Virus In Fulminant Hepatitis Research Articles

Molecular adsorbent recirculating system therapy in a rare case of fulminant hepatitis

Background: Acute hepatitis C virus infection leading to fulminant hepatitis is very rare whereas Hepatitis C virus (HCV) infection is one of the main causes of chronic liver disease worldwide. The repertoire of substances that accumulate in the blood in fulminant hepatic failure cause neurological abnormalities, aggravate injury to the liver and other organs, suppress the ability of residual hepatocytes to perform organ-specific functions (sick cell syndrome), and inhibit the hepatic regenerative response especially in fulminant hepatitis Virus C which has subacute clinical evolution and takes time to manifest. Liver support technology is evolving as different techniques become available that assist the remaining functional cell mass by providing specific liver functions. Case Presentation: We report a case of Fulminant C virus Hepatitis, successfully treated with albumin dialysis Molecular Adsorbent Recirculating System (MARS). At time of admittance the patient presented: Model End-stage Liver Disease (MELD)-36; Child Turcotte Pugh (CTP)-C(13); Sequential Organ Failure Assestment (SOFA)-12, Glasgow Coma Score (GCS)-11. The patient underwent six sessions of MARS in Intensive Care Unit (ICU) in association with standard medical therapy (SMT). The patient survived and was discharged from the hospital in good condition after 40 days without liver transplantation (LT).

The role of hepatitis C virus in fulminant viral hepatitis in an area with endemic hepatitis A and B

Background/Aims: The role of hepatitis C virus in fulminant hepatitis remains controversial and needs further investigation. The aim of this study was to examine the role of hepatitis C virus in fulminant hepatitis in an area with endemic hepatitis A and B. Methods: Serological markers of hepatitis C virus were studied in 62 adults from Taiwan with fulminant viral hepatitis. Results: Of 62 patients, 5 (8.1%) were infected with acute type B hepatitis, 11 (17.7%) were infected with acute non-A, non-B hepatitis, and the remaining 46 (74.2%) were hepatitis B surface antigen (HBsAg) positive but immunoglobulin M (IgM) antibody to hepatitis B core antigen negative. Of the latter, 11 (23.9%) were IgM antibody to hepatitis D virus positive, 16 (34.8%) had high-titered serum hepatitis B virus DNA (>1000 pg/mL) and were suspected to have hepatitis B virus reactivation, and the other 19 (41.3%) had no identified causes. Serum hepatitis C virus RNA was found in 5 (45.5%) of 11 patients with fulminant non-A, non-B hepatitis, 3 (27.3%) of 11 HBsAg carriers with delta superinfection, and 6 (31.6%) of 19 HBsAg carriers with fulminant hepatitis of undetermined cause. Conclusions: Nearly half of fulminant non-A, non-B hepatitis and about 20% of HBsAg carriers with superimposed fulminant hepatitis in Taiwan could be attributed to hepatitis C virus infection.

Hepatitis B virus precore mutation and fulminant hepatitis in the United States. A polymerase chain reaction-based assay for the detection of specific mutation.

Hepatitis B virus (HBV) variants with precore mutation(s) resulting in the absence of HBeAg production have been associated with the occurrence of fulminant hepatitis in Japan, Israel, and southern Europe, where the prevalence of this HBV strain appears common. In areas such as United States, where HBV infection is not endemic, the role of this mutant virus in fulminant hepatitis is unknown. We developed an amplification refractory mutation detection system to detect specifically the presence of the G to A mutation at nucleotide position 1898, which is the most frequently observed mutation resulting in a precore stop codon. In addition, this method provided a quantitative measurement of the relative ratio of one strain to the other. Using this system, we tested HBV strains for the presence of the stop codon mutation in sera from 40 cases of fulminant hepatitis B occurring in the United States. Serum HBV DNAs from 28 patients were analyzed successfully. A mixture of wild-type and mutant strains in various ratios were observed in 15 patients, wild type exclusively in 11, and mutant exclusively in 2. Four of these patients had undergone liver transplantation for HBV-associated cirrhosis and developed fulminant HBV-associated hepatitis after transplantation. Pre- and posttransplant serum samples from one patient were analyzed: a mixture of wild-type and mutant HBV strains was detected in both samples. Our study demonstrated that both wild-type and mutant HBV strains are associated with fulminant hepatitis, and that in some patients in the United States, factors other than precore mutations contribute to the development of fulminant hepatitis.

Diagnostic significance of IgM antibody to hepatitis delta virus in fulminant hepatitis B

The prevalence of hepatitis delta virus (HDV) infection was studied in 25 adult patients with fulminant hepatitis who were admitted consecutively to our unit from February, 1986, to September, 1988. Enzyme and radioimmunoassays were used for the detection of serological markers of HAV, HBV, and HDV (HDAg, IgM anti-HD, total [IgG] anti-HD) infections. Two hundred twenty-nine serum samples (three to 19 samples/patient) were tested for serological markers of HDV infection. Of the 25 patients, 17 (68%) were HBsAg-positive, and the remaining eight (32%) were HBsAg-negative on admission to the hospital. All patients were seropositive for IgM anti-HBc. Serological markers of HDV infection were detected in 13 (52%) of the 25 patients. In particular, HDV infection was observed in nine (53%) of the 17 HBsAg-positive and in four (50%) of the eight HBsAg-negative patients with type B fulminant hepatitis. Survival was 16.7% for patients with hepatitis B and 57.8% for patients with B and D coinfection. Coinfections were responsible for fulminant hepatitis in 100% of drug addicts and 40% in patients who were not drug addicts. All patients with HBV/HDV coinfections became seropositive for IgM anti-HD. The results show that HDV infection has a significant role (52%) in type B fulminant hepatitis in an area with a moderate prevalence of HBV infections, that it should be tested in cases with early clearance of HBsAg, and that it does not seem to be accompanied by a high fatality rate.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Identification of toga-like virus in fulminant hepatitis attributed to minocycline therapy.

Identification of toga-like virus in fulminant hepatitis attributed to minocycline therapy.

Fulminant hepatitis-virus B in a three months old infant: therapeutic trial with specific anti-HB globulins in antibody excess.

A newborn of normal birthweight received fresh blood transfusions and procoagulant fractions during his first days for a haemorrhagic disease. Three months later the infant had acute liver failure. Liver biopsy revealed a massive hepatic necrosis and an Australia antigen was detected. 1ml/kg of anti-HB gamma globulin was administered after each of two exchange transfusions (200 ml/kg). Anti-HB antibodies were detected after gamma globulin therapy. Once the passively administered antibodies had disappeared, the HB titer increased, and the child seemed physically and mentally normal seven months after the infection. These observations are difficult to interpret but immunity of the child seems possible.