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Dingshinn Chen - One of the best experts on this subject based on the ideXlab platform.
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Posttransfusion Hepatitis revisited by Hepatitis C antibody assays and polymerase chain reaction.
Gastroenterology, 1992Co-Authors: Jintown Wang, Jinchuan Sheu, Teh Hong Wang, Jaw-town Lin, Chang-yi Wang, Dingshinn ChenAbstract:Sera of 40 patients with posttransfusion non-A, non-B Hepatitis were tested for Hepatitis C and B viral genomes by polymerase chain reaction and for Hepatitis C antibodies by synthetic peptide immunoassays. Five were then considered to have chronic Hepatitis before transfusion. Six patients without Hepatitis C markers and Hepatitis B virus DNA recovered. In 29 recipients who became positive for Hepatitis C virus RNA, posttransfusion Hepatitis C was diagnosed. Of them, 5 were Hepatitis B surface antigen carriers. Synthetic peptide immunoassays detected 28 whereas anti-C100 assay detected 23 of the 29 acute Hepatitis C patients. Anticapsid antibody appeared earlier than the antinonstructural antibody in 10 seroconverters. They appeared simultaneously in 15 seroconverters but anticapsid antibody appeared later then the antinonstructural antibody in 3 Hepatitis B carriers. Transient suppression of Hepatitis B surface antigenemia was found in 2, whereas elevated Hepatitis B virus DNA was found in 3 carriers during acute Hepatitis C superinfection. In 2 carriers whose Hepatitis C became chronic, both Hepatitis B and C viral genomes persisted throughout 2 years of followup. Therefore these assays define posttransfusion Hepatitis C more precisely, and there seems no significant interference between chronic Hepatitis B and C virus infections.
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A prospective study of posttransfusion Hepatitis in Taiwan.
Journal of Hepatology, 1991Co-Authors: Teh Hong Wang, Jintown Wang, Jinchuan Sheu, Juei-low Sung, Dingshinn ChenAbstract:In a follow-up study of 6 months or more of two hundred and ninety-six patients who had received blood transfusion, 37 (12.5%) developed acute posttransfusion Hepatitis. Patients with posttransfusion Hepatitis had significantly higher donor numbers and transfusion amounts than patients without Hepatitis. Frequency was not related to the age, sex or Hepatitis B carriage of recipients. There were no cases of fulminant Hepatitis. Of 37 patients with Hepatitis, 36 were diagnosed as non-A, non-B Hepatitis and one as Hepatitis B. Twenty-two (59.5%) of the 36 patients with non-A, non-B Hepatitis seroconverted to Hepatitis C antibody. Two of these were positive for Hepatitis C antibody before transfusion and 12 were negative for Hepatitis C antibody. Thirty-three of the 36 patients were followed-up for more than 6 months after the onset of Hepatitis. While 13 of the 33 patients recovered, the remaining 20 (60.6%) patients still had persistent liver test abnormalities 6 months after the onset of Hepatitis. Seventeen (85%) of the 20 patients who developed chronic Hepatitis were Hepatitis C antibody positive. In contrast, only four (30%) of the 13 patients who recovered after acute Hepatitis were positive for the Hepatitis C antibody. Chronicity rate was not related to the patient's sex, age, transfusion amount or donor number. Our results suggest a high frequency of posttransfusion Hepatitis C in Taiwan and that the infection has a high risk of chronicity.
Ansgar W Lohse - One of the best experts on this subject based on the ideXlab platform.
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overlap syndromes the international autoimmune Hepatitis group iaihg position statement on a controversial issue
Journal of Hepatology, 2011Co-Authors: Kirsten Muri Boberg, Ansgar W Lohse, Michael P Manns, R W Chapman, Gideon M Hirschfield, Erik SchrumpfAbstract:Some patients present with overlapping features between disorders within the spectrum of autoimmune liver diseases ( i.e. autoimmune Hepatitis (AIH), primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC)) and are commonly classified as having an "overlap syndrome". Standardized definitions of "overlap syndromes" are lacking. The aim of this report by the International Autoimmune Hepatitis Group (IAIHG) is to evaluate if there are important reasons to classify conditions with overlapping features between autoimmune liver diseases as separate diagnostic entities. Definition of diagnostic criteria for overlap conditions can only be arbitrary. The IAIHG scoring system for diagnosis of AIH has been widely used to diagnose "overlap syndromes", but was not intended for such use and has not proven to be an efficient tool for this purpose. Some patients with overlapping features between a cholestatic and hepatitic disorder appear to benefit from treatment with a combination of ursodeoxycholic acid and immunosuppressants, but this strategy is not evidence-based, and it seems unjustified to define new diagnostic groups in this regard. The IAIHG suggests that patients with autoimmune liver disease should be categorized according to the predominating feature(s) as AIH, PBC, and PSC/small duct PSC, respectively, and that those with overlapping features are not considered as being distinct diagnostic entities. The IAIHG scoring system should not be used to establish subgroups of patients. Patients with PBC and PSC with features of AIH should be considered for immunosuppressive treatment. Due to the low prevalence of such "overlap syndromes", prospective interventional therapeutic trials cannot be expected in the foreseeable future.
