Familial Cluster of Fulminant Hepatitis A Infection

Durst, Ronen; Goldsmidt, Neta; Namestnick, Julia; Safadi, R.; Ilan, Yaron

doi:10.1097/00004836-200105000-00023

Cited by 20 publications

(12 citation statements)

References 10 publications

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“…Some studies suggested the relationship between disease severity and viral load, 30,31 some strains or amino acid change in the 2B region. [31][32][33][34] Fourth, histopathological evaluation was performed in only one patient. To understand the underlying mechanisms of AKI, histopathological evaluations should be performed on available patients.…”

Section: Discussionmentioning

confidence: 99%

Clinical features and outcomes of acute kidney injury among patients with acute hepatitis A

Choi

Song

Han

et al. 2011

Journal of Clinical Virology

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Section: Discussionmentioning

confidence: 99%

Clinical features and outcomes of acute kidney injury among patients with acute hepatitis A

Choi

Song

Han

et al. 2011

Journal of Clinical Virology

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“…It has been suggested that disease severity depends on host factors including age and underlying chronic liver disease [Muraoka, 1990;Vento et al, 1998]. On the other hand, it was reported that young healthy persons were also at risk for severe complications, based on the outbreak of an urban epidemic of hepatitis A in the United States [Willner et al, 1998], in which a cluster of fulminant hepatitis A was reported [Durst et al, 2001]. Analysis of factors contributing to disease severity revealed no significant differences in patients' factors including age [Fujiwara et al, 1995[Fujiwara et al, , 2000], suggesting that viral factors and the individual immune responses might determine the severity.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis A viral load in relation to severity of the infection

Fujiwara

Kojima

Yasui

et al. 2010

Journal of Medical Virology

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A correlation between hepatitis A virus (HAV) genomes and the clinical severity of hepatitis A has not been established. The viral load in sera of hepatitis A patients was examined to determine the possible association between hepatitis A severity and HAV replication. One hundred sixty-four serum samples from 91 Japanese patients with sporadic hepatitis A, comprising 11 patients with fulminant hepatitis, 10 with severe acute hepatitis, and 70 with self-limited acute hepatitis, were tested for HAV RNA. The sera included 83 serial samples from 20 patients. Viral load was measured by real-time RT-PCR. The detection rates of HAV RNA from fulminant, severe acute, and acute hepatitis were 10/11 (91%), 10/10 (100%), and 55/70 (79%), respectively. Mean values of HAV RNA at admission were 3.48 ± 1.30 logcopies/ml in fulminant, 4.19 ± 1.03 in severe acute, and 2.65 ± 1.64 in acute hepatitis. Patients with severe infection such as fulminant hepatitis and severe acute hepatitis had higher initial viral load than patients with less severe infection (P < 0.001). Viremia persisted for 14.2 ± 5.8 days in patients with severe infection and 21.4 ± 10.6 days in those with acute hepatitis after clinical onset (P = 0.19). HAV RNA was detectable quantitatively in the majority of the sera of hepatitis A cases during the early convalescent phase by real-time PCR. Higher initial viral replication was found in severely infected patients. An excessive host immune response might follow, reducing the viral load rapidly as a result of the destruction of large numbers of HAV-infected hepatocytes, and in turn severe disease might be induced.

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“…Recently, a study of 3 familial cases of FH A suggested that some strains of HAV might be particularly pathogenic. 22 HAV strains isolated to date have been divided into 7 genotypes based on the criterion of 15% to 20% nucleotide sequence diversity over a 168-base segment at the VP1/2A junction. In our series, patients infected by genotype IA strains (which predominate in France) had a lower incidence of FH, but the difference was not significant in multivariate analysis.…”

Section: Discussionmentioning

confidence: 99%

Viral and clinical factors associated with the fulminant course of hepatitis A infection

2003

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Fulminant hepatitis is a severe complication of hepatitis A virus infection. Its mechanism is unknown. Liver transplantation can be necessary, but spontaneous recovery is frequent. There are no data on the level of viral replication according to the clinical form of hepatitis A. We reviewed the files of 50 patients with acute hepatitis A. Nineteen patients had fulminant hepatitis (defined by encephalopathy and factor V <50%), and, from them, 10 patients underwent transplantation. Hepatitis A virus (HAV) RNA was quantified by real-time PCR on sera obtained at admission. The genotype was determined by phylogenetic analysis of HAV RNA. HAV RNA was detected in serum by RT-PCR in 39 out of 50 patients. Encephalopathy and low factor V level were significantly related to female gender, HAV PCR negativity (9/19 vs. 5/31, respectively; P ‫؍‬ .03), a low serum HAV RNA level (log, 3.6 ؎ 0.6 vs. 4.4 ؎ 0.9, respectively; P ‫؍‬ .02), genotypes other than IA, and acetaminophen intake. In multivariate analysis, low or undetectable HAV viral load and a high bilirubin level were independently associated with both low factor V levels and fulminant hepatitis and also with death or transplantation. In conclusion, HAV-related liver failure is due to an excessive host response associated with a marked reduction in viral load. The infection is spread chiefly by fecal-oral transmission and is a public health problem throughout the world. The main complication of HAV infection is fulminant hepatitis (FH), i.e., acute liver failure with encephalopathy, which occurs in less than 1% of cases. It appears to be more frequent in adults than in children. 1 In the United States, about one third of adults have anti-HAV antibodies, and 100 deaths per year are attributed to HAV-related acute liver failure. 1 This is also a frequent cause of death among children in developing countries. 2 Liver transplantation has markedly changed the prognosis of HAV-related acute liver failure in industrialized countries 3 and is currently indicated for patients with deep coma and low factor V levels. However, HAV-related FH resolves spontaneously more frequently than FH of other origins, and the decision to transplant or not to transplant is thus particularly difficult. Auxiliary liver transplantation may be appropriate in this setting, pending possible regeneration of the native liver. 4,5 Few data have been published on viral replication during acute hepatitis A, and viral load in patients with FH A has not yet been studied. There are several HAV genotypes, IA being most prevalent in industrialized countries. 6 Little information is available on the possible relation between the severity of hepatitis A and the infecting genotype. We applied real-time quantitative polymerase chain reaction (PCR) to stored sera from 50 patients with acute hepatitis A, of whom 19 had FH, to examine the possible relation between HAV viral load, HAV genotype, and the clinical course.

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Familial Cluster of Fulminant Hepatitis A Infection

Cited by 20 publications

References 10 publications

Clinical features and outcomes of acute kidney injury among patients with acute hepatitis A

Clinical features and outcomes of acute kidney injury among patients with acute hepatitis A

Hepatitis A viral load in relation to severity of the infection

Viral and clinical factors associated with the fulminant course of hepatitis A infection

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