Hepatitis after liver transplantation: The role of the known and unknown viruses

Terrault, Norah A.; Ferrell, Linda D.; Detmer, Jill; Kolberg, Janice A.; Collins, Mark L.; Viele, Maurene; Lake, John R.; Roberts, John P.; Ascher, Nancy L.; Wright, Teresa L.

doi:10.1002/lt.500040603

Cited by 28 publications

(10 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[42][43][44][45][46][47][48] The predominant finding is mononuclear portal inflammatory infiltrate associated with variable-interface hepatitis. Bile duct damage and venous endothelial inflammation are not conspicuous.…”

Section: Idiopathic Posttransplantation Chronic Hepatitismentioning

confidence: 99%

“…49 During the early 1990s, several studies using polymerase chain reaction techniques to detect HCV RNA identified HCV as a major cause of otherwise unexplained posttransplantation hepatitis. [50][51][52][53] However, many patients included in these studies underwent transplantation before routine screening of HCV in donors was performed, and a similar prevalence of posttransplantation hepatitis continues to be seen in patients who have undergone transplantation since the advent of HCV screening and who [46][47][48]54 Hepatitis G virus has been found in association with chronic hepatitis in two studies of long-term posttransplantation biopsies. 47,48 However, no correlation was found between the presence of hepatitis G virus infection and the development of graft hepatitis.…”

Section: Idiopathic Posttransplantation Chronic Hepatitismentioning

confidence: 99%

See 1 more Smart Citation

Recurrent autoimmune hepatitis after liver transplantation: Diagnostic criteria, risk factors, and outcome

Hübscher

2001

Liver Transpl

109

View full text Add to dashboard Cite

Approximately 20% to 30% of patients undergoing liver transplantation for autoimmune hepatitis (AIH) develop features of recurrent disease. Diagnostic criteria for recurrent AIH are similar to those used in the nontransplanted liver and include, in varying combinations, biochemical, serological, and histological abnormalities and steroid dependency. However, these criteria are more difficult to apply in the liver allograft because of potential interactions between recurrent AIH and other complications of liver transplantation, particularly rejection, and the uncertain effects of long-term immunosuppression. In the absence of other reliable diagnostic markers, a number of studies have used the histological finding of chronic hepatitis as the main or sole criterion for diagnosing recurrent AIH. However, this also lacks diagnostic specificity because there are many other possible causes of chronic hepatitis in the liver allograft. In addition, approximately 20% to 40% of biopsies performed on patients as part of routine annual review have histological features of chronic hepatitis, for which no definite cause can be identified. Risk factors that have been associated with the development of recurrent AIH include suboptimal immunosuppression, HLA phenotype, disease type and severity in the native liver, and duration of follow up. In many cases in which recurrent AIH seems to be related to underimmunosuppression, biochemical and histological features rapidly resolve once adequate immunosuppression is restored. However, in other cases, recurrent AIH behaves more aggressively, with progression to cirrhosis and graft failure. Areas that require further study include developing uniform criteria for the diagnosis of recurrent AIH, identifying risk factors for severe recurrent disease, and determining optimal levels of immunosuppression that minimize the impact of disease recurrence without exposing patients to the risks of overimmunosuppression. (Liver Transpl 2001;7:285-291.) R ecurrence of autoimmune hepatitis (AIH) after liver transplantation has been reported in several studies. [1][2][3][4][5][6][7][8][9][10][11][12] The reported rate of recurrence ranges from 11% to 83%, with 20% to 30% documented in most studies. Occasional studies have failed to find evidence of recurrent AIH. 13 There is considerable variation in the criteria used to diagnose recurrent AIH and the reported outcome of disease recurrence, and risk factors for recurrent AIH are also poorly understood. The study by Gonzalez-Koch et al, 14 which appears in this edition of Liver Transplantation, provides further evidence that AIH recurs after liver transplantation, but also highlights some problems that exist in diagnosing disease recurrence in the liver allograft. Diagnostic CriteriaThe main problem with establishing a diagnosis of AIH is the lack of a single specific diagnostic marker. In the native liver, AIH is diagnosed on the basis of a constellation of findings, including the presence of positive features that support a diagnosis of AIH and the a...

show abstract

Section: Idiopathic Posttransplantation Chronic Hepatitismentioning

confidence: 99%

Section: Idiopathic Posttransplantation Chronic Hepatitismentioning

confidence: 99%

Recurrent autoimmune hepatitis after liver transplantation: Diagnostic criteria, risk factors, and outcome

Hübscher

2001

Liver Transpl

109

View full text Add to dashboard Cite

show abstract

“…Recurrent hepatitis C leads to chronic hepatitis and liver cirrhosis in a significant proportion of patients and lowers graft and patient survival. 7 The difficulty for the local pathologist in diagnosing recurrent hepatitis C arises in two scenarios. The first scenario is early recurrent hepatitis C when there are only small numbers of lymphocytes in the portal tracts and lobules with occasional acidophil bodies (case 1, Figure 1a).…”

