Cases reported "Hepatitis B, Chronic"

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1/114. Highly active antiretroviral therapy used to treat concurrent hepatitis B and human immunodeficiency virus infections.

    We report a case of simultaneous infection with hepatitis b virus (HBV) and human immunodeficiency virus type 1 (hiv-1) in a 26-year-old Japanese homosexual man. He was admitted to our hospital for acute hepatitis caused by HBV. At that time, HIV-1antibody (Ab) was not detected in his serum. After 6 months, he was readmitted to our hospital for further examination of his liver because of confined liver enzyme abnormalities. Anti-HIV- Ab was detected in his serum by both enzyme immunosorbent assay (EIA) and particle agglutination (PA). His serum hiv-1 RNA level was 50 x 10(4) copies/ml and serum levels of HBV dna polymerase (dna-P) and HBV dna were 6535cpm and 3 plus (>1000 copies/ml). His clinical course and laboratory data suggested progression from acute to chronic hepatitis related to coinfection with hiv-1. The diagnosis was chronic active hepatitis caused by HBV as an opportunistic infection due to coinfection with hiv-1. We began highly active antiretroviral therapy (HAART) because interferon (IFN) therapy was ineffective. HAART was started at an initial dosage of 600 mg zidovudine (AZT), 300 mg lamivudine (3TC), and 2400 mg indinavir (IDV) daily. After 4 weeks, the serum level of HBV dna-polymerase (p) had decreased markedly to 37cpm and that of hiv-1 RNA had decreased to below the sensitivity threshold, indicating considerable suppression of the replication of these viruses by the treatment. But HBV dna remained at low levels. Although the incidence of HBV infection in patients with hiv-1 infection has been reported to be high in the united states and europe, simultaneous HBV and hiv-1 infection leading to persistent HBV infection is rare.
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2/114. Successful treatment of decompensated chronic viral hepatitis by bursal disease virus vaccine.

    Three cases of women with chronic liver inflammation caused by hepatitis B (two) and C (one) viral infections, were followed up to twelve years after diagnosis. As conventional therapy was ineffective and the patients progressed into decompensated liver disease, they were superinfected with massive doses of an attenuated variant (MTH-68/B) of the apathogenic avian Bursal disease virus (a double-stranded RNA virus from the birnaviridae family). Clinical symptoms and biochemical abnormalities were resolved in two patients following few months of virus treatment. Cirrhosis was stabilized and significant clinical improvement was achieved in the third patient--who before the virus therapy was moribund with recurring, diuretic-resistant ascites, variceal bleedings, portal encephalopathy and renal failure. To our knowledge, these are the first recorded cases of decompensated chronic viral hepatitis which went to long-lasting remission or were stabilized by superinfection with an apathogenic virus.
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3/114. Antiviral treatment for human immunodeficiency virus patients co-infected with hepatitis b virus: combined effect for both infections, an obtainable goal?

    A large percentage of human immunodeficiency virus (HIV) patients have serological evidence of a past or present hepatitis b virus infection (HBV). Long-term survival is increasing for HIV patients because of highly active antiretroviral therapy. Therefore, the chronic hepatitis B infection may become an important determinant of disease outcome in these co-infected patients. We describe two HIV/HBV co-infected patients who were treated with extended antiviral therapy, initially indicated for the HIV infection. lamivudine, a suppressor of viral replication in both infections, was one of these antiviral drugs. One patient showed a severe rebound of the HBV after withdrawal of lamivudine, the other patient developed a mutant hepatitis b virus after 18 months of treatment. This mutation was exclusively induced by lamivudine. These patients show that, with improved HIV-related survival, the HBV infection should be monitored carefully, thereby enabling the physician to interfere with therapy when necessary.
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4/114. A novel deletion mutant of hepatitis b virus surface antigen.

