therapy with Hu-alpha-IFN, infiltration of inflammatory cells in the portal region was improved compared with earlier findings. Immediate and/or prolonged adverse side effects were not observed during or after administration of Hu-alpha-IFN. For the present, we propose these six conditions for use of Hu-alpha-IFN in children with HBV infection. Children should: (a) be more than 1 year old; (b) have abnormal liver function for more than 6 months; (c) have a liver biopsy demonstrating CAH; (d) have moderate elevation of DNAP activity; (e) be eAg positive; and (f) be unresponsive to other treatments.
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PMID:Therapeutic effects of human leukocyte interferon on chronic active hepatitis B in children. 398 64

Alpha fetoprotein (AFP) was detected in sera (351 samples) of 128 patients with viral hepatitis by radioimmunoassay. 77 positive tests for AFP were obtained. These positive results were demonstrated on 1 or more samples taken from 40 (31%) of the 128 patients studied; the highest value obtained was 4400 ng/ml. Hepatitis B antigen (HBAg) was positive in 26/40 (65%) of patients in whom AFP was detected during the disease process. However, 58/88 (66%) who were seronegative for AFP also demonstrated HBAg in their sera. Chi-square analysis revealed no significant difference in occurrence of detectable AFP between HBAg seropositive and seronegative patients. Individuals seropositive for AFP had no statistically different concentration of the protein than patients seropositive or seronegative for HBAg. 24 patients' sera were tested serially over a 2-week period. Both the peak glutamic-pyruvic transaminase (GPT) and peak total bilirubin levels were in a higher range in those 10/24 patients seropositive (P .001) for AFP than in the 14/24 who were seronegative. Appearance of AFP was related to the severity of liver tissue destruction, as reflected by serum GPT. However, peak AFP levels were attained 5-16 days after peak serum GPT appeared in the circulation.
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PMID:The detection of alpha 1-fetoprotein in patients with viral hepatitis. 480 61

Peripheral T-cell subsets in 77 patients with hepatitis B surface antigen (HBsAg)-positive chronic liver diseases were studied by indirect immunofluorescence using murine monoclonal antibodies against all peripheral T cells (OKT3), T-helper/inducer cells (OKT4), and T-cytoxic/suppressor cells (OKT8). OKT4/OKT8 ratios were significantly reduced in patients with hepatitis B e antigen (HBeAg)-positive chronic liver diseases, including 28 patients with chronic active hepatitis (CAH) (P less than 0.001) and 15 with chronic persistent hepatitis (CPH) (P less than 0.001). OKT4/OKT8 ratios were significantly lower in 21 HBeAg-negative patients with CAH (P less than 0.05), as compared to those of 17 normal controls, while T-cell subsets in 13 patients with HBeAg-negative CPH were essentially normal. Low OKT4/OKT8 ratios significantly correlated with HBeAg positivity (P less than 0.001) and CAH (P less than 0.05), as assessed with multiple regression. There was a significant negative correlation between OKT4/OKT8 ratios and serum glutamic-pyruvic transaminase (SGPT) levels (r = -0.37; P less than 0.01). It was concluded that in chronic hepatitis B virus infection, low OKT4/OKT8 ratios are closely related to active viral replication and more severe histological and biochemical activity.
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PMID:Peripheral T-cell subsets in chronic type B hepatitis: correlation with biochemical and histological activities and hepatitis B e antigen/antibody status. 623 72

Examinations of 4457 blood donors (about 80% were men aged 18 to 30) revealed an increased level of serum glutamic-pyruvic transaminase (SGPT) in 82 (1.8%). Specific markers of viral hepatitis C were detected in 15.9%, of hepatitis B in 12.0%, of hepatitis D in 2.0%, of hepatitis E in 8.0%, of hepatitis A in 2.0% of sera with high SGPT levels. Mandatory screening of blood donors revealed specific markers of viral hepatitis in 15.9% of cases, additional testing detected these markers in 10.9% cases more. A conclusion is made that an increase of SGPT activity is an independent surrogate marker of viral hepatitis.
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PMID:[Alanine aminotransferase--a surrogate marker of viral hepatitis]. 774 Jul 84

