Hepatitis C Virus–Associated Fulminant Hepatic Failure

Farci, Patrizia; Alter, Harvey J.; Shimoda, Akihiro; Govindarajan, Sugantha; Cheung, Ling; Melpolder, Jacqueline C.; Sacher, Ronald A.; Shih, James Wai Kuo; Purcell, Robert H.

doi:10.1056/nejm199608293350904

Cited by 173 publications

(88 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It has been claimed in published studies that the staining was evident in hepatocyte cytoplasm and was granular in appearance. 19,21,24 In agreement with these studies, positive staining after immunohistochemical detection of HCV antigens was observed using the commercial monoclonal antibody Tordji-22 on the majority of HCVrecurrent liver biopsy tissue sections. This staining was confined to hepatocyte cytoplasm and was granular in appearance, as described previously using this commercial monoclonal antibody and other anti-HCV antibodies.…”

Section: Discussionsupporting

confidence: 71%

“…[19][20][21]30 Therefore, the claim that this monoclonal antibody detected HCV antigen in severely damaged liver tissue from a case of fulminant hepatitis must be viewed with caution. 19 In support of our finding, other groups have reported that the commercial monoclonal antibody Tordji-22 has been associated with both low sensitivity 21,31 and nonspecificity 32 when tested on chronic HCV-infected patients and HCV-positive liver allograft recipients. Vartanian et al 30 observed diffuse, cytoplasmic staining of biopsy specimens from patients with HCV, HBV, and nonviral liver disease tested with Tordji-22.…”

Section: Discussionmentioning

confidence: 99%

“…This antibody had been generated against a fusion protein created from the carboxy terminal end of NS3 and the amino terminal end of NS4. Tordji-22 has recently been used to detect HCV antigens in both nontransplant 19,20 and posttransplantation liver tissue. 20,21 Initially, our results indicated a strong correlation between the location of HCV antigens and areas of liver injury, particularly regions of hepatocyte ballooning.…”

confidence: 99%

See 2 more Smart Citations

Nonspecificity of monoclonal antibody tordji-22 for the detection of hepatitis C virus in liver transplant recipients with cholestatic hepatitis

Doughty

McCaughan

1999

Liver Transpl

View full text Add to dashboard Cite

Detection of hepatitis C virus (HCV) antigens in liver tissue provides important diagnostic and pathological information. Limited studies have been performed on tissue taken after liver transplantation for HCV. In this study, serial post-liver transplantation biopsy tissue from patients with recurrent HCV was tested, with particular interest in patients showing severe cholestatic hepatitis. HCV-related antigens were detected using the commercial monoclonal antibody, Tordji-22. Initial results were promising, showing intense positive staining, especially in areas of hepatocyte ballooning. HCV-negative donor tissue was consistently negative by staining. However, as a final control for the level of tissue damage, HCV negative posttransplantation biopsy tissue showing hepatocyte ballooning was examined. These tissues also showed positive staining. All attempts to eliminate this nonspecific interaction failed. In conclusion, Tordji-22 was associated with nonspecificity in this posttransplantation population, and care is warranted when using this monoclonal antibody.

show abstract

Section: Discussionsupporting

confidence: 71%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Nonspecificity of monoclonal antibody tordji-22 for the detection of hepatitis C virus in liver transplant recipients with cholestatic hepatitis

Doughty

McCaughan

1999

Liver Transpl

View full text Add to dashboard Cite

show abstract

“…But the most important finding of our study was a significant association between viral evolution and hepatic injury. Strikingly, biochemical evidence of liver damage was invariably associated with the presence of a mono-or oligoclonal viral population, an unexpected finding thus far documented only in patients with fulminant hepatitis C (16,25). By contrast, in children with normal or slightly elevated ALT values, we documented the generation of a complex quasispecies, with a progressive increase in both the number of viral variants and their genetic diversity.…”

Section: Discussionmentioning

confidence: 47%

Evolution of hepatitis C viral quasispecies and hepatic injury in perinatally infected children followed prospectively

