2005
DOI: 10.1155/2005/853947
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Parvovirus B19 in an Immunocompetent Adult Patient with Acute Liver Failure: An Underdiagnosed Cause of Acute Non-A-E Viral Hepatitis

Abstract: There are occasional pediatric reports of parvovirus B19-associated transient acute hepatitis and hepatic failure. A case of a 34-year-old immunocompetent woman who developed severe and prolonged but self-limited acute hepatitis and myelosuppression following acute parvovirus B19 infection is reported. Parvovirus B19 may be the causative agent in some adult cases of acute non-A-E viral hepatitis and acute liver failure.

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Cited by 22 publications
(18 citation statements)
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“…First, several reports have suggested a pathogenic role for parvovirus B19 in the development of acute hepatitis [7-9] and fulminant liver failure of unknown aetiology [10,11]. Furthermore, persistence of B19 DNA in liver and bone marrow has been associated with acute liver disease and aplastic anaemia [9,12,13].…”
Section: Discussionmentioning
confidence: 99%
“…First, several reports have suggested a pathogenic role for parvovirus B19 in the development of acute hepatitis [7-9] and fulminant liver failure of unknown aetiology [10,11]. Furthermore, persistence of B19 DNA in liver and bone marrow has been associated with acute liver disease and aplastic anaemia [9,12,13].…”
Section: Discussionmentioning
confidence: 99%
“…Although according to the clinical data in our department, the incidence of superinfection with hepatitis A was similar to that with hepatitis E in chronic hepatitis B in southeast China, since the virulence of hepatitis A virus is much lower than that of hepatitis E virus, [28][29][30] fatal liver failure resulted from hepatitis B superinfected by hepatitis A in only 1.4% (4/ 282) of patients. Because of the introduction of diagnostic kits for hepatitis C in the early 1990s 31 and because the blood products in China became more strictly filtered in the middle 1990s, the incidence of chronic hepatitis B superinfected with hepatitis C obviously decreased after 1998 ( 36,37 Inconsistent results have been reported as to whether liver failure is caused by serum conversion of HBeAg to anti-HBe as a result of a precore region mutation of the hepatitis B virus. 3,[38][39][40][41] Although the sequences of precore region mutations of hepatitis B virus were not routinely checked in this study, if the serum conversion of HBeAg to anti-HBe caused by a precore region mutation could result in fatal liver failure exacerbated by an acute attack of chronic hepatitis B, the frequency of HBeAg(+) and anti-HBe(−) in the group in which causes were not clear should be lower than that in the group with superinfections.…”
Section: Discussionmentioning
confidence: 99%
“…Molecular testing for parvovirus B19 DNA was not performed in either case (1). Ho et al reported a case of a 34-year-old woman presenting with 6 weeks of polyarthritis, sore throat, anorexia, and fever and 4 weeks of right upper quadrant abdominal pain and jaundice (4). Laboratory testing was consistent with acute hepatitis.…”
Section: Case Reportmentioning
confidence: 99%