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)

We compared the response and the relapse rates of HBeAb-positive patients treated with interferon-alpha for 6 or 12 months. Thirty-eight HBeAb-positive patients which chronic hepatitis B were randomly allocated into two groups: Group I (19 patients receiving 10 MU of recombinant interferon-alpha 2b three times a week for 2 months, followed by 5 MU three times a week for 2 months and then 3 MU three times a week for 2 months); Group II (19 patients receiving 10 MU of recombinant interferon-alpha 2b three times a week for 2 months, followed by 5 MU three times a week for 2 months and then 3 MU three times a week for 8 months). At the end of treatment, alanine aminotransferase normalization was higher but not more significant in Group I than in II (53% vs 26%), while hepatitis B virus DNA clearance was similar in both groups (21% in Group I vs 26% in Group II). However, at 12 months of follow-up, biochemical relapses occurred only in Group I (60% vs 0% in Groups I and II, respectively). Five complete responders cleared hepatitis B surface antigen at that time. In conclusion, prolonged treatment of HBeAb patients is efficient in reducing the biochemical relapse.
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PMID:Efficacy of prolonged interferon-alpha treatment in chronic hepatitis B patients with HBeAb: comparison between 6 and 12 months of therapy. 909 75

Currently, the only therapy of proven benefit in chronic hepatitis B is interferon-alpha which leads to a long-term benefit in only one-third of patients. New therapies for hepatitis B fall into three categories; antiviral chemotherapy, immunomodulation with cell-based therapies, vaccines or cytokines, and gene therapy such as with antisense oligonucleotides, ribozymes or viral mutants. The most promising immediate approach to therapy is with the new nucleoside antivirals--lamivudine and famciclovir. These drugs are well absorbed orally, result in profound inhibition of circulating hepatitis B virus, and, in some cases, loss of hepatitis B e antigen and improvement in serum aminotransferases. Controlled trials of long-term famciclovir and lamivudine therapy currently underway aim to show whether these drugs are safe and can provide sustained inhibition of viral replication and attentant improvement in liver disease.
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PMID:New therapies for chronic hepatitis B. 909 77

Systemic vasculitides are a heterogeneous group of diseases. Having only a partial understanding of the aetiologies and pathogenetic mechanisms of these disorders explains the difficulties encountered in classifying and treating patients. Nevertheless, some important points have been established. Classification is mainly based on the size of vessels affected and, from the polyarteritis nodosa group, microscopic polyangiitis (MPA) has been separated from classic polyarteritis nodosa (c-PAN). The latter is a rare disease which is, in a small number of cases, the consequence of hepatitis B or C virus (HBV/HCV) infection. In the other cases of c-PAN and in MPA, the aetiology is unknown as for Churg-Strauss syndrome (CSS) and Wegener's granulomatosis (WG). MPA, CSS and WG are mainly antineutrophil cytoplasmic antibodies (ANCA)-related vasculitides. ANCA play a part in the pathogenesis of diseases and are sometimes useful markers for diagnosis and follow-up. Vasculitis treatments should be chosen according to classification, aetiology, pathogenetic mechanisms, severity and predictable outcome. In virus-associated vasculitides, treatment is based on the combination of antiviral agents and symptomatic or immunomodulating therapies. HBV-related PAN and HCV-related cryoglobulinaemia respond to interferon-alpha and to plasma exchange. Responses are excellent in HBV-PAN but usually partial in HCV-cryoglobulinaemia, and relapses occur in the majority of cases. MPA, c-PAN, WG and other vasculitides respond to corticosteroids and cytotoxic agents, mainly cyclophosphamide. Treatment duration and ways of administration can vary from one disease to another. Plasma exchange is not recommended as the first-line treatment. Immunoglobulins and other immunomodulating treatments are indicated in limited cases and their indications necessitate further prospective studies.
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PMID:Classification and management of necrotising vasculitides. 912 67

