1/24. Autoimmune hepatitis in a genetically susceptible patient: is it triggered by acute viral hepatitis A?The pathogenic mechanisms for autoimmune hepatitis (AIH) are not completely known. Susceptibility to AIH is associated with the human leukocyte antigens (HLA) class II: DR3 and DR4. Nevertheless, AIH does not have a strong genetic predisposition, suggesting that other factors are involved. Perhaps the strongest evidence of a viral cause for AIH exists for hepatitis c virus. AIH has been reported to develop rarely after acute infection with hepatitis a virus. We report on a 55-year-old woman in whom AIH developed during the convalescence period of serologically proven acute viral hepatitis type A. HLA class II DRB1*0401, which was reported to be associated with AIH with a moderate coarse and late appearance in life, was found in this patient. Steroid therapy was followed by a complete clinical remission. Our case supports the possibility that acute hepatitis A may trigger the development of AIH in a genetically susceptible subject.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
2/24. Efficacy of lamivudine for the treatment of hepatitis b virus infection after liver transplantation in children.BACKGROUND: There is at present very little information about hepatitis b virus (HBV) infection in children after liver transplantation. This is the first study to assess the safety and efficacy of lamivudine in this patient population. methods: We describe three children aged 5-14 years who underwent liver transplantation for fulminant hepatitis A, hyperoxaluria, and cystic fibrosis. Despite adequate immunoprophylaxis, two of the children who were serum hepatitis B surface antigen-positive before transplantation (HBV dna-negative by hybridization) had a reactivation of the disease, and one had a de novo HBV infection, at 12-18 months after transplantation. lamivudine 3 mg/kg was administered on a compassionate-use basis for 14-36 months. RESULTS: After 1 month of therapy, HBV dna disappeared from the serum in all patients by hybridization and in two patients by polymerase chain reaction. In all three children, alanine transaminase levels normalized. One child developed lamivudine resistance after 22 months with no evidence of hepatic decompensation. Repeated liver histological studies revealed progression of hepatic fibrosis in one child. All children remained serum hepatitis B surface antigen- and hepatitis B e antigen-positive. No adverse effects of the drug were noted. CONCLUSION: lamivudine is beneficial and well tolerated in children with HBV infection after liver transplantation.- - - - - - - - - - ranking = 3keywords = antigen (Clic here for more details about this article) |
3/24. Presence of oligoclonal T cells in cerebrospinal fluid of a child with multiphasic disseminated encephalomyelitis following hepatitis a virus infection.We have investigated the clonality of beta-chain T-cell receptor (TCR) transcripts from the cerebrospinal fluid (CSF) and peripheral blood from a 7-year old child who developed a multiphasic disseminated encephalomyelitis following an infection with hepatitis a virus. We amplified beta-chain TCR transcripts by nonpalindromic adaptor (NPA)-PCR-Vbeta-specific PCR. TCR transcripts from only five Vbeta families (Vbeta13, Vbeta3, Vbeta17, Vbeta8, and Vbeta20) were detected in CSF. The amplified products were combined, cloned, and sequenced. sequence analysis revealed in the CSF substantial proportions of identical beta-chain of TCR transcripts, demonstrating oligoclonal populations of T cells. Seventeen of 35 (48%) transcripts were 100% identical, demonstrating a major Vbeta13.3 Dbeta2.1 Jbeta1.3 clonal expansion. Six of 35 (17%) transcripts were also 100% identical, revealing a second Vbeta13 clonal expansion (Vbeta13.1 Dbeta2.1 Jbeta1.2). Clonal expansions were also found within the Vbeta3 family (transcript Vbeta3.1 Dbeta2.1 Jbeta1.5 accounted for 5 of 35 transcripts [14%]) and within the Vbeta20 family (transcript Vbeta20.1 Dbeta1.1 Jbeta2.4 accounted for 3 of 35 transcripts [8%]). These results demonstrate the presence of T-cell oligoclonal expansions in the CSF of this patient following infection with hepatitis a virus. Analysis of the CDR3 motifs revealed that two of the clonally expanded T-cell clones exhibited substantial homology to myelin basic protein-reactive T-cell clones. In contrast, all Vbeta TCR families were expressed in peripheral blood lymphocytes. Oligoclonal expansions of T cells were not detected in the peripheral blood of this patient. It remains to be determined whether these clonally expanded T cells are specific for hepatitis A viral antigen(s) or host central nervous system antigen(s) and whether molecular mimicry between hepatitis A viral protein and a host protein is responsible for demyelinating disease in this patient.- - - - - - - - - - ranking = 2keywords = antigen (Clic here for more details about this article) |
