Development of autoimmune hepatitis following liver transplantation for primary biliary cirrhosis

Jones, David; James, Oliver; Portmann, Bernard; Burt, Alastair D.; Williams, Roger; Hudson, Mark

doi:10.1002/hep.510300103

Cited by 102 publications

(75 citation statements)

References 30 publications

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“…The outcome and specific treatment of this complication are not well known. Although steroid dose increase has been suggested for the treatment of this condition, 1,2,7,8,10 there are no reports specifically addressed to this important issue. In this article we describe the evolution of de novo AIH in a representative series of patients treated and not treated with steroids.…”

Section: Discussionmentioning

confidence: 99%

“…We studied HLA class I and II polymorphism by standard complement-dependent microcytotoxicity assays and/or by PCR with sequence-specific primers for the following antigens/alleles: A (1,2,3,11,23,24,25,26,29,30,31,32,33,34,66,68,69,80), B (7,8,13,18,27,35,37,38,39,41,42,44,45,47,48,49,50,51,52,53,55,56,57,58,60,61,62,63,64,65,67,70,73), Cw (1,2,3,4,…”

Section: Methodsmentioning

confidence: 99%

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Response to steroids in de novo autoimmune hepatitis after liver transplantation

et al. 2002

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Graft dysfunction associated with autoimmune phenomena has been recently described in liver transplant recipients without previous autoimmune disease. However, the natural history, diagnostic criteria, and definitive therapeutic approach of de novo autoimmune hepatitis (de novo AIH) are poorly understood. We report 12 cases of de novo AIH 27.9 ؎ 24.5 months after liver transplantation: the outcome of 7 patients treated with steroids is compared with a group of 5 nontreated patients. Nontreated patients lost the graft after 5.8 ؎ 2.6 months from de novo AIH onset. All treated patients were alive after 48.4 ؎ 14 (29-65) months from de novo AIH onset, and none of them lost the graft. However, 5 patients relapsed in relation to steroid tapering. All patients presented an atypical antiliver/ kidney cytosolic autoantibody, associated to classical autoantibodies in 10 cases. Histological study showed several degrees of lobular necrosis and inflammatory infiltrate. HLA antigen frequencies and matching were compared with 2 control groups (16 orthotopic liver transplantation [LTX] patients without de novo AIH and 929 healthy blood donors); de novo AIH patients showed a higher prevalence of HLA-DR3 (54.5% vs. 25.9%, P ‫؍‬ .04) than healthy controls, which was not observed in LTX patients without de novo AIH. In conclusion, this new disease should be included in the differential diagnosis of unexplained graft dysfunction. In addition, treatment with steroids results in a dramatically improved outcome. However, maintenance therapy is usually required. (HEPATOLOGY 2002;35:349-356.)

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Response to steroids in de novo autoimmune hepatitis after liver transplantation

et al. 2002

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“…The possibility that autoimmune hepatitis 25 might have developed in the last patient can be excluded because such characteristic markers as ANA and hypergammaglobulinemia were absent.…”

Section: Discussionmentioning

confidence: 99%

Disease recurrence after living liver transplantation for primary biliary cirrhosis: A clinical and histological follow-up study

Hashimoto¹,

Shimada²,

Noguchi³

et al. 2001

Liver Transplantation

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“…Patients without AIH before transplantation can develop autoantibodies either as a complication of otherwise typical rejection 11,12,29 or in association with new-onset AIH. [30][31][32][33][34][35][36] "Non-organ-specific" autoantibodies have been detected in up to 71% of patients after liver transplantation, 37 emphasizing the need for clinicopathological correlation.…”

Section: Practical Problems and Approach To Biopsy Interpretationmentioning

confidence: 99%

Liver biopsy interpretation for causes of late liver allograft dysfunction

2006

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Evaluation of needle biopsies and extensive clinicopathological correlation play an important role in the determination of liver allograft dysfunction occurring more than 1 year after transplantation. Interpretation of these biopsies can be quite difficult because of the high incidence of recurrent diseases that show histopathological, clinical, and serological features that overlap with each other and with rejection. Also, more than one insult can contribute to allograft injury. In an attempt to enable centers to compare and pool results, improve therapy, and better understand pathophysiological disease mechanisms, the Banff Working Group on Liver Allograft Pathology herein proposes a set of consensus criteria for the most common and problematic causes of late liver allograft dysfunction, including late-onset acute and chronic rejection, recurrent and new-onset viral and autoimmune hepatitis, biliary strictures, and recurrent primary biliary cirrhosis and primary sclerosing cholangitis. A discussion of differential diagnosis is also presented. (HEPATOLOGY 2006;44:489-501.)

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Development of autoimmune hepatitis following liver transplantation for primary biliary cirrhosis

Cited by 102 publications

References 30 publications

Response to steroids in de novo autoimmune hepatitis after liver transplantation

Response to steroids in de novo autoimmune hepatitis after liver transplantation

Disease recurrence after living liver transplantation for primary biliary cirrhosis: A clinical and histological follow-up study

Liver biopsy interpretation for causes of late liver allograft dysfunction

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