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phenprocoumon induced liver disease ranges from mild acute Hepatitis to sub acute liver failure
Journal of Hepatology, 2004Co-Authors: Carl Cristoph Schimanski, Margie Mohler, Jurgen Burg, Sonja Kanzler, Peter R Galle, G Otto, Thomas Hohler, Ansgar W LohseAbstract:Abstract Background/Aims Except for bleeding complications, other serious adverse reactions of coumarin anticoagulants such as hepatotoxicity or skin necrosis are comparatively rare. Nonetheless, a small number of coumarin-induced (sub-) acute liver failures has been published. Methods A retrospective analysis was performed of patients treated for liver disease between 1992 and 2002 at our department to evaluate the incidence, clinical findings and histopathology of coumarin-induced hepatotoxicity. Results The retrospective analysis revealed eight cases of phenprocoumon-induced hepatotoxicity, including three cases of (sub-) acute liver failure which resulted in two orthotopic liver transplantations and one fatal outcome. Five patients with phenprocoumon-induced Hepatitis recovered well after anticoagulation was switched to another coumarin derivate or subcutaneous low molecular weight heparin. In all patients liver injury was predominantly of an hepatitic type. In the cases of (sub-) acute liver failure massive confluent liver cell necroses were histologically present, whereas among patients without liver failure mild portal to moderate active lobular Hepatitis were observed. A retrospective analysis by BfArM (German Federal Institute for Drugs and Medical Devices) revealed 4390 cases of possible phenprocoumon-related adverse reactions since 1990, 2% of which had presented with Hepatitis and 0.2% with liver failure. Conclusions Phenprocoumon-induced liver disease is an uncommon complication, which can, however, cause (sub-) acute liver failure.
Roger Williams - One of the best experts on this subject based on the ideXlab platform.
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Hepatitis c and e in non a non b fulminant hepatic failure a polymerase chain reaction and serological study
Journal of Hepatology, 1994Co-Authors: Richard Sallie, Antonio Eduardo Silva, Michael Purdy, Heather Smith, Karen Mccaustland, Christopher Tibbs, Bernard S Portmann, Adrian Eddleston, Daniel P Bradley, Roger WilliamsAbstract:A significant proportion of patients with fulminant hepatic failure have clinical, biochemical and histological features suggestive of acute viral Hepatitis, without serological evidence of either Hepatitis A or B. The contribution of Hepatitis C to such cases of non-A non-B fulminant hepatic failure is presently uncertain while Hepatitis E is well recognized as a cause of fulminant hepatic failure in endemic areas. Nested polymerase chain reaction for detection of both Hepatitis C and E virus as well as two serological assays for anti-Hepatitis C virus and anti-Hepatitis E virus western blotting (both IgG and IgM) were performed on acute sera of 42 consecutive cases of non A, non B-fulminant hepatic failure and on convalescent sera of 17 of 20 patients who underwent orthotopic liver transplantation. Fresh liver tissue, obtained at the time of transplantation, was also studied by polymerase chain reaction in eight cases. Evidence of an acute Hepatitis E virus infection (Hepatitis E virus RNA amplified from serum by polymerase chain reaction or serum IgM positive to western blot) was found in eight patients. One patient had anti-HCV at presentation but assays on later sera proved negative. Convalescent sera and sera obtained after orthotopic liver transplantation were all negative to both anti-HCV assay systems, but HCV RNA was not found in either serum or liver tissue in any case. While these findings suggest sporadic Hepatitis E virus infection may be an important cause of fulminant hepatitic failure outside endemic areas, most cases of presumed non A, non B-fulminant hepatic failure appear to be due to a viral agent(s) other than Hepatitis A, B, C, D, or E, or to some as yet undefined toxic or metabolic process