    HBsAg is the most important serological marker for acute or chronic hepatitis B. Nevertheless, there are reports of HBsAg-negative virus carriers, either with anti-HBc as the only marker for hepatitis b virus (HBV) infection or even positive for anti-HBs and anti-HBc. We report isolates from a patient, in which a deletion in the HBs-gene was associated with persisting viremia in the presence of anti-HBs. The 62-year-old female, infected most likely by her husband, had detectable markers of chronic active hepatitis B, such as HBsAg, HBeAg, and anti-HBc-IgM, for 2 years. The patient then seroconverted to anti-HBs, although HBeAg and anti-HBc-IgM remained detectable. At this time, semiquantitative polymerase chain reaction showed about 10(4) viral genomes per milliliter of serum. Direct sequencing of the amplified products revealed a major population of dna molecules with a deletion of nucleotide 31 of the HBs-gene, which up to now has not been described. This deletion led to a frame-shift and introduced a stop-codon after 21 amino acids of the sHBsAg. We suspect that this deletion, and the resulting HBsAg lacking the major epitopes recognized by specific antibodies, could favor ongoing viral replication, despite the presence of anti-HBs. However, because the reading frame of the polymerase was also severely damaged by this deletion, it is assumed that a minor population of intact genomes was present to help in the formation of virus particles.
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5/114. Fatal virus-associated hemophagocytic syndrome associated with coexistent chronic active hepatitis B and acute hepatitis c virus infection.

    A 28-year-old man was admitted to our department with intermittent fever, hepatosplenomegaly and pancytopenia. Liver parameters and serum ferritin were markedly elevated. bone marrow biopsy showed hypocellularity, histiocytic hyperplasia, and hemophagocytosis consistent with a virus-associated hemophagocytic syndrome (VAHS). There was serological evidence of chronic active hepatitis B and acute hepatitis c virus infection. The patient died despite aggressive immunosuppressive and supportive treatment. autopsy revealed signs of acute viral hepatitis with cholestasis. histiocytes engaged in hemophagocytosis were observed in bone marrow and spleen. The condition was interpreted as VAHS associated with chronic active hepatitis B and acute hepatitis c virus infection. To our knowledge this is the first report of a hemophagocytic syndrome in that setting.
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6/114. Quantitative dna analysis of low-level hepatitis B viremia in two patients with serologically negative chronic hepatitis B.

    Low-level viremia due to hepatitis b virus (HBV) was demonstrated in the sera of two patients diagnosed previously as having non-B, non-C chronic hepatitis. Both patients had a "silent" HBV infection, because they were negative for both hepatitis B surface antigen (HBsAg) and anti-hepatitis B core antibody. The TaqMan chemistry polymerase chain reaction (PCR) amplified the HBV dna, enabling quantitation of the virus in their sera. Their serum HBV dna concentrations were low: the amount of each HBV S or X gene amplified showed there were approximately 10(3) copies/ml and HBV dna was detected occasionally during clinical follow-up. Positive HBsAg staining in liver tissues was demonstrated by an immunoperoxidase technique. Vertical transmission of silent HBV from one patient to her daughter was confirmed. Direct nucleotide sequencing of the amplified HBV X region revealed several mutations, suggesting reduced viral replication. One patient had a T-to-C mutation at the extreme 5'-terminus of the direct repeat 2 region and the other exhibited a coexisting X region with a 155-nucleotide deletion. These findings suggest that HBV replication is suppressed considerably in patients with silent hepatitis B.
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7/114. Chronic active hepatitis B exacerbations in human immunodeficiency virus-infected patients following development of resistance to or withdrawal of lamivudine.