Farci¹,

Quinti

Farci³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

Perinatal infection with hepatitis C virus (HCV) is characterized by a wide range of alanine aminotransferase (ALT) levels. The mechanisms responsible for this variability are unknown. We examined whether the evolution of the HCV quasispecies was associated with different ALT profiles in perinatally infected children. Sequences within HCV envelope 1 and 2 genes, inclusive of the hypervariable region 1, the viral load, and the nascent humoral immunity were analyzed in serial serum samples from 12 perinatally infected children prospectively followed for a median of 53 months. These patients were selected to represent two different ALT patterns during the first year of life: 6 had high levels (maximum values ranging from 4.2 to 30 times the normal upper limit), and 6 had normal or slightly elevated levels (<2 times the normal upper limit). Two patterns of viral evolution were identified according to the ALT profiles. Biochemical evidence of hepatic injury was invariably associated with a mono-or oligoclonal viral population, whereas mild or no liver damage correlated with the early emergence of a heterogeneous viral quasispecies. Consistent with selective immune pressure, amino acid changes occurred almost exclusively within the hypervariable region 1 and were temporally associated with antibody seroconversion; at this time, the difference in genetic diversity between the two groups was highly significant (P ‫؍‬ 0.002). The two patterns of viral evolution persisted over time and did not correlate with viral load or genotype. Our study demonstrates that, in perinatally infected children, the evolution of HCV quasispecies correlates with hepatic injury.perinatal hepatitis C virus infection ͉ genetic variability ͉ alanine aminotransferase levels M aternal-infant transmission is the dominant route for acquisition of hepatitis C virus (HCV) infection in children in developed countries, with an estimated transmission rate of Ϸ5% (1-3). Age and mode of infection are assumed to influence the progression of HCV disease in adults, but limited data are available on the natural history of perinatally acquired HCV infection (4, 5). Recent studies suggest that 80% of these children develop chronic infection (6-8), a rate similar to that documented in adults (9) but higher than that reported in children with posttransfusion HCV infection (10). Persistent HCV infection in infants and children is associated with minimal or mild liver damage and very rarely with advanced liver disease (5,(11)(12)(13)(14). However, perinatal HCV infection is associated with a wide range of aminotransferase levels during the first year of life (5, 7). Whereas some infants reach serum concentrations of alanine aminotransferase (ALT) compatible with acute hepatitis, others show normal or slightly elevated levels (5, 7). The mechanisms responsible for the different ALT profiles seen in perinatal HCV infection are unknown but are likely the result of a complex interplay between viral factors and host immunity. One of the most effective strategies enacted ...

show abstract

“…However, in a significant proportion of patients, the cause of the fulminant hepatitis cannot be established despite systematic screening to detect rare viruses and other less common causes which include: Wilson's disease, ischemic hepatitis, Budd-Chiari syndrome, Reye's syndrome and malignancy. In addition, some rare cases of fulminant hepatitis related to hepatitis C virus infection have been described in the literature [12].…”

Section: Causesmentioning

confidence: 99%

Fulminant Hepatitis: Definitions, Causes and Management

Morabito¹,

Adebayo²

2014

Health

View full text Add to dashboard Cite

Fulminant hepatitis (FH) is a rare and devastating syndrome caused by a variety of hepatic insults. It characterized by severe metabolic derangements, neurologic complications and ultimately, multiorgan failure. Liver transplantation is the gold standard therapy for patients with irreversible FH. The major areas of current research in this field include the development of: hepatic support devices, strategies to accelerate hepatic regeneration and criteria for accurate prognostic classification of patients. This review aims to focus on the definitions, aetiologies and management strategies for FH.

show abstract

Hepatitis C Virus–Associated Fulminant Hepatic Failure

Cited by 173 publications

References 23 publications

Nonspecificity of monoclonal antibody tordji-22 for the detection of hepatitis C virus in liver transplant recipients with cholestatic hepatitis

Nonspecificity of monoclonal antibody tordji-22 for the detection of hepatitis C virus in liver transplant recipients with cholestatic hepatitis

Evolution of hepatitis C viral quasispecies and hepatic injury in perinatally infected children followed prospectively

Fulminant Hepatitis: Definitions, Causes and Management

Contact Info

Product

Resources

About