Double-shelled virus-like particles (60 nm) and long cytoplasmic tubular structures were found in the cytoplasm of hepatocytes from areas of collapsed and regenerating areas of hepatectomised liver in a 13-year-old boy who received a liver graft for fulminant hepatitis attributed to sporadic non-A,
Fulminant hepatitis in patients undergoing liver transplantation: Evidence for a non-A, non-B, non-C, non-D, and non-E syndrome
β Scribed by Ferraz, M. Lucia ;Silva, A. Eduardo ;Macdonald, Graeme A. ;Tsarev, Sergei A. ;Di Biscelgie, Adrian M. ;Lucey, Michael R.
- Publisher
- Wiley (John Wiley & Sons)
- Year
- 1996
- Tongue
- English
- Weight
- 596 KB
- Volume
- 2
- Category
- Article
- ISSN
- 1074-3022
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β¦ Synopsis
Fulminant hepatic failure (FHF) in the absence of serum markers of hepatitis A (HAV) or B (HBV) infection or another cause is called non-A, non-B (NANB) FHF. The pathogenetic role of viral infection in NANB FHF remains controversial. To better define this relationship, we studied patients who underwent orthotopic liver transplantation (OLT) for FHF. Thirty-six patients with FHF underwent transplantation between 1987 and 1992. Pre-OLT serum was available for 24 patients, 14 with NANB FHF (all female; mean age, 32 years), and 10 (3 males, 7 females; mean age, 20 years) with a defined origin for FHF who formed the control group. Sera were tested using polymerase chain reaction for HAV, HCV, HDV, and HEV RNA and HBV DNA, and also serologically for antibodies to these viruses. In the NANB group, pre-OLT serum was negative for all viruses tested. Four patients ulminant hepatic failure (FHF) is a syndrome in F which massive liver injury or impairment is associated with the rapid development of hepatic encephalopathy. FHF develops as a consequence of toxic injury, viral infection, metabolic disorders, hepatic vascular catastrophes, drug reactions, and neoplastic infiltration. Before the availability of liver transplantation, FHF resulted in death in up to 80% of patients2 Depending on the population studied, between 25% and 40% of patients have no obvious precipitant for fulminant liver fai1u1-e.~ In the absence of serological markers of hepatitis A or B infection or From the
π SIMILAR VOLUMES
could be attributed to hepatitis C infection. 5 Rarely, acute Patients presenting with clinical and laboratory feahepatitis E has been identified among U.S. or European patures consistent with a diagnosis of acute non-A, non-B tients with a history of recent travel to underdeveloped counhepatitis we
In a patient who followed the typical clinical course of fulminant hepatitis attributable to "sporadic" non-A,non-B (NANB) hepatitis and who finally received treatment by orthotopic liver grafting, three, apparently separate, viruslike agents (26, 45, and 80 nm) and cytoplasmic, reticular tubular st
## Abstract Many cases of acute hepatitis remain undiagnosed and the hepatitis E virus (HEV) is emerging in industrialized countries. The aim of this study was to assess the role HEV as causative agent in acute nonβA, nonβB, and nonβC hepatitis patients in Hungary. 10.5% of the 264 acute nonβA, non
To assess the contribution of hepatitis C virus to non-A, non-B fulminant hepatitis in Japan, we compared 10 mqjor clinical features among 7 patients with type B fulminant hepatitis (type B group), 13 patients with non-A, non-B fulminant hepatitis with evidence of hepatitis C virus infection (type C
been linked with FHF in neonates, pregnancy, immunocom-Members of the herpes virus family and hepatitis B promised patients, and apparently healthy individuals. [5][6][7][8] Epvirus (HBV) have been implicated as etiologic agents in stein-Barr virus (EBV) infection may cause acute liver failure non-A