Section: Recurrent Hepatitis Cmentioning

confidence: 99%

The impact of pathologist experience on liver transplant biopsy interpretation

et al. 2006

View full text Add to dashboard Cite

We studied the impact of pathologist experience on liver transplant biopsy interpretation for cases designated 'nonspecific' by pathologists at a nontransplant center. Among 102 consecutive liver transplant biopsies from 92 patients performed at the Foothills Medical Center, 30 liver biopsies from 23 patients were designated 'nonspecific' by the local pathologist. These biopsy slides were independently reviewed by an expert in liver transplant pathology at a major US transplant center. The expert pathologist was given only the information on the original requisition. In seven biopsies from five patients, there was full agreement between the external expert and the local pathologist. In 10 biopsies from six patients, the expert concurred with the initial assessment but emphasized critical negatives such as 'no evidence of rejection or recurrent hepatitis'. A discrepant diagnosis was found in 13 biopsies from 12 patients. In five biopsies from four patients, the revised diagnoses were inaccurate due to insufficient or misleading clinical information on the requisition. In eight biopsies from eight patients, the revised diagnoses were proven to be correct by clinicopathologic correlation. Our study shows that pathology expertise helped to clarify the diagnosis in about 27% of cases, which justifies the cost of obtaining a second opinion in difficult biopsies. Misinterpretation by the expert pathologist in up to 17% of biopsies highlights the importance of direct communication between hepatologist and pathologist in order to achieve a correct diagnosis. Familiarity with those cases with relatively uncommon histology, a diligent search for subtle morphologic changes, and use of standard terminology could improve the quality of liver transplant biopsy interpretation in a nontransplant center.

show abstract

“…This suspicion has been supported by reports of transfusion-associated cryptogenic cirrhosis in the nontransplantation population 1 and the finding of unexplained posttransplantation graft hepatitis in 22% of liver transplant recipients in a recent report from San Francisco. 2 Despite earlier enthusiasm that an agent(s) responsible for NANE hepatitis had been identified, neither hepatitis G (HGV)/GB virus-C nor TT virus (TTV) subsequently has been shown to result in significant liver disease in either the immunocompetent population [3][4][5][6][7][8][9][10][11][12] or among liver transplant recipients. [13][14][15][16][17] Recently, a novel DNA virus referred to as SEN virus (SEN V) has been identified and characterized.…”

mentioning

confidence: 99%

A cross-sectional study of SEN virus in liver transplant recipients

Yoshida

Buczkowski

Giulivi

et al. 2001

Liver Transplantation

View full text Add to dashboard Cite

T here has been a long-standing suspicion within the medical community that unidentified hepatotrophic viruses are responsible for both acute and chronic viral marker-negative hepatitis, an entity referred to as Non A to Non E (NANE) hepatitis. This suspicion has been supported by reports of transfusion-associated cryptogenic cirrhosis in the nontransplantation population 1 and the finding of unexplained posttransplantation graft hepatitis in 22% of liver transplant recipients in a recent report from San Francisco. 2 Despite earlier enthusiasm that an agent(s) responsible for NANE hepatitis had been identified, neither hepatitis G (HGV)/GB virus-C nor TT virus (TTV) subsequently has been shown to result in significant liver disease in either the immunocompetent population 3-12 or among liver transplant recipients. [13][14][15][16][17] Recently, a novel DNA virus referred to as SEN virus (SEN V) has been identified and characterized. 18 This virus is reported to be an unenveloped linear structure with an average length of 3,900 nucleotides. Eight genotypes (SEN V:A through H) have been identified. SEN V appears to have a high prevalence among blood transfusion recipients, 19 intravenous drug users, and those coinfected with hepatitis C virus (HCV) or HIV. 20 Furthermore, the incidence of SEN V in some reports appears to be greater in those who develop NANE hepatitis than those who do not, 19 which leads to the suggestion that an association with NANE hepatitis exists.Liver transplant recipients are at high risk for acquiring previously undetected transfusion-associated viruses. Aside from the transplanted allograft itself and the unavoidable transfusion of passenger blood cells, many receive blood products in the pretransplantation treatment of complications of decompensated cirrhosis (e.g., blood transfusions for variceal bleeds, albumin infusions during paracentesis of ascites), as well as during transplantation surgery and in the posttransplantation period (i.e., red blood cell and platelet transfusions, frozen plasma, hepatitis B immune globulin, and volume expansion with albumin). Likewise, liver transplant recipients are significantly immunosuppressed, and it is well accepted by the transplant community that recurrent HCV 21 and hepatitis B virus (HBV) 22 post-

show abstract

Hepatitis after liver transplantation: The role of the known and unknown viruses

Cited by 28 publications

References 13 publications

Recurrent autoimmune hepatitis after liver transplantation: Diagnostic criteria, risk factors, and outcome

Recurrent autoimmune hepatitis after liver transplantation: Diagnostic criteria, risk factors, and outcome

The impact of pathologist experience on liver transplant biopsy interpretation

A cross-sectional study of SEN virus in liver transplant recipients

Contact Info

Product

Resources

About