Patients with biopsy-proven chronic hepatitis C, who failed to respond to a previous course of either recombinant (rIFN-alpha) or lymphoblastoid (Ly IFN-alpha) interferon-alpha, were randomized to receive either leucocyte (Le) IFN-alpha (patients) or a second course of the same IFN-alpha (controls), to compare the efficacy and safety of these treatment schedules. All patients received the same dose of IFN-alpha as was used during their previous treatment (3 million units (MU) or 6 MU three times weekly) for 6 months. Patients with a normal alanine aminotransferase (ALT) value at month 6 were treated for a further 6 months. All patients were followed-up for 12 months after treatment. A total of 69 patients were enrolled, 44 in the Le IFN-alpha group and 25 in the control group. At the end of the treatment period, 13 of the 44 patients (29.5%) in the Le IFN-alpha group had a biochemical response (normal ALT) and six of 44 (13.6%) patients had undetectable serum hepatitis C virus (HCV) RNA. At the end of the follow-up period, 10 patients (22.7%) had normal ALT values and serum HCV RNA was undetectable in three (6.8%). None of the patients in the control group showed normal ALT values at any time. Genotype 1b tended to be more frequent among non-responders (61 vs 45%): basal gamma-glutamyl transpeptidase (gamma-GT) values were lower in responders than in non-responders (33.3 +/- 11.70 Ul-1 vs 58.4 +/- 33.04; P = 0.01). Le IFN-alpha was well tolerated by all patients. These results support the use of Le IFN-alpha in patients with chronic hepatitis C who are non-responders to a previous treatment with recombinant or lymphoblastoid IFN-alpha.
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PMID:Human leucocyte interferon-alpha in chronic hepatitis C resistant to recombinant or lymphoblastoid interferon-alpha: a randomized controlled trial. 918 30

Interleukin-12, a cytokine with an important role against intracellular pathogens, promotes Th1 cell development, cellmediated cytotoxicity, and interferon-gamma production. We investigated the immunoregulatory role of IL-12 in 72 chronic hepatitis B virus (HBV) carriers, 33 of whom were monitored longitudinally during interferon-alpha treatment. Serum levels of IL-12 heterodimer, IL-12 p40 subunit, IL-4, and Th1 cytokines were determined by specific ELISAs, and hepatitis B core antigen-specific T cell response by a proliferation assay. Chronic HBV carriers had higher serum levels of IL-12 and IL-12 p40 in comparison with controls (P < 0.01), suggesting that IL-12 production is not impaired. The longitudinal analysis revealed a further substantial increase (> 2.5x baseline level) of bioactive IL-12 and Th1 cytokines in patients who cleared HBV and seroconverted to anti- hepatitis B e, unlike the 23 nonresponders with persistent HBV replication (P < 0.01). The IL-12 peak followed the peak of hepatocytolysis by 9.8+/-2.8 wk and occurred either before or simultaneously with hepatitis B e seroconversion. Hepatitis B core antigen-specific T cell proliferation closely correlated with hepatocytolysis and increased significantly in all patients (8 responders and 15 nonresponders) who developed hepatitis flare, irrespective of the virological outcome. These results provide in vivo evidence that IL-12 may have an important role for viral clearance in chronic HBV infection.
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PMID:Interleukin-12 induction of Th1 cytokines is important for viral clearance in chronic hepatitis B. 918 27

We have reported the Keio multicenter randomized trial of interferon-alpha 2b treatment for chronic hepatitis C, hypothesizing that disappearance of serum hepatitis C virus (HCV) ribonucleic acid (RNA) during the first 2 days by one does administration of interferon is a predictive factor of final response to the high-dose interferon treatment. In this study we quantified HCV RNA by multicyclic reverse transcription-polymerase chain reaction in the stored sera of the same patients with our previous study. The multivariate analysis confirmed that the pretreatment HCV RNA levels and HCV genotype were significantly correlated with the response to the 6-month course interferon treatment. Although the relationship between decreased HCV RNA titers within the first 2 days after one dose administration of interferon and the efficacy of the therapy was not obtained, the cases in which HCV RNA disappeared within 2 days significantly responded to the 6-month course treatment (73.7% vs 12.5% in other cases, p < 0.01). The present study has confirmed the hypothesis suggested in the previous study that clearance of HCV RNA during the first 2 days has a predictive value for the final outcome.
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PMID:Disappearance of serum hepatitis C virus RNA within two days after one dose interferon administration is predictive for response to high-dose interferon-alpha 2b treatment for chronic hepatitis C. Keio Interferon-alpha 2b Study Group. 921 90