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Hepatitis b virus reinfection after orthotopic liver transplantation serological and clinical implications
Journal of Hepatology, 1992Co-Authors: John Ogrady, Heather M Smith, Susan E Davies, Helena M Daniels, Peter T Donaldson, K C Tan, Bernard Portmann, Graeme J M Alexander, Roger WilliamsAbstract:The implications of Hepatitis B virus (HBV) reinfection after liver transplantation were studied in 29 patients followed for 1.7-15 years. Of 20 patients with HBV infection alone, nine were HBeAg and HBV DNA seronegative and 11 had evidence of HBV replication as measured by HBeAg or HBV DNA seropositivity. Nine patients had co-existing HBV and delta virus (HDV) infection. Five patients became HBsAg seronegative after transplantation (four immediately and one after an hepatitic episode). Of the 20 patients with HBV infection alone, 17 had evidence of viral replication after transplantation with markedly increased HBV DNA levels. Five patients with HDV infection had HBV DNA in serum, but in significantly lower amounts than in those with HBV infection alone. Twenty-five episodes of graft dysfunction attributed to recurrent HBV infection occurred in 19 patients (65.5%). Thirteen episodes (in 12 patients) were self-resolving acute hepatitic illnesses. Six patients had a rapidly progressive illness leading to graft loss within 6 weeks, with the distinctive histological features termed fibrosing cholestatic Hepatitis (FCH). Liver function tests in these patients showed markedly abnormal serum bilirubin and prothrombin times, but only modest increases in serum transaminase levels. An additional six patients lost their graft as a consequence of HBV recurrence through various pathogenetic mechanisms including possible (but unproven) FCH, chronic active Hepatitis or late-onset hepatic failure. Co-existing HDV infection appeared to confer some medium-term protection from graft loss.
Teh Hong Wang - One of the best experts on this subject based on the ideXlab platform.
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Posttransfusion Hepatitis revisited by Hepatitis C antibody assays and polymerase chain reaction.
Gastroenterology, 1992Co-Authors: Jintown Wang, Jinchuan Sheu, Teh Hong Wang, Jaw-town Lin, Chang-yi Wang, Dingshinn ChenAbstract:Sera of 40 patients with posttransfusion non-A, non-B Hepatitis were tested for Hepatitis C and B viral genomes by polymerase chain reaction and for Hepatitis C antibodies by synthetic peptide immunoassays. Five were then considered to have chronic Hepatitis before transfusion. Six patients without Hepatitis C markers and Hepatitis B virus DNA recovered. In 29 recipients who became positive for Hepatitis C virus RNA, posttransfusion Hepatitis C was diagnosed. Of them, 5 were Hepatitis B surface antigen carriers. Synthetic peptide immunoassays detected 28 whereas anti-C100 assay detected 23 of the 29 acute Hepatitis C patients. Anticapsid antibody appeared earlier than the antinonstructural antibody in 10 seroconverters. They appeared simultaneously in 15 seroconverters but anticapsid antibody appeared later then the antinonstructural antibody in 3 Hepatitis B carriers. Transient suppression of Hepatitis B surface antigenemia was found in 2, whereas elevated Hepatitis B virus DNA was found in 3 carriers during acute Hepatitis C superinfection. In 2 carriers whose Hepatitis C became chronic, both Hepatitis B and C viral genomes persisted throughout 2 years of followup. Therefore these assays define posttransfusion Hepatitis C more precisely, and there seems no significant interference between chronic Hepatitis B and C virus infections.
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A prospective study of posttransfusion Hepatitis in Taiwan.