4/24. factor viii levels during the course of acute hepatitis in a haemophiliac.A 51-year-old patient with haemophilia since childhood (usual factor viii level 14%) developed acute viral hepatitis type B two months after an operation which had been covered by cryoprecipitate. The course of the hepatitis following admission was severe with encephalopathy and ascites. Evidence of intravascular coagulation with an increased radioactive fibrinogen turnover was also present. The factor viii level measured by a one-stage clotting factor assay rose rapidly to 200% of normal and remained at this level for two weeks, and factor-VIII-related antigen as measured by electroimmunoassay also became greatly elevated (900% of normal). The possible mechanisms underlying those surprising changes are discussed.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
5/24. Acute glomerulonephritis complicating australia antigen-negative viral hepatitis.A case of acute glomerulonephritis complicating australia antigen-negative hepatitis in a 17-year-old man is described. The literature relating the onset of glomerulonephritis to virus infection is general, and to that of hepatitis in particular, is reviewed.- - - - - - - - - - ranking = 5keywords = antigen (Clic here for more details about this article) |
6/24. Relapsing hepatitis A. review of 14 cases and literature survey.We have reviewed our experience with 14 cases of relapsing hepatitis A (RH-A), as well as 68 cases reported in the literature. Relapse occurs in 3 to 20% of patients with acute hepatitis A, and rarely takes the form of a polyphasic disease (multiple relapses). After a stage of typical hepatitis A, remission phase ensues, with partial or complete resolution of clinical and biochemical manifestations. Relapse usually occurs after a short period (usually less than 3 weeks). Relapse is usually clinically milder than the first phase, with variable liver function abnormalities and a tendency toward more marked cholestatic features. Not uncommonly, immune manifestations occur during this phase, including purpura, nephritis, and arthralgia, with common laboratory findings of rheumatoid factor as well as false-positive reaction to HCV-EIA tests. The clinical course in relapsing hepatitis A is almost always benign, and uneventful recovery is the rule with few exceptions. Steroid treatment, first reported in the present series, resulted in marked clinical improvement. Preliminary results suggest that R-HA is associated with a continuing viremia as well as shedding of virus in stools during the relapse phase. The pathogenesis of R-HA probably involves an interaction between persistent viral infection and immune mechanisms responding to the continuing antigenic stimulation.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
7/24. Autoimmune hepatitis triggered by acute hepatitis A.The patient was a 57-year-old woman presenting with jaundice as the chief complaint. She began vomiting on July 10, 2003. jaundice was noted and admitted to our hospital for thorough testing. Tests on admission indicated severe hepatitis, based on: aspartate aminotransferase (AST), 1 076 IU/L; alanine aminotransferase (ALT), 1 400 IU/L; total bilirubin (TB), 20.9 mg/dL; and prothrombin time rate (PT%), 46.9%. Acute hepatitis A (HA) was diagnosed based on negative hepatitis B surface antigen and hepatitis c virus rna and positive immunoglobulin (Ig) M HA antibody, but elevation of anti-nuclear antigen (X320) and IgG (3 112 mg/dL) led to suspicion of autoimmune hepatitis (AIH). plasma exchange was performed for 3 d from July 17, and steroid pulse therapy was performed for 3 d starting on July 18, followed by oral steroid therapy. Liver biopsy was performed on August 5, and the results confirmed acute hepatitis and mild chronic inflammation. Levels of AST and ALT normalized, so dose of oral steroid was markedly reduced. Steroid therapy was terminated after 4 mo, as the patient had glaucoma. Starting 3 mo after cessation of steroid therapy, levels of AST and ALT began to increase again. Another liver biopsy was performed and AIH was diagnosed based on serum data and biopsy specimen. Oral steroid therapy was reinitiated. Levels of AST and ALT again normalized. The present case was thus considered to represent AIH triggered by acute HA.