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Marion Koopmans - One of the best experts on this subject based on the ideXlab platform.

  • Chronic Hepatitis e virus infection in liver transplant recipients
    Liver Transplantation, 2008
    Co-Authors: Elizabeth B Haagsma, Arie P Van Den Berg, Robert J Porte, Cornelis A Benne, Harry Vennema, Johan Reimerink, Marion Koopmans
    Abstract:

    Hepatitis E virus (HEV) infection is known to run a self-limiting course. Sporadic cases of acute Hepatitis due to infection with HEV genotype 3, present in pig populations, are increasingly recognized. Zoonotic transmission seems infrequent. The entity of unexplained Chronic Hepatitis after liver transplantation has been recognized. Detection of HEV in 2 liver transplant recipients triggered a review of these cases. Freeze-stored sera were available for retrospective analysis. HEV antibodies were determined. For virus detection and identification, a fragment of the gene encoding the major capsid protein (open reading frame 2) was amplified by reverse-transcription polymerase chain reaction and sequenced to identify the genotype. Two months after liver transplantation, case A developed unexplained Chronic Hepatitis, which developed into cirrhosis. Retransplantation followed 7 years later, after which Chronic Hepatitis recurred. In retrospect, HEV RNA was present in serum 3 weeks after the first transplantation and remained present afterwards. HEV RNA was also present in retransplant liver tissue. HEV antibodies appeared late after retransplantation. Case B developed unexplained Chronic Hepatitis 7 years after transplantation. Retransplantation was needed 5 years later, after which no signs of Hepatitis recurred. In retrospect, the period of Chronic Hepatitis up to the retransplantation coincided with HEV RNA in serum. In case B, antibodies developed, the viral load was much lower than in case A, and the virus seemed to be cleared after retransplantation. Genotyping in both cases revealed 2 unique strains of genotype 3. In conclusion, Chronic HEV infection may develop in immunosuppressed patients, who may then serve as long-term carriers of the virus. We hypothesize that HEV may be the cause of Chronic Hepatitis in liver transplant recipients.

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

  • Endotheliitis-like changes in Chronic Hepatitis C.
    Histology and Histopathology, 1997
    Co-Authors: Lory J, Zimmermann A
    Abstract:

    Liver biopsies in Hepatitis C frequently show bile duct damage, lymphoid follicles, large and small droplet fat, hepatocyte multinucleation. Mallory body-like material, and activation of sinusoidal inflammatory cells. Even though these lesions are useful parameters in the diagnosis of Hepatitis C, their specificity remains uncertain. Endotheliitis-like changes of small portal veins have been described for various liver diseases, including viral Hepatitis. The aim of the present study was to investigate the prevalence and severity of endotheliitis-like changes in Chronic Hepatitis C in comparison with Chronic Hepatitis B. For this purpose, liver biopsies of 50 patients with Chronic Hepatitis C and 48 patients which Chronic Hepatitis B were systematically analyzed for the presence of endotheliitis-like changes. Endotheliitis-like changes were defined as lymphocytic infiltration of venous walls, subendothelial lymphocyte accumulation, adherence of lymphocytes to the endothelium, and endothelial cell damage. Endotheliitis-like change severity was graded (borderline/questionable; slight to moderate; severe), and endotheliitis-like changes were analyzed in small portal veins and in central veins. Endotheliitis-like changes were significantly more frequent in Chronic Hepatitis C than in Chronic Hepatitis B (41.5% vs. 6.9%; p < 0.05). In Chronic Hepatitis C, endotheliitis-like changes predominated in small portal veins, but 27% of small hepatic veins were involved as well. The findings indicate that endotheliitis-like changes may represent a useful histological parameter in the diagnosis of Chronic Hepatitis C.

  • Endotheliitis-like changes in Chronic Hepatitis C.
    Histology and Histopathology, 1997
    Co-Authors: Lory J, Zimmermann A
    Abstract:

    Liver biopsies in Hepatitis C frequently show bile duct damage, lymphoid follicles, large and small droplet fat, hepatocyte multinucleation. Mallory bodylike material, and activation of sinusoidal inflammatory cells. Even though these lesions are useful parameters in the diagnosis of Hepatitis C, their specificity remains uncertain. Endotheliitis-like changes of small portal veins have been described for various liver diseases, including viral Hepatitis. The aim of the present study was to investigate the prevalence and severity of endotheliitis-like changes in Chronic Hepatitis C in comparison with Chronic Hepatitis B. For this purpose, liver biopsies of 50 patients with Chronic Hepatitis C and 48 patients which Chronic Hepatitis B were systematically analyzed for the presence of endotheliitis-like changes. Endotheliitis-like changes were defined as lymphocytic infiltration of venous walls, subendothelial lymphocyte accumulation, adherence of lymphocytes to the endothelium, and endothelial cell damage. Endotheliitis-like change severity was graded (borderline/questionable; slight to moderate; severe), and endotheliitis-like changes were analyzed in small portal veins and in central veins. Endotheliitis-like changes were significantly more frequent in Chronic Hepatitis C than in Chronic Hepatitis B (41.5% vs. 6.9%; p

Brian J Mcmahon - One of the best experts on this subject based on the ideXlab platform.

