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Jean-claude Homberg - One of the best experts on this subject based on the ideXlab platform.

  • Brief Definitive Report ANTI-LIVER-KIDNEY MICROSOME ANTIBODY RECOGNIZES A 50,000 MOLECULAR WEIGHT PROTEIN OF THE ENDOPLASMIC RETICULUM
    2013
    Co-Authors: Fernando Alvarez, Jean-claude Homberg, Olivier Bernard, Gert Kreibich
    Abstract:

    Children with autoimmune Chronic Active Hepatitis can be separated into two groups depending on the presence in the serum of either smooth muscle antibody (SMA) or liver-kidney microsome antibody (LKMA) (1). The latter can be detected by immunofluorescence as a cytoplasmic staining of hepatocytes and of kidney tubular cells in sections from the respective rat organs (2). Indeed, it has been shown by immunoelectron microscopy that LKMA binds to constitutents of the endoplasmic reticulum of rat hepatocytes (3). Using recent developments in cell fractionation and immunological techniques, we have determined that the antigen recognized by LKMA is an integral membrane protein of 50,000 mol wt located primarily in the smooth endoplasmic reticulum. Materials and Methods Sera. LKMA-positive sera were obtained from five children with Chronic Active Hepatitis as proven by liver biopsy (immunofluorescence LKMA titer, 1:500 to 1:100,000; serum gamma globulin levels, 13.5-43 g/i). As a control we studied the sera from 20 children with various Chronic inflammatory liver diseases whose sera were negative fo

  • characterization of the liver cytosol antigen type 1 reacting with autoantibodies in Chronic Active Hepatitis
    Hepatology, 1992
    Co-Authors: Nisen Abuaf, Emmanuelle Soulier, Syria Laperche, Catherine Johanet, Pascale Chretien, Eric Martini, Jean-claude Homberg
    Abstract:

    An autoantibody to liver cytosol was previously described in childhood autoimmune Chronic Active Hepatitis type 2. The antigen, liver cytosol antigen type 1, was for the first time partially purified using gel filtration and ion exchange chromatography, and it was characterized using immunodiffusion, immunoblot and sodium dodecyl sulfate—polyacrylamide gel electrophoresis analysis of the immunoprecipitate. Immunoblot detected a unique antigenic peptide at 62 kD from human cytosol and at 58 kD from rat cytosol. The same peptides were also detected when immuno-precipitates of liver cytosol antigen type 1 and autoantibodies to liver cytosol antigen were submitted to sodium dodecyl sulfate—polyacrylamide gel electrophoresis. A polymeric structure, probably a tetramer, is suggested for native liver cytosol antigen type 1 because in gel filtration chromatography liver cytosol antigen type 1 was eluted as a protein of a molecular weight between 240 and 290 kD when human liver cytosol was fractionated and between 220 and 270 kD from rat liver cytosol. Liver cytosol antigen type 1 is probably poor in carbohydrates because it was not stained by periodic acid—Schiff stain. The autoantibodies to liver cytosol were frequently found in association with antiliver kidney microsomal autoantibodies type 1, which are directed against the cytochrome P-450 of the IID6 subfamily. Antiliver kidney microsomal autoantibodies type 1 but not antiliver cytosol autoantibodies were found in association with antibodies to Hepatitis C virus. Autoantibodies to liver cytosol antigen type 1 seem to be a more specific marker for autoimmune Hepatitis type 2 than antiliver kidney microsomal antibodies type 1 autoantibodies. (HEPATOLOGY 1992;16:892–898.)

Henry A. Homburger - One of the best experts on this subject based on the ideXlab platform.

  • frequency and significance of antibodies to liver kidney microsome type 1 in adults with Chronic Active Hepatitis
    Gastroenterology, 1992
    Co-Authors: Albert J Czaja, Michael P. Manns, Henry A. Homburger
    Abstract:

    To assess the frequency of antibodies to liver/kidney microsome type 1 (anti-LKM1) in patients with Chronic Active Hepatitis, 131 such patients were tested by an indirect immunofluorescence assay. Of 62 patients with type 1 autoimmune Hepatitis, none were seropositive. In contrast, 3 of 11 patients with autoimmune Hepatitis and antimitochondrial antibodies (27%) were seropositive for anti-LKM1. Each had responded to corticosteroid therapy, and retesting of sera confirmed that each had been misclassified as antimitochondrial antibody positive. None of the patients with Chronic Active Hepatitis B (14 patients) or C (24 patients) had anti-LKM1. Similarly, none of the 20 patients with cryptogenic disease had these antibodies. It is concluded that anti-LKM1 is specific for type 2 autoimmune Hepatitis and is infrequent in adult patients seen at a referral center in the United States for Chronic Active Hepatitis. Anti-LKM1 reactivity may be misinterpreted as antimitochondrial antibody reactivity by indirect immunofluorescence. Chronic Hepatitis B and C virus infections are not important stimuli for the production of anti-LKM1, and testing for anti-LKM 1 is unlikely to clarify the nature of cryptogenic disease.