Virological response to treatment of chronic hepatitis B is defined as the loss of serum hepatitis B virus DNA (HBV DNA) and hepatitis B e antigen (HBeAg). The quantitative measurement of HBV DNA is useful for monitoring and predicting the response to therapy with interferon-alpha (IFN-alpha). In this study, we evaluated whether quantitative measurement of serum HBeAg and IgM antibody to hepatitis B core antigen (HBcAb) could also be used in this manner. Using a microparticle-capture enzyme immunoassay (IMx), a standard curve of fluorescence rate vs HBeAg concentration was constructed to provide quantitative results. The IgM HBcAb index was also measured using a microparticle enzyme immunoassay and serum HBV DNA was measured by a solution hybridization assay. We studied 48 patients who were initially positive for HBeAg and HBV DNA and who were treated with IFN-alpha2b. Their sera were serially evaluated for HBeAg concentration, and results were compared with HBV DNA levels. In the 14 patients who responded to IFN, similar disappearance curves were observed with good intraindividual correlation between the levels of the two markers. In the 34 non-responders, HBeAg levels decreased during treatment but never became negative; HBV DNA levels also decreased during treatment and became transiently undetectable in six patients, falsely suggesting treatment success. The IgM HBcAb index paralleled changes in alanine aminotransferase (ALT) concentration and did not provide additional information. Multiple logistic regression indicated that baseline ALT and HBeAg concentrations were independent predictors of the response to treatment and the addition of neither HBV DNA nor IgM HBcAb improved the model. We conclude that quantitative measurement of HBeAg provides information similar to that of HBV DNA in monitoring and predicting the response to treatment; this technique could be readily adaptable to clinical laboratories.
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PMID:Quantitative assessment of serum hepatitis B e antigen, IgM hepatitis B core antibody and HBV DNA in monitoring the response to treatment in patients with chronic hepatitis B. 927 24

Fifty percent of healthy hepatitis B surface antigen carriers may have histologically proven chronic hepatitis. Our aim was to study the benefit of interferon-alpha in healthy patients. Twenty-nine hepatitis B surface antigen carriers with normal liver enzymes and with serum hepatitis B virus DNA were randomized into two groups: Group I, 14 patients treated with 9 megaunits of interferon alpha-2a thrice weekly for six months, and Group II, 15 control patients. A liver biopsy was obtained from each patient at study initiation. A second biopsy was available in nine treated patients and six controls. During treatment, a significant increase in alanine amino transferase levels was observed in treated patients as compared with the controls (P < 0.05). After treatment, transaminase levels decreased to normal values. No differences between treated and control patients were observed in clearance of hepatitis B virus markers. A significant increase in the total histological activity index between base line and final liver biopsies was observed in treated patients (P < 0.05). It is concluded that interferon alpha treatment may induce a biochemical and histological activation of liver disease. Accordingly, interferon alpha should not be administered to healthy hepatitis B surface antigen carriers, at least with the schedule used in this work.
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PMID:Activation of liver disease in healthy hepatitis B surface antigen carriers during interferon-alpha treatment. 929 36

This study compared rates of spontaneous hepatitis B e antigen (HBeAg)-positive to -negative seroconversion in chronic carriers of hepatitis B virus (HBV) with rates reported during interferon-alpha therapy. Four hundred fifty-four Asian-American HBeAg-positive HBV carriers, followed for 1-10 years, were tested approximately every 6 months for HBeAg. Patients with alanine aminotransferase levels > or = 50 IU/mL at entry had 1067.3 seroconversions/10(5) person-months in the 5- to 19-year age group, 1753.3 in the 20- to 34-year group, and 1257.2 in the 35- to 50-year group. Published data indicate that 30% of children and 33% of adults seroconvert during interferon-alpha treatment and follow-up. In our study population, spontaneous seroconversion occurred in 15% of children (95% confidence interval [CI], 8%-27%), 23% of adults 20-34 years (95% CI, 15%-34%), and 17% of adults 35-50 years (95% CI, 10%-28%) during the same interval. The high rate of spontaneous seroconversion should be weighed in decisions to treat HBV carriers with interferon-alpha.
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PMID:Spontaneous seroconversion in hepatitis B e antigen-positive chronic hepatitis B: implications for interferon therapy. 933 40

A 43-year-old Japanese man who was positive for hepatitis B surface (HBs) antigen and HB e antibody, underwent chemotherapy for non-Hodgkin's lymphoma. After the chemotherapy he suffered from acute exacerbation of hepatitis because of reactivation of HBV. Recovery was achieved with interferon-alpha, glucagon-insulin therapy, and plasma exchange. Mutations were detected in codons 97, 100, 129, and 131 of the core region of HBV. The peptide encoded from the core region including such mutations possibly had greater antigenicity to induce cytotoxic T cell activity in the host. Core region mutations may be a crucial cause of the acute exacerbation of hepatitis B seen after chemotherapy.
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PMID:Acute exacerbation of hepatitis due to reactivation of hepatitis B virus with mutations in the core region after chemotherapy for malignant lymphoma. 934 95


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