- - - - - - - - - - ranking = 2keywords = antigen (Clic here for more details about this article) |
8/24. vasculitis with hepatitis B antigenemia: long-term observation in nine patients.The development of generalized necrotizing vasculitis in association with hepatitis B antigenemia is the first example in man of a chronic rheumatic disease presumably caused by a viral infection. This report reviews the experience in nine biopsy-proven cases of hepatitis B-associated necrotizing vasculitis followed for up to six years. The natural history of the disease is emphasized and the manifestations of patients with vasculitis who carry hepatitis B antigen are compared with those of vasculitis patients who are antigen negative.- - - - - - - - - - ranking = 7keywords = antigen (Clic here for more details about this article) |
9/24. cytomegalovirus mononucleosis in a healthy adult: association with hepatitis, secondary Epstein-Barr Virus antibody response and immunosuppression.A 35 year old previously healthy physician had clinical manifestations of a mononucleosis illness complicated by arthralgia, vesicular pharyngitis and hepatitis. Initially, the patient had cytomegalovirus (CMV) viremia (predominantly in polymorphonuclear leukocytes) followed by the presence of CMV in the urine, throat and semen. He also had an antibody response to the Epstein-Barr virus which appeared to be a secondary type. During the acute phase of illness, only 7 per cent of the patient's lymphocytes formed spontaneous T cell rosettes as compared to a normal value of 65 to 70 per cent. Concurrently, evidence of abnormal delayed hypersensitivity was manifested by the loss of reactivity to mumps skin test antigen. All clinical and laboratory abnormalities except for the persistence of CMV in the pharynx, urine and semen returned to normal after resolution of the clinical illness.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
10/24. Persistence of hepatitis a virus in fulminant hepatitis and after liver transplantation.A peroxidase-labelled, specific mouse monoclonal antibody to hepatitis a virus (HAV) and an in situ hybridization technique (streptavidin-biotin-horseradish peroxidase reaction) with an HAV-specific cDNA probe (recombinant plasmid pAWHA comprising 1.8 kb of the HAV-specific cDNA, located toward the 3' end of the genome) were used to detect HAV in liver tissues in two patients with fulminant viral hepatitis type A treated by liver transplantation after a protracted (day 40: case 1) and relapsing (day 60: case 2) clinical course. HAV antigens and HAV-specific genomic sequences were detected in the hepatectomy tissues and in serial biopsies of the liver grafts through to final follow-up at 2 months (case 2) or death at 7 months after re-grafting for chronic rejection (case 1). In the fulminant liver parenchyma, numerous degenerating and some surviving hepatocytes were positive and randomly scattered. The immunoperoxidase staining was predominantly cytoplasmic and often granular. The localization of the cDNA probe was predominantly nuclear/perinuclear but was occasionally cytoplasmic. High-titre IgM-anti-HAV antibodies persisted until death (case 1) or resolution (5 months) of an acute hepatitis (case 2), which occurred at 2 months, accompanied by HAV antigen (ELISA), in stool. Intact replicating virus particles must have been present in one or more sites in each case, including extrahepatic locations, with a viraemia as the most likely explanation for subsequent reinfection of the grafts.- - - - - - - - - - ranking = 2keywords = antigen (Clic here for more details about this article) |
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