The molecular mechanisms responsible for hepatocyte death and the events leading to viral clearance in hepatitis B virus (HBV) infections are not well understood. Elucidation of the mechanisms involved have been complicated by the difficulty of infecting human hepatocytes with HBV in vitro and the lack of an appropriate animal model. We report an animal model of human HBV infection by in vivo transfection. We have directly introduced a replication-competent, cloned HBV construct into rat liver by using a membrane fusion-promoting cationic lipid. HBV mRNA and 3.2-kb HBV DNA were expressed in the liver by this in vivo transfection method. In the majority of rats, HBV virions and hepatitis B e antigen were found in the blood 3-7 days after transfection, after which antibody to the e antigen appeared. Two to three weeks after the transfection, glutamic-pyruvic transaminase levels were elevated in serum, hepatocyte death and lymphocyte infiltration were observed in the vicinity of the portal vein of liver, and HBV virions were no longer detected in the serum. Thus, transfection of HBV into rats resulted in histological and serological changes comparable to HBV-induced acute hepatitis in humans. In contrast, no hepatocellular injury was observed in T-lymphocyte-deficient nude rats transfected with the same HBV construct, and viremia was substantially prolonged, providing direct evidence that T lymphocytes play an essential role in liver cell injury and in the clearance of HBV. This rat hepatitis model will be useful for studying pathogenesis of HBV infection.
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PMID:Acute hepatitis in rats expressing human hepatitis B virus transgenes. 787 2

Intercellular adhesion molecule-1 (ICAM-1) is expressed on the hepatocyte membrane in patients with chronic hepatitis B and C. We assayed levels of the soluble form of this molecule (sICAM-1) in serum by an enzyme-linked immunosorbent assay method; we then analyzed the results in relation to hepatitis activity. Fifty-one patients with chronic hepatitis (22 with type B and 29 with type C) and 10 normal controls were examined. The serum levels of sICAM-1 in hepatitis B and C were significantly higher (P < 0.01) than in normal controls. The serum level of sICAM-1 was correlated with serum glutamic-pyruvic transaminase level (P < 0.01), and the level of sICAM-1 in patients in whom exacerbation was seen was significantly higher (P < 0.05) than that in patients in a remission. There was no relationship between the serum level of sICAM-1 and the degree of ICAM-1 expression on the hepatocyte membrane. These results suggest that the serum level of sICAM-1 reflects the degree of activity of chronic hepatitis B and C.
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PMID:Soluble intercellular adhesion molecule-1 in serum in chronic hepatitis B and C. 795 56

We previously developed a method for introducing foreign genes into liver tissue using liposomes with incorporated hemagglutinating virus of Japan (HVJ, Sendai virus), and found that liver cells transfected with the E. coli beta-galactosidase gene or the gene for hepatitis B virus (HBV) surface protein (HBsAg) expressed these proteins in vivo. Here, we analyzed cellular reactions leading to hepatitis in the liver by expressing the genes of HBV in vivo. Lymphocytes were eluted directly from liver transfected with the HBsAg genes and shown to be cytotoxic only to cells expressing HBsAg in vitro. These lymphocytes were identified as cytotoxic T lymphocytes with the CD4- CD8+ phenotype. Transfer of these lymphocytes to transgenic mice with the whole HBV genome led to elevation of the serum glutamic-pyruvic transaminase (SGPT) level, indicating the induction of hepatitis due to the cytotoxic T lymphocytes in vivo. Similarly, direct transfer of the gene for the HBV secretory core protein (HBeAg) induced expression of HBeAg in hepatocytes and the appearance of antibody against HBeAg in the serum. However, using this system, we found that the lymphocytes infiltrating the transfected liver showed no cytotoxicity specific for HBeAg. These results indicate that expression of HBsAg, one of the components of virions, in animal liver induced hepatitis efficiently through generation of specific cytotoxic T lymphocytes (CTL) without any expression of the other viral components. This in vivo experimental system should be useful for evaluating how expression of a given gene induces cellular reactions and intrinsic functions in the living body.
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PMID:Use of the hemagglutinating virus of Japan (HVJ)-liposome method for analysis of infiltrating lymphocytes induced by hepatitis B virus gene expression in liver tissue. 839 62


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