Cases reported "Hepatitis D"

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1/15. Acute delta hepatitis without hepatitis B surface antigen detectable in the blood.

    The case is described of a 42-year-old man suffering from acute delta hepatitis without hepatitis B surface antigen (HBsAg) being detectable in his blood. Tests on the patient's blood were negative for anti-HBcIgM and HBeAg but positive for anti-HBs, anti-HBe, HDAg and anti-DIgM. It is well known that the delta antigen-antibody system is detectable only in HBsAg carriers except rarely in persons recently recovered from acute hepatitis b virus (HBV) and delta infection. We report one of the rare cases in which the circulating HBsAg as well as anti-HBcIgM and HBeAg were not found in the patient's serum, thus indicating the absence of recent infection with HBV.
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2/15. Transplantation of hepatitis B surface antigen-positive livers into hepatitis b virus-positive recipients and the role of hepatitis delta coinfection.

    The scarcity of liver donors requires consideration of grafts from sources not previously used. allografts from hepatitis B surface antigen (HBsAg)-carriers without a significant liver disease have been proposed for liver transplant recipients with hepatitis b virus (HBV)-related cirrhosis and hepatocellular carcinoma (HCC). Combination prophylaxis schemes against HBV post-liver transplantation (LT) recurrence are currently available; the efficacy of those schemes in HBV-related cirrhosis and HCC must be assessed. This report describes the allocation of HBsAg-positive grafts in three HBsAg-positive recipients, with HBV-related cirrhosis and evolving HCC lesions, two of them with hepatitis Delta virus (HDV) coinfection. patients were administered anti-hepatitis B immunoglobulins (HBIGs) and lamivudine in order to prevent HBV recurrence. In spite of anti-HBV prophylaxis, HBV infection did persist after LT in all patients (no serum clearance of HBsAg). HBV replication assessed by serum HBV deoxyribonucleic acid (dna) presence was detected in the first month after LT in the 3 recipients. A prompt HDV reinfection with a clinical and histological pattern of hepatitis was observed in the 2 HBV / HDV coinfected recipients. In 1 of them, an evolving chronic hepatitis required a second LT. The non-HDV-infected patient showed an uneventful follow-up, but the lack of the neutralizing effect of HBIGs and the high risk of escape mutants forced the addition of adefovir-dipivoxil to lamivudine, in order to prevent viral variants and hepatitis recurrence. In conclusion, allografts from HBsAg-positive donors in HBsAg-positive recipients are associated with the persistence of the HBsAg after LT due to the failure of HBIG prophylaxis, even if lamivudine does inhibit virion production. This condition favors HDV replication and HDV hepatitis recurrence in coinfected patients. The allocation of HBsAg-positive grafts in HBsAg-positive recipients could be justified only in recipients without HDV coinfection and a combined prophylaxis with lamivudine and adefovir-dipivoxil is currently the best way to manage escape mutants in these recipients.
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3/15. hepatitis delta virus super-infection in a co-infected patient with the human immunodeficiency virus type 1 and a surface antigen-negative hepatitis b virus variant.

    Human immunodeficiency virus infection has a major impact on the natural history of chronic hepatitis B and favours the emergence of viral mutants. We describe an acute hepatitis D virus superinfection in an hiv-1-infected patient under HAART treatment who was previously a chronic carrier of a surface negative HBV variant resistant to lamivudine.
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4/15. A long-term follow-up of five patients with hepatitis delta virus in japan.

    From 1973 to 1989 five patients with hepatitis delta virus having anti-hepatitis delta antibodies continuously in the serum for more than 5 years were identified among 1019 hepatitis b virus carriers who were being followed-up for more than 3 years (mean 8.9 years). Of the five patients with antibodies, three had a history of blood transfusion, in two cases the transfusion was massive, and one patient had been addicted to narcotics given intravenously 35 years before. In the remaining patient, the route of superinfection could not be determined. Hepatitis delta antigen was detected in hepatocyte nuclei of one of the three patients in whom liver biopsies were performed and there was chronic persistent hepatitis detected by an indirect immunoperoxidase technique. During the follow-up, hepatocellular carcinoma developed in one case but the clinical prognosis was favourable in the remaining four cases.
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5/15. Pre-S1 and Pre-S2 gene-encoded proteins in liver and serum in chronic hepatitis delta infection.

    Frozen cryostat sections and sera from 30 patients with chronic delta infection were examined for pre-S1 and pre-S2 gene-encoded proteins, and the results were compared to markers in liver and serum HBV and HDV replication. Pre-S1 and pre-S2 were detected by indirect immunofluorescence (IF) in the liver in all 26 patients with histochemically demonstrable HBsAg. Pre-S peptides were found by double IF to have a predominantly cytoplasmic expression and to be located in the same hepatocytes expressing HBsAg. Liver cells expressing hepatitis delta antigen (HDAg) were frequently negative or very weakly positive for HBsAg and pre-S peptides, but occasional HDAg positive hepatocytes were also strongly positive for HBsAg and for pre-S peptides, particularly pre-S2. Circulating pre-S1 was detected in 24 patients (80%) and pre-S2 in 27 (90%). Detection of pre-S peptides in liver and serum was independent of HBV and HDV replication and of the HBV-dna integration state. There was no correlation between the amount of circulating pre-S peptides and serum HBV-dna and HDV-rna. These results indicate that in chronic HDV infection, formation and secretion of pre-S peptides and of HBsAg occur independently of HBV and HDV replication and secretion. They further indicate that in the acquisition by replicating HDV of an HBV-derived envelope in the liver, both HBsAg and pre-S peptides are concomitantly available but circulating HDV-rna is not invariably associated with the presence of these peptides in serum.
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6/15. Course of hepatitis delta virus infection in auxiliary liver grafts in patients with delta virus cirrhosis.