Takeshi Okanoue - One of the best experts on this subject based on the ideXlab platform.

  • Hepatitis b virus dna in liver serum and peripheral blood mononuclear cells after the clearance of serum Hepatitis b virus surface antigen
    Journal of Medical Virology, 2004
    Co-Authors: Yoshiki Murakami, Masahito Minami, Yukiko Daimon, Takeshi Okanoue
    Abstract:

    The integration of Hepatitis B virus (HBV) DNA in the liver of Chronic HBV carriers has been documented extensively. However, the status of the viral genome during acute infection has not been assessed conclusively. While HBV DNA sequences are detected often in serum, liver, and peripheral blood mononuclear cells (PBMCs) after the clearance of serum the Hepatitis B virus surface antigen (HBsAg), the precise status of the viral genome, and in particular the possible persistence of integrated genomes in PBMCs, has not been established. A highly sensitive PCR-derived assay (Alu-PCR) was employed to re-examine liver and PBMC specimens obtained from patients with acute (n = 19) and Chronic (n = 22) Hepatitis in whom serum HBsAg was present (n = 12) (HBV-related Chronic Active Hepatitis) or absent with anti-HCV (n = 10) (HCV-related Chronic Active Hepatitis). Viral integration was demonstrated in 3 out of 19 liver specimens from patients with acute Hepatitis and 12 out of 12 specimens from patients with Chronic Hepatitis. Viral integration was also observed in 4 out of 7 PBMC samples from HBV-related Chronic Active Hepatitis patients and 2 out of 10 liver and PBMC samples from HCV-related Chronic Active Hepatitis patients. In one liver specimen from an acute Hepatitis patient, HBV DNA was found integrated in the intronic sequence of the tumour necrosis factor (TNF)-induced protein gene; viral integration into cellular sequences was also found in the PBMCs of four HBV-related Chronic Active Hepatitis and two HCV-related Chronic Active Hepatitis. The results demonstrate the early integration of HBV genome during acute viral infections and the persistence of the viral genome in an integrated form in PBMCs.

  • ischemic colitis during interferon alpha treatment for Chronic Active Hepatitis c
    Journal of Gastroenterology, 1996
    Co-Authors: Hisashi Tada, Takeshi Okanoue, Shoichi Saitoh, Yoshihiro Nakagawa, Hirofumi Hirana, Michio Morimoto, Toshihide Shima, Kazuhiko Shimamoto, Kei Kashima
    Abstract:

    Between 1991 and 1994, at Hoshigaoka Koseinenkin Hospital, we treated 280 patients with Chronic Hepatitis C with interferon (IFN), and ischemic colitis occurred in two patients (0.7%) during the treatment. Melena appeared in case 1 in the 2nd month after the initiation of IFN-alpha treatment, and in case 2 in the 6th month. In both patients, longitudinal ulcerations in the descending colon were revealed by urgent colonoscopy, and these resolved within 2 weeks after discontinuation of the IFN treatment. It appears that ischemic colitis was associated with the IFN treatment, suggesting that attention should be paid to this possible complication.

Roger Williams - One of the best experts on this subject based on the ideXlab platform.

  • relapse following treatment withdrawal in patients with autoimmune Chronic Active Hepatitis
    Hepatology, 2007
    Co-Authors: J.e. Hegarty, Kayhan Nouri T Aria, Bernard Portmann, Adrian L W F Eddleston, Roger Williams
    Abstract:

    A prospective study was performed to evaluate the outcome of treatment withdrawal in 30 patients with “autoimmune” Chronic Active Hepatitis in remission for periods of 1.5 to 9 years on maintenance corticosteroid and azathioprine therapy. Reactivation of disease, with marked rises in serum aminotransferase level (mean 668 ± S.D. 458 IU per liter) and accompanied by severe symptoms, occurred in 25 (87%) patients within 52 weeks (median 9 weeks; range 5 to 52) and was associated with the histological features of piecemeal necrosis and lobular Hepatitis in all 20 liver biopsies examined. Age, sex, duration of disease and remission, presence of cirrhosis, autoantibody status, or immunoglobulin levels did not differentiate patients who relapsed from those who remained in remission. The response to reinstitution of treatment with prednisolone was satisfactory in 25 patients and clinical and biochemical abnormalities resolved within 10 weeks (median 6; range 3 to 10), death occurred in one patient within 48 hr of readmission to hospital.

