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
Microbial Structures in a Patient With Sporadic Non-A, Non-B Fulminant Hepatitis Treated by Liver Transplantation
β Scribed by Elizabeth A. Fagan; David S. Ellis; Bernard Portmann; George M. Tovey; Roger Williams; Professor Arie J. Zuckerman
- Publisher
- John Wiley and Sons
- Year
- 1987
- Tongue
- English
- Weight
- 658 KB
- Volume
- 22
- Category
- Article
- ISSN
- 0146-6615
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β¦ Synopsis
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, non-B hepatitis. The patient died on the ninth postoperative day from acute graft failure. Although virus-like particles were not found, instead, gram-negative rods were identified in the necrotic graft and the most likely cause of death was a gram-negative septicaemia with a Shwartzman-like reaction localized to the liver.
π SIMILAR VOLUMES
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 underw
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
## Abstract Toga virusβlike particles (typically 60β70 nm: enveloped with small surface spikes) were detected in the native hepatectomy specimens in 7 of 18 patients grafted for acute liver failure attributed to sporadic nonβA, nonβB hepatitis and in 2 patients grafted for fulminant hepatitis attri
## Abstract An experimental model of sporadic nonβA nonβB hepatitis involving a Fab nonimmune binding activity in stools was established in the rhesus monkey. The first animal was inoculated intravenously with a stool extract from a French patient who had never left the country and in whom postβtra
Electron microscopic observations were carried out on five HBsAg carrier chimpanzees infected with delta (delta) agent and two chimpanzees infected with human non-A, non-B hepatitis. The cytoplasmic tubular structures, which have been recognized in the liver of chimpanzees infected with human non-A,