  • Chronic Hepatitis b
    Hepatology, 2001
    Co-Authors: Brian J Mcmahon
    Abstract:

    PREAMBLE These guidelines have been written to assist physicians and other health care providers in the recognition, diagnosis, and management of patients Chronically infected with the Hepatitis B virus (HBV). They are intended to suggest preferable approaches to the clinical management of Chronic Hepatitis B. The recommendations are flexible and are not intended as the only acceptable approach to management and treatment. As the appropriate course of treatment will vary in light of the relevant facts and circumstances surrounding each individual patient with Chronic Hepatitis B, guidelines are not intended to define the applicable standard of medical care and may be updated periodically as new information becomes available. These guidelines were developed under the auspices of, and approved by, the Practice Guidelines Committee of the American Association for the Study of Liver Diseases. They should be taken as guidelines and not “standards of care.” Data used to support the recommendations made were obtained by a literature search of peer-reviewed articles concerning the natural history, diagnosis, and treatment of Chronic Hepatitis B. In addition, the proceedings of a recent National Institutes of Health workshop on the “Management of Hepatitis B” were considered in the development of these guidelines. 1 The strength of each recommendation is categorized based on the quality of evidence in the literature according to the rating system indicated in Table 1. 2

Marie Danjoux - One of the best experts on this subject based on the ideXlab platform.

  • Hepatitis e virus and Chronic Hepatitis in organ transplant recipients
    The New England Journal of Medicine, 2008
    Co-Authors: Nassim Kamar, Janick Selves, Jeanmichel Mansuy, Leila Ouezzani, Jeanmarie Peron, Joelle Guitard, Olivier Cointault, Laure Esposito, Florence Abravanel, Marie Danjoux
    Abstract:

    Hepatitis E virus (HEV) is considered an agent responsible for acute Hepatitis that does not progress to Chronic Hepatitis. We identified 14 cases of acute HEV infection in three patients receiving liver transplants, nine receiving kidney transplants, and two receiving kidney and pancreas transplants. All patients were positive for serum HEV RNA. Chronic Hepatitis developed in eight patients, as confirmed by persistently elevated aminotransferase levels, serum HEV RNA, and histologic features of Chronic Hepatitis. The time from transplantation to diagnosis was significantly shorter and the total counts of lymphocytes and of CD2, CD3, and CD4 T cells were significantly lower in patients in whom Chronic disease developed.

Elizabeth B Haagsma - One of the best experts on this subject based on the ideXlab platform.

  • Chronic Hepatitis e virus infection in liver transplant recipients
    Liver Transplantation, 2008
    Co-Authors: Elizabeth B Haagsma, Arie P Van Den Berg, Robert J Porte, Cornelis A Benne, Harry Vennema, Johan Reimerink, Marion Koopmans
    Abstract:

    Hepatitis E virus (HEV) infection is known to run a self-limiting course. Sporadic cases of acute Hepatitis due to infection with HEV genotype 3, present in pig populations, are increasingly recognized. Zoonotic transmission seems infrequent. The entity of unexplained Chronic Hepatitis after liver transplantation has been recognized. Detection of HEV in 2 liver transplant recipients triggered a review of these cases. Freeze-stored sera were available for retrospective analysis. HEV antibodies were determined. For virus detection and identification, a fragment of the gene encoding the major capsid protein (open reading frame 2) was amplified by reverse-transcription polymerase chain reaction and sequenced to identify the genotype. Two months after liver transplantation, case A developed unexplained Chronic Hepatitis, which developed into cirrhosis. Retransplantation followed 7 years later, after which Chronic Hepatitis recurred. In retrospect, HEV RNA was present in serum 3 weeks after the first transplantation and remained present afterwards. HEV RNA was also present in retransplant liver tissue. HEV antibodies appeared late after retransplantation. Case B developed unexplained Chronic Hepatitis 7 years after transplantation. Retransplantation was needed 5 years later, after which no signs of Hepatitis recurred. In retrospect, the period of Chronic Hepatitis up to the retransplantation coincided with HEV RNA in serum. In case B, antibodies developed, the viral load was much lower than in case A, and the virus seemed to be cleared after retransplantation. Genotyping in both cases revealed 2 unique strains of genotype 3. In conclusion, Chronic HEV infection may develop in immunosuppressed patients, who may then serve as long-term carriers of the virus. We hypothesize that HEV may be the cause of Chronic Hepatitis in liver transplant recipients.