Cases reported "Hepatitis, Chronic"

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1/37. A case of autoimmune hepatitis with a high titer of antimitochondrial antibody and normal gamma-globulinemia.

    We report here a patient with chronic active hepatitis who had no markers for hepatitis viruses and no hyper-gamma-globulinemia, but had high titers of antimitochondrial antibody. serum levels of alkaline phosphatase were normal, and antinuclear antibody, antismooth muscle antibody, and antiliver kidney microsome antibody tested negative. The titers of antimitochondrial antibody exceeded 1:640, and the positivity for anti-M2 was ascertained by using both ELISA and immunoblot with beef-heart mitochondria and a recombinant pyruvate dehydrogenase E2 subunit as antigens. This patient responded to ursodeoxycholic acid (UDCA) therapy in the beginning, but her hepatitis flared up during UDCA therapy. In contrast, she responded completely to corticosteroid therapy. The clinical course and histological findings of this patient strongly suggest that this patient has autoimmune hepatitis.
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2/37. Successfully resected hepatoblastoma in a young adult with chronic hepatitis B: report of a case.

    hepatoblastoma usually occurs in children, but a few cases have also been reported in adults. We report the unusual case of hepatoblastoma in an 18-year-old adult with chronic hepatitis B. He visited a local hospital with right upper abdominal pain. Abdominal ultrasound showed a large mass in the right lobe of his liver. He was referred to our hospital and admitted for further examination. At admission, liver function tests gave slightly elevated results (aspartate aminotransferase (AST) 103 IU/l, alanine aminotransferase (ALT) 63 IU/l). A test for hepatitis virus revealed that he was a hepatitis B surface antigen (HBsAg) carrier and had experienced seroconversion. His alpha-fetoprotein (AFP) was elevated to 1 548 000 IU/ml. Abdominal ultrasound showed a 109 x 96 x 80-mm mass with mosaic pattern in the right lobe of the liver and right portal vein thrombus. Abdominal computed tomography (CT) demonstrated a large low-density mass occupying the right lobe, with some high-density parts that showed calcification. From these results, we diagnosed hepatoblastoma in a young adult. A right lobectomy was performed. Pathological examination showed a highly differentiated hepatoblastoma. Adjuvant chemotherapy was performed with cisplatin and pirarubicin. The patient has been well and free of recurrence for 12 months, and his AFP level remains almost normal.
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3/37. mutation of the core region of HBV-dna and submassive hepatic necrosis in patients with anti-HBe-positive chronic hepatitis B.

    Three patients with submassive hepatic necrosis developed acute liver failure during the severe reactivation of chronic hepatitis B. The activity of hepatitis B virus (HBV) dna polymerase increased in all three patients immediately before the onset of hepatic failure. Liver biopsy specimens obtained before and after the episode of submassive hepatic necrosis showed progression to advanced liver cirrhosis. The nucleotide sequences of the precore and core regions of HBV-dna were investigated in two of the three patients and in another two patients with piecemeal and bridging necrosis. The nucleotide and amino acid sequences of the HBV-dna core region changed after reactivation in the the two patients with submassive hepatic necrosis, while the sequences in the other two patients with piecemeal necrosis remained unchanged before and after reactivation. These results suggest that the antigenicity of the HBV-dna core region may have been changed before and after severe reactivation. Due to mutation at the core region, a different type of epitope would be expressed on the hepatocytes after submassive hepatic necrosis, which would not be a target for the cytotoxic T cell. This was evident by the continuation of the normal serum GPT for 5 and 9 years, respectively.
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4/37. hepatitis c virus antibody in hepatocellular carcinoma in taiwan.

    The prevalence of antibody to hepatitis c virus (anti-HCV) was investigated in patients with hepatocellular carcinoma (HCC), and correlated with the clinical features. Anti-HCV was detected in 129 histology or aspiration cytology proven HCC patients and 54 healthy controls. Anti-HCV was examined by the HCV EIA (Abbott laboratories). All healthy controls were anti-HCV-negative. Nineteen of 81 (23.5%) hepatitis B surface antigen (HBsAg)-positive HCC patients were positive for anti-HCV. Anti-HCV was found among 60.4% (29/48) of HCC patients without detectable HB-sAg. Forty-eight of 129 (37.2%) HCC patients were positive for anti-HCV. There was a significant difference in the prevalence of anti-HCV between patients with HBsAg (23.5%) and those without HBsAg (60.4%, P = 0.0001). However, irrespective of the status of HBsAg, there was no statistical difference in sex, age, routine liver function tests, alpha-fetoprotein concentration, or associated cirrhosis between patients with anti-HCV and those without. The results imply that hepatitis c virus may play a role in the pathogenesis of HCC.
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5/37. A case of HBs antigen negative fulminant hepatitis with IgM antibody to hepatitis B core antigen persisting more than seven years.