  • identification of Hepatitis b virus dna in the liver by in situ hybridisation using a biotinylated probe relation to hbcag expression and histology
    Journal of Hepatology, 1993
    Co-Authors: Nikolai V Naoumov, Adrian L W F Eddleston, Helena M Daniels, Fergus Davison, Graeme J M Alexander, Roger Williams
    Abstract:

    The cellular localisation of Hepatitis B virus (HBV)-DNA in liver tissue was studied by in situ hybridisation using biotinylated and radiolabelled probes on samples from HBsAg carriers with a spectrum of disease and related to the presence of HBV-DNA in serum and intrahepatic HBcAg expression. Sixteen of the 31 patients studied were seropositive for HBV-DNA; nine had Chronic Active Hepatitis and seven had Chronic persistent Hepatitis. HBV-DNA was detected in the liver tissue in seven of these patients. In each, HBV-DNA was detected in both cytoplasm and nuclei. All seven also had nuclear and/or cytoplasmic HBcAg which in six was associated with Chronic Active Hepatitis. HBcAg (without tissue HBV-DNA) was detected in the remaining nine patients with an exclusively nuclear pattern in two. Fifteen patients were seronegative for HBV-DNA. HBV-DNA was not detected in the tissue of any of these. Three of these were HBcAg positive but in each this was confined to occasional nuclei and each had inActive disease. The close association between the presence of detectable HBV-DNA in tissue, cytoplasmic HBV-DNA expression and Chronic Active Hepatitis in one group and a failure to detect HBV-DNA in those with nuclear HBcAg and benign disease suggests that there may be two distinct patterns of HBV replication in Chronic HBV carriers which may influence the development of liver damage.

Yasuni Nakanuma - One of the best experts on this subject based on the ideXlab platform.

  • distribution of cytokeratin 19 positive biliary cells in cirrhotic nodules hepatic borderline nodules atypical adenomatous hyperplasia and small hepatocellular carcinomas
    Modern Pathology, 1995
    Co-Authors: Tadashi Terada, Masahiro Hoso, Yasuni Nakanuma
    Abstract:

    : Borderline nodule (BN) in the cirrhotic liver is considered to be a precancerous lesion leading to hepatocellular carcinoma (HCC). We investigated the distribution of cytokeratin 19 (CK 19)-positive biliary cells, recognizable by a monoclonal antibody AE1, in normal livers, Chronic Active Hepatitis, cirrhosis, BN, and small HCC. The CK 19-positive biliary cells in the hepatic parenchyma were clearly divisible into two types (I and II). Type I cells were located within the hepatic parenchyma as small clusters forming small tubules (intraparenchymal ductules). Type II cells were bile ductules located in the peripheral rim of the hepatic lobules or hepatocellular lesions (peripheral ductular reaction) and were continuous with proliferated bile ductules in fibrous septae or portal tracts. In Chronic Active Hepatitis and regenerative nodules of cirrhosis, a few type I cells and a variable number of type II cells were present. In the BN, all cases harbored a few type I cells as well as a variable number of type II cells. The type II cells in the BN were fewer in number and more randomly distributed than those in Chronic Active Hepatitis and cirrhosis. Malignant foci in some BNs lacked CK 19-positive biliary cells. In small HCC, no CK 19-positive biliary cells were found; instead, AE1-positive HCC cells were present in three cases (17%). Although a great majority of type I cells corresponded to intraparenchymal ductules, some type I cells in the BN were composed of rather large tubules considered as interlobular bile ducts.(ABSTRACT TRUNCATED AT 250 WORDS)

  • mixed types of Chronic Active Hepatitis and primary biliary cirrhosis associated with the anti phospholipid antibody syndrome a case report
    Hepato-gastroenterology, 1993
    Co-Authors: R Saeki, Masashi Unoura, Yasuni Nakanuma, Shuichi Kaneko, S Terasaki, Hidero Ogino, T Wakabayashi, S Kawara, Kenichi Kobayashi
    Abstract:

    An understanding of the pathogenesis of mixed types of Chronic Active Hepatitis and primary biliary cirrhosis is important for the treatment of the patients. A 40-year-old Japanese woman with antiphospholipid syndrome has been treated with prednisolone for two years since she was diagnosed as having a mixed type of Chronic Active Hepatitis and primary biliary cirrhosis. Biochemical tests for liver function were normal during treatment. Laparoscopy revealed a white liver, and histology demonstrated disappearance of the findings of piecemeal necrosis or Chronic nonsuppurative destructive cholangitis in the specimen. Steroid treatment of patients with mixed types of Chronic Active Hepatitis and primary biliary cirrhosis is controversial, since it is contra-indicated in some. Although the clinical features of the patients varies from one to another, this case suggests that the autoimmune mechanism of some patients may resemble autoimmune Hepatitis rather than primary biliary cirrhosis, and treatment with steroid is effective.