    Two patients, with decompensated liver cirrhosis due to a chronic hepatitis type D, received an auxiliary partial liver graft. Both grafts were infected by hepatitis B and D virus. The appearance of hepatitis B and D antigens in the graft were investigated in serial liver biopsies in relation to light microscopical and biochemical changes. One week after transplantation HDAg could already be demonstrated in 1-50 percent of hepatocytic nuclei, in one graft combined with HBsAg along the cell membranes. In the three-week biopsies the expression of HBsAg had increased. After 7-9 weeks both grafts showed biochemical and histological evidence of an acute hepatitis; at that time HBcAg and HBeAg had appeared in the nucleus and cytoplasm of many hepatocytes. Thereafter HBcAg and HBeAg expression in the liver tissue decreased slowly, and acute hepatitis transformed into chronic hepatitis. Two and three years after transplantation both grafts showed good function, with only minimal fibrosis in one and severe fibrosis in the other. HDAg and HBsAg expression persisted, while HBc and HBeAg disappeared in the one with minimal fibrosis and decreased in the other. It is concluded that the course of HBV with HDV co-infection in liver grafts includes an excellent medium-term prognosis.
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7/15. Sanded nuclei in delta patients.

    Sanded nuclei are nuclei with eosinophilic inclusions identified by light microscopy in cases of chronic hepatitis b virus infection. In hematoxylin and eosin-stained sections, these inclusions have an almost homogeneous, finely granular texture giving a sandy appearance. They have been related to excess hepatitis B core antigen formation. We have studied liver biopsies from two HBsAg positive immunosuppressed patients with numerous sanded nuclei, morphologically identical to those previously described in hepatitis B. Immunohistochemically, sanded nuclei showed a strong nuclear positivity for delta antigen, but were negative for hepatitis B core antigen. Hepatitis B core particles were not demonstrable by electron microscopy. To our knowledge, this is the first time that sanded nuclei have been related to hepatitis delta virus (HDV) infection.
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8/15. Hepatitis D virus infection in children with acute or chronic hepatitis b virus infection in taiwan.

    To investigate the prevalence and clinical features of hepatitis D virus infection (HDV) in childhood, total antibody to hepatitis D antigen (anti-HD) in serum samples from 247 children (29 with acute hepatitis B, 68 with chronic hepatitis B, and 150 with asymptomatic hepatitis B surface antigen (HBsAg) carriers with normal liver function profiles) were studied using solid-phase competitive radioimmunoassay. Anti-HD was detected in three of the 29 children with acute hepatitis B and in only one of the 68 with chronic hepatitis B; none of the serum specimens from 150 asymptomatic carriers with normal liver function profile showed detectable anti-HD. All three children with HDV coinfection cleared HBsAg and seroconverted to anti-HBs, whereas one with superinfection finally had normal liver function without clearance of HBsAg. To identify possible sources of HDV infection, HBV markers and anti-HD in family members were also examined. One 4-month-old infant boy became infected through a blood transfusion from his hepatitis B e antigen (HBeAg)-positive carrier father, who had anti-HD. A 4-month-old infant girl was infected through close contact with her HBeAg-negative carrier father, who had HDV superinfection. The infection sources remained undefined in another two patients. The mothers of these four children were seronegative for anti-HD, indicating that perinatal transmission is not the usual mode of HDV infection in taiwan. The natural course of either acute or chronic HBV infections in childhood in taiwan may be more closely related to HBV itself, or to some other yet unrecognized factor, rather than to HDV infection.
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9/15. Permanent HBsAg clearance in chronic hepatitis B viral infection following acute delta superinfection.

    Three patients are described with chronic hepatitis b virus infection for three to six years before hepatitis delta virus superinfection occurred. Liver biopsy performed in two patients prior to their delta illness revealed chronic persistent hepatitis and chronic active hepatitis, respectively. Within one to seven months of the acute delta event, all three patients lost their circulating hepatitis B surface antigen. Subsequently, delta antibody also cleared. Clinical well-being and normal transaminases were documented over 10-44 months of follow-up. Although most cases of delta infection in chronic hepatitis B result in severe or progressive disease, a small number of patients may develop clearance of the HBsAg with clearance of both B and delta infections.
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10/15. Cytopathic liver injury in acute delta virus hepatitis.

    Hepatitis delta-virus (the delta-agent) is now recognized as a cause of acute hepatitis, fulminant hepatitis, chronic hepatitis, and cirrhosis in hepatitis B surface antigen-positive hosts. This report describes the clinical course and liver biopsy histopathology of acute delta-hepatitis in a young American woman with presumed chronic hepatitis B infection. The liver biopsy specimen features included severe cytotoxic and cytopathic hepatocellular damage, small droplet vacuolar liver cell degeneration, and few parenchymal inflammatory cells, lesions resembling epidemic delta-hepatitis in Venezuelan Indians and experimental chimpanzee delta-superinfection. This case suggests that this form of cytopathic liver injury is an important morphologic expression of delta-virus hepatitis that deserves wider diagnostic recognition.
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