Journal of Hepatology, 1991Co-Authors: Teh Hong Wang, Jintown Wang, Jinchuan Sheu, Juei-low Sung, Dingshinn ChenAbstract:In a follow-up study of 6 months or more of two hundred and ninety-six patients who had received blood transfusion, 37 (12.5%) developed acute posttransfusion Hepatitis. Patients with posttransfusion Hepatitis had significantly higher donor numbers and transfusion amounts than patients without Hepatitis. Frequency was not related to the age, sex or Hepatitis B carriage of recipients. There were no cases of fulminant Hepatitis. Of 37 patients with Hepatitis, 36 were diagnosed as non-A, non-B Hepatitis and one as Hepatitis B. Twenty-two (59.5%) of the 36 patients with non-A, non-B Hepatitis seroconverted to Hepatitis C antibody. Two of these were positive for Hepatitis C antibody before transfusion and 12 were negative for Hepatitis C antibody. Thirty-three of the 36 patients were followed-up for more than 6 months after the onset of Hepatitis. While 13 of the 33 patients recovered, the remaining 20 (60.6%) patients still had persistent liver test abnormalities 6 months after the onset of Hepatitis. Seventeen (85%) of the 20 patients who developed chronic Hepatitis were Hepatitis C antibody positive. In contrast, only four (30%) of the 13 patients who recovered after acute Hepatitis were positive for the Hepatitis C antibody. Chronicity rate was not related to the patient's sex, age, transfusion amount or donor number. Our results suggest a high frequency of posttransfusion Hepatitis C in Taiwan and that the infection has a high risk of chronicity.
Jintown Wang - One of the best experts on this subject based on the ideXlab platform.
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Posttransfusion Hepatitis revisited by Hepatitis C antibody assays and polymerase chain reaction.
Gastroenterology, 1992Co-Authors: Jintown Wang, Jinchuan Sheu, Teh Hong Wang, Jaw-town Lin, Chang-yi Wang, Dingshinn ChenAbstract:Sera of 40 patients with posttransfusion non-A, non-B Hepatitis were tested for Hepatitis C and B viral genomes by polymerase chain reaction and for Hepatitis C antibodies by synthetic peptide immunoassays. Five were then considered to have chronic Hepatitis before transfusion. Six patients without Hepatitis C markers and Hepatitis B virus DNA recovered. In 29 recipients who became positive for Hepatitis C virus RNA, posttransfusion Hepatitis C was diagnosed. Of them, 5 were Hepatitis B surface antigen carriers. Synthetic peptide immunoassays detected 28 whereas anti-C100 assay detected 23 of the 29 acute Hepatitis C patients. Anticapsid antibody appeared earlier than the antinonstructural antibody in 10 seroconverters. They appeared simultaneously in 15 seroconverters but anticapsid antibody appeared later then the antinonstructural antibody in 3 Hepatitis B carriers. Transient suppression of Hepatitis B surface antigenemia was found in 2, whereas elevated Hepatitis B virus DNA was found in 3 carriers during acute Hepatitis C superinfection. In 2 carriers whose Hepatitis C became chronic, both Hepatitis B and C viral genomes persisted throughout 2 years of followup. Therefore these assays define posttransfusion Hepatitis C more precisely, and there seems no significant interference between chronic Hepatitis B and C virus infections.
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A prospective study of posttransfusion Hepatitis in Taiwan.
Journal of Hepatology, 1991Co-Authors: Teh Hong Wang, Jintown Wang, Jinchuan Sheu, Juei-low Sung, Dingshinn ChenAbstract:In a follow-up study of 6 months or more of two hundred and ninety-six patients who had received blood transfusion, 37 (12.5%) developed acute posttransfusion Hepatitis. Patients with posttransfusion Hepatitis had significantly higher donor numbers and transfusion amounts than patients without Hepatitis. Frequency was not related to the age, sex or Hepatitis B carriage of recipients. There were no cases of fulminant Hepatitis. Of 37 patients with Hepatitis, 36 were diagnosed as non-A, non-B Hepatitis and one as Hepatitis B. Twenty-two (59.5%) of the 36 patients with non-A, non-B Hepatitis seroconverted to Hepatitis C antibody. Two of these were positive for Hepatitis C antibody before transfusion and 12 were negative for Hepatitis C antibody. Thirty-three of the 36 patients were followed-up for more than 6 months after the onset of Hepatitis. While 13 of the 33 patients recovered, the remaining 20 (60.6%) patients still had persistent liver test abnormalities 6 months after the onset of Hepatitis. Seventeen (85%) of the 20 patients who developed chronic Hepatitis were Hepatitis C antibody positive. In contrast, only four (30%) of the 13 patients who recovered after acute Hepatitis were positive for the Hepatitis C antibody. Chronicity rate was not related to the patient's sex, age, transfusion amount or donor number. Our results suggest a high frequency of posttransfusion Hepatitis C in Taiwan and that the infection has a high risk of chronicity.