    A 33-year old dentist developed fulminant hepatitis. At admission, a test for IgM antibody to hepatitis B core antigen (IgM anti-HBc) was positive, while tests for HBsAg and HBeAg were negative. He was cured of the disease, but in follow-up examinations from 1983 to 1990 IgM anti-HBc was continuously detected with radioimmunoassay while HBsAg and HBV-dna were absent in the serum. However, HBcAg was found in a biopsied liver specimen and a small quantity of HBV-dna was detectable by polymerase chain reaction assay. These observation suggest that the continuous detection of IgM anti-HBc without HBsAg in serum is due to persistent HBV infection and HBV replication in the liver.
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6/37. 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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7/37. The effects of recombinant interleukin 2 on HBe antigen positive chronic hepatitis B.

    Recombinant interleukin (IL-2) was administered to 16 patients with HBe antigen-positive chronic active hepatitis in which the diagnosis was ascertained histologically. In 7 of the 16 patients, a decrement of the serum HBe antigen value was observed (Group A). In group A, the findings showed an increment of peripheral Leu 11-positive cells and NK and LAK cell activity, an acute exacerbation during and after IL-2 administration, disappearance of HBc antigen observed in liver biopsy histology, and decrement of serum dna-p activity. However, seroconversion of HBs antigen was not observed and no case showed the elimination status of continuous HB virus infection. On the other hand, in the other 9 patients (Group B), these changes were not observed and the existence of a HLA type difference between Group A and B was shown by HLA analysis. These results indicated that the immune responses mediated by IL-2 may play an important role in the development of chronic hepatitis B, and these results may be regulated genetically.
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8/37. Chronic active "lupoid" hepatitis and HLA system; report of 6 cases.

    During the 12 years from 1977 to 1988 in Tottori University Hospital, 6 cases (4.2%) with chronic active "lupoid" hepatitis were encountered among 143 patients with histologically proven chronic active hepatitis. hla antigens were studied; BW 22 and CW 1 were strongly associated, and A 11 was rather associated with the rare disorder in japan. These results suggested that Japanese patients with chronic active "lupoid" hepatitis have different HLA markers from those in Caucasian patients, which may be attributable to rare specificity in the HLA system rather than different mechanisms of pathogenesis.
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9/37. Chronic active hepatitis following splenectomy for autoimmune thrombocytopenia.

    Two patients with immune thrombocytopenic purpura underwent splenectomy following the failure of steroid therapy. In neither patient was there evidence of liver disease prior to the splenectomy. Both had autoimmune parameters before the operation. They both received blood compounds; one patient remained negative for hepatitis B surface antigen (HBsAg) and antibodies, and the other had anti-HBs and anti-HBc. antibodies for hepatitis c virus were found in both patients. In the two patients hepatitis developed 4 and 6 weeks, respectively, following splenectomy, and liver biopsies performed 6 months and 2 years post splenectomy revealed chronic active hepatitis. The relationship between the two disorders is discussed and a possible role of the splenectomy in the development of chronic active hepatitis in these two cases is suggested.
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10/37. Redevelopment of hepatitis B surface antigen after renal transplantation.

    A patient with chronic hepatitis b virus (HBV) and chronic renal failure received a renal transplantation. Hepatitis B surface antigen (HBsAg) disappeared, and antibodies to HBsAg appeared 10 months before transplantation. Liver tests showed no abnormality at transplantation. Six months later, chronic hepatitis reactivated, antibodies to HBsAg disappeared, and HBsAg reappeared. hepatitis b virus dna was demonstrated with polymerase chain reaction in the serum collected before transplantation. This observation suggests that low level HBV replication was present before transplantation despite the absence of detectable HBsAg and was reactivated under immunosuppressive therapy after transplantation.
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