    lamivudine is a nucleoside analog with activity against human immunodeficiency virus (HIV) and hepatitis b virus (HBV). patients coinfected with HIV and HBV may have hepatitis flares when lamivudine therapy is discontinued or when resistance of HBV to lamivudine emerges. This retrospective, descriptive study conducted in three tertiary care medical centers describes patients coinfected with HIV type 1 and HBV who presented with a spectrum of clinical and subclinical hepatitic responses to lamivudine withdrawal or resistance. One patient had fulminant hepatic failure and a second patient had subclinical hepatitis when lamivudine therapy was discontinued and a more efficacious antiretroviral regimen was substituted. Three patients had flares of hepatitis after 13 to 18 months of lamivudine therapy. lamivudine withdrawal or emergence of lamivudine-resistant mutants in patients coinfected with HIV and HBV may result in severe hepatitis. Clinicians caring for patients with coinfection with HIV and HBV should be aware of the possibility that a hepatitis B flare may occur in previously asymptomatic carrier patients.
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8/114. Antigenic characterization of pre- and post-liver transplant hepatitis B surface antigen sequences from patients treated with hepatitis B immune globulin.

    BACKGROUND/AIMS: The success of treatment with hepatitis B hyperimmune globulin in preventing recurrence of hepatitis b virus infection in patients undergoing orthotopic liver transplantation depends on maintaining levels of anti-HBs sufficient to neutralise hepatitis b virus and also on patient compliance. Breakthrough infections may occur, and these have been associated with the emergence of variants in HBsAg. methods: Three patients, two who relapsed and one who had no evidence of hepatitis b virus infection post-orthotopic liver transplantation were studied. polymerase chain reaction and sequencing of pre- and post-orthotopic liver transplantation samples was followed by antigenic analysis of the in vitro expressed cloned sequences. RESULTS: In two patients who were treated with hyperimmune globulin, amino acid variation in the region of the immunodominant B cell epitopes of HBsAg occurred. Sequencing of clones revealed fluctuating variant sequences over time. One had clinical relapse and immune escape was evident on in vitro antigenic analysis. Patient two lost HBsAg reactivity post-orthotopic liver transplantation. There was loss of an antigenically critical cysteine molecule; sequencing of clones revealed that this was the dominant species. The third patient relapsed when protective levels of anti-HBs were not maintained; HBsAg showed no variation compared to a standard subtype sequence. CONCLUSION: These data provide strong experimental evidence of immune escape. It appears that hyperimmune globulin provides the selection pressure. In these patients, HBsAg negativity does not exclude infection of the transplanted liver.
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9/114. Disappearance of hepatitis b virus core deletion mutants and successful combined kidney/liver transplantation in a patient treated with lamivudine.

    hepatitis b virus (HBV) core deletion variants with enhanced viral replication are associated with rapid deterioration of liver function in renal allograft recipients. antiviral agents such as famciclovir and lamivudine offer new treatment strategies for these patients. Appearance, accumulation and persistence of HBV core deletion mutants were closely monitored in a kidney transplant recipient with liver cirrhosis before and after initiation of antiviral treatment. Under treatment with famciclovir HBV dna concentration decreased by 50 %, HBV mutants persisted. After replacement of famciclovir by lamivudine HBV replication was reduced below the detection limit. lamivudine was well tolerated and liver function improved. After successful combined kidney/liver transplantation the patient became HBsAg and HBV dna (detected by PCR) negative under continuous hyperimmune globulin and lamivudine treatment. Antiviral therapy with lamivudine may be useful in treatment of progressive liver disease associated with HBV core deletion mutants in renal allograft recipients and may enable successful liver transplantation.
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10/114. Case report: lamivudine therapy for submassive hepatic necrosis due to reactivation of hepatitis B following chemotherapy.

    This report describes the case of a 53-year-old woman who developed severe hepatitis following chemotherapy for breast carcinoma. The patient was hepatitis B surface antigen positive, e antigen negative and e antibody positive and had high levels of hepatitis b virus-dna. Liver biopsy revealed submassive hepatic necrosis, consistent with reactivation of hepatitis B. Treatment with lamivudine resulted in rapid loss of hepatitis b virus-dna, resolution of hepatitis and clinical recovery.
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