High Incidence of Antitissue Antibodies in Patients Experiencing Chronic Liver Allograft Rejection1

Dubel, Laurence; Farges, Olivier; Johanet, Catherine; Sebagh, Mylène; Bismuth, H

doi:10.1097/00007890-199804270-00011

Cited by 77 publications

(62 citation statements)

References 22 publications

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“…One series described the presence of ANA or ASM antibodies in 71% of patients who developed chronic rejection. 4 Antibodies were detectable before or at the time of diagnosis of chronic rejection. The prevalence of antibody formation was significantly greater than in patients with HCV recurrence posttransplantation without chronic rejection, of whom 16% had detectable antibodies, and in patients without graft dysfunction in which the prevalence of autoantibodies was 7%.…”

Section: Discussionmentioning

confidence: 99%

“…This form of graft dysfunction occurred in association with serologic and histologic features compatible with autoimmune hepatitis (AIH) in patients who underwent transplantation for etiologies other than AIH. 1 Although graft dysfunction in association with the presence of autoantibodies has been described in adults, [2][3][4] it has not been characterized. A recent report described 2 patients who underwent transplantation for primary biliary cirrhosis (PBC) who developed an autoimmune-type reaction in their liver allograft.…”

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Graft dysfunction mimicking autoimmune hepatitis following liver transplantation in adults

et al. 2001

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In children, a type of graft dysfunction associated with autoimmune features has been described. We have identified 7 adult liver-transplant (LT) recipients from a series of over 1,000 consecutive transplant recipients who presented between 0.3 years and 7.2 years following transplantation with characteristic symptoms, autoantibody profiles, and histologic findings of autoimmune disease. The indications for transplantation were Ecstasy overdose, alcohol-related cirrhosis, primary sclerosing cholangitis (PSC) (2), primary biliary cirrhosis (PBC), hepatitis C cirrhosis, and cryptogenic cirrhosis. Two patterns of de novo autoantibody development were noted; anti-liver-kidney-microsome (LKM) antibody development at high titer in association with an aspartate transaminase (AST) > 500 and antinuclear ( Long-term follow-up of large numbers of liver-transplant recipients has led to a reasonably clear understanding of the causes of graft dysfunction. Liver-function test abnormalities are most commonly associated with rejection, sepsis, vascular compromise, biliary complications, lymphoproliferative disease, and recurrence of the original disease. In some circumstances, the cause of graft dysfunction may be impossible to ascertain. A recent report described a unique form of graft dysfunction occurring in pediatric liver allograft recipients late after liver transplantation (LT). This form of graft dysfunction occurred in association with serologic and histologic features compatible with autoimmune hepatitis (AIH) in patients who underwent transplantation for etiologies other than AIH. 1 Although graft dysfunction in association with the presence of autoantibodies has been described in adults, 2-4 it has not been characterized. A recent report described 2 patients who underwent transplantation for primary biliary cirrhosis (PBC) who developed an autoimmune-type reaction in their liver allograft. 5 In this report, we describe a characteristic form of graft dysfunction in adults akin to the de novo AIH syndrome described in children, 1 except for a more severe graft dysfunction that may result in graft loss. The entity occurred in a group of liver allograft recipients who underwent transplantation at King's College Hospital for indications other than AIH over a 10-year period. PATIENTS AND METHODSOver a 12-year period of observation (1988-99), 7 adults from a series of more than 1,700 adult LT recipients had a characteristic form of graft dysfunction. The indications for transplantation were Ecstasy-induced acute liver failure, alcohol-related cirrhosis, primary sclerosing cholangitis (PSC) (2), PBC, hepatitis C cirrhosis, and cryptogenic cirrhosis. Of these, 4 were male, 3 were female, and all were white. Demographic features are summarized in Table 1. The median age at transplantation was 33.4 years (range, 19-58 years). All 7 patients received cadaveric grafts, and postoperative immunosuppression was achieved with cyclosporine to maintain trough concentrations of 150 to 250 g/L in the first 6 months and 100 to 200 g/L the...

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Section: Discussionmentioning

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Graft dysfunction mimicking autoimmune hepatitis following liver transplantation in adults

et al. 2001

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“…Recipient dendritic cell antigen uptake and self-reactive T and/or B lymphocyte priming 10 triggers "autoantibody" production and immunity directed against non-major histocompatibility complex determinants. Some non-major histocompatibility complex cytoplasmic, nuclear, and matrix protein antigens [11][12][13][14] (reviewed in Graft [15][16][17][18] ) are shared by the donor and recipient, whereas others may be donor-specific.…”

Section: Immunological Considerationsmentioning

confidence: 99%

“…Antimitochondrial antibodies and antinuclear antibodies often persist after transplantation in patients with PBC or AIH, albeit at lower titers, even without histopathological evidence of recurrent disease. 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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“…Likewise, no histological features of acute or chronic rejection were found. 9,10 Tacrolimus is a fungal macrolide with immunosuppressive activity 10 to 200 times greater than that of cyclosporine. Despite its distinct structure, tacrolimus, like cyclosporine, selectively inhibits CD4 ϩ lymphocyte activation and proliferation.…”

Section: Case Reportmentioning

confidence: 99%

Successful tacrolimus therapy for a severe recurrence of type 1 autoimmune hepatitis in a liver graft recipient

Hurtova

Duclos‐Vallée

Johanet

et al. 2001

Liver Transplantation

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High Incidence of Antitissue Antibodies in Patients Experiencing Chronic Liver Allograft Rejection1

Abstract: These results show a strong association between chronic allograft rejection and the development of antitissue antibodies and suggest that these antibodies could be used to identify patients at high risk of developing chronic rejection after liver transplantation.

Cited by 77 publications

References 22 publications

Graft dysfunction mimicking autoimmune hepatitis following liver transplantation in adults

Graft dysfunction mimicking autoimmune hepatitis following liver transplantation in adults

Liver biopsy interpretation for causes of late liver allograft dysfunction

Successful tacrolimus therapy for a severe recurrence of type 1 autoimmune hepatitis in a liver graft recipient

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