Non-A, non-B fulminant hepatitis is also non-E and non-C

S. K. Kuwada, V. M. Patel, F. B. Hollinger, H. J. Lin, P. O. Yarbough, R. H. Wiesner, D. Kaese, Jorge Rakela

Research output: Contribution to journalArticle

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Abstract

Objectives: to define the roles of the hepatitis C and E viruses (HCV and HEV) in non-A, non-B (NANB) fulminant hepatitis. Methods: we utilized the polymerase chain reaction to amplify HCV and HEV RNA sequences and assays to detect antibodies to HCV and HEV in the acute phase sera of eight presumed viral NANB and seven nonviral NANB fulminant hepatic failure (FHF) patients. Results: none of the 15 patients had detectable HCV or HEV RNA or elevated HCV and IgM-HEV antibody titers in their acute phase sera. Three patients, all with features of autoimmune hepatitis, had raised IgG-HEV antibody titers. Due to the possibility of serologically undetectable hepatitis B virus (HBV) infection in fulminant hepatitis patients, we performed polymerase chain reaction amplification of HBV genomic DNA in acute phase sera of the presumed viral NANB FHF patients and subsequently found no evidence of HBV DNA. Conclusions: we did not find evidence implicating HCV or HEV in presumed viral NANB FHF or as agents contributing to or causing the liver failure in nonviral NANB FHF patients with autoimmune hepatitis, drug- induced hepatotoxicity, or halothane hepatotoxicity.

Original languageEnglish (US)
Pages (from-to)57-61
Number of pages5
JournalAmerican Journal of Gastroenterology
Volume89
Issue number1
StatePublished - 1994

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Hepatitis
Acute Liver Failure
Hepatitis B virus
Autoimmune Hepatitis
Serum
Hepatitis E virus
Polymerase Chain Reaction
Hepatitis C Antibodies
Antibodies
DNA
Liver Failure
Halothane
Virus Diseases
Hepacivirus
Immunoglobulin M
Immunoglobulin G
RNA
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Kuwada, S. K., Patel, V. M., Hollinger, F. B., Lin, H. J., Yarbough, P. O., Wiesner, R. H., ... Rakela, J. (1994). Non-A, non-B fulminant hepatitis is also non-E and non-C. American Journal of Gastroenterology, 89(1), 57-61.

Non-A, non-B fulminant hepatitis is also non-E and non-C. / Kuwada, S. K.; Patel, V. M.; Hollinger, F. B.; Lin, H. J.; Yarbough, P. O.; Wiesner, R. H.; Kaese, D.; Rakela, Jorge.

In: American Journal of Gastroenterology, Vol. 89, No. 1, 1994, p. 57-61.

Research output: Contribution to journalArticle

Kuwada, SK, Patel, VM, Hollinger, FB, Lin, HJ, Yarbough, PO, Wiesner, RH, Kaese, D & Rakela, J 1994, 'Non-A, non-B fulminant hepatitis is also non-E and non-C', American Journal of Gastroenterology, vol. 89, no. 1, pp. 57-61.
Kuwada SK, Patel VM, Hollinger FB, Lin HJ, Yarbough PO, Wiesner RH et al. Non-A, non-B fulminant hepatitis is also non-E and non-C. American Journal of Gastroenterology. 1994;89(1):57-61.
Kuwada, S. K. ; Patel, V. M. ; Hollinger, F. B. ; Lin, H. J. ; Yarbough, P. O. ; Wiesner, R. H. ; Kaese, D. ; Rakela, Jorge. / Non-A, non-B fulminant hepatitis is also non-E and non-C. In: American Journal of Gastroenterology. 1994 ; Vol. 89, No. 1. pp. 57-61.
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AB - Objectives: to define the roles of the hepatitis C and E viruses (HCV and HEV) in non-A, non-B (NANB) fulminant hepatitis. Methods: we utilized the polymerase chain reaction to amplify HCV and HEV RNA sequences and assays to detect antibodies to HCV and HEV in the acute phase sera of eight presumed viral NANB and seven nonviral NANB fulminant hepatic failure (FHF) patients. Results: none of the 15 patients had detectable HCV or HEV RNA or elevated HCV and IgM-HEV antibody titers in their acute phase sera. Three patients, all with features of autoimmune hepatitis, had raised IgG-HEV antibody titers. Due to the possibility of serologically undetectable hepatitis B virus (HBV) infection in fulminant hepatitis patients, we performed polymerase chain reaction amplification of HBV genomic DNA in acute phase sera of the presumed viral NANB FHF patients and subsequently found no evidence of HBV DNA. Conclusions: we did not find evidence implicating HCV or HEV in presumed viral NANB FHF or as agents contributing to or causing the liver failure in nonviral NANB FHF patients with autoimmune hepatitis, drug- induced hepatotoxicity, or halothane hepatotoxicity.

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