Outcome of Autoimmune Hepatitis After Liver Transplantation1

Prados, Elisa; Cuervas-Mons, Valentín; Mata, Manuel de la; Fraga, Enrique; Rimola, Antoni; Prieto, M.; Clemente, G.; Vicente, Emilio; Casanovas, Teresa; Fábrega, Emilio

doi:10.1097/00007890-199812270-00013

Cited by 144 publications

(154 citation statements)

References 21 publications

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“…Criteria used to distinguish rejection from AIH can be melded into generalized criteria applicable to other causes of late liver allograft dysfunction, [39][40][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55][56] including: (1) histopathological evidence of liver injury showing a pattern compatible with the diagnosis (liver tests are usually elevated in a pattern consistent with the diagnosis); (2) positive serological, molecular biological, immunological, or radiographic evidence of pathogen or possible cause of injury; and (3) other causes of similar histopathological changes and elevated liver tests, if present, have been reasonably excluded. Table 1 shows approximate incidences, risk factors, and clinical, immunological, and radiological observations for common causes of late dysfunction.…”

Section: Generalized Criteriamentioning

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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Section: Generalized Criteriamentioning

confidence: 99%

Liver biopsy interpretation for causes of late liver allograft dysfunction

2006

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“…5,9,11,16 Our experience was too small to establish these associations. Similarly, we were unable to show that the principal program of immunosuppression (tacrolimus or cyclosporine) was an important determinant of recurrence.…”

Section: Discussionmentioning

confidence: 88%

“…3,4 Furthermore, autoantibodies and hypergammaglobulinemia disappear in most patients within 2 years. 1,2 Despite these successes, recurrent disease is possible, 2,3,[5][6][7][8][9][10][11][12][13] and recent reports have indicated that it may lead to cirrhosis and graft failure. 2,8,12 Furthermore, the immunoreactive propensity of the recipient may contribute to greater frequencies of acute rejection, steroid-resistant rejection, and chronic rejection, especially if corticosteroids are withdrawn in the posttransplantation period.…”

mentioning

confidence: 99%

“…2,8,12 Furthermore, the immunoreactive propensity of the recipient may contribute to greater frequencies of acute rejection, steroid-resistant rejection, and chronic rejection, especially if corticosteroids are withdrawn in the posttransplantation period. [12][13][14][15] The reasons for recurrent disease are unclear, but associations have been made with corticosteroid withdrawal, 5,9,11,16 implantation of an HLA-DR3-negative liver into a HLA-DR3-positive recipient, 5,6,17 immunosuppressive regimens based on tacrolimus, 8,10,12 and pediatric propensities for aggressive disease. 8 However, findings in various centers have been discrepant regarding the prevalence of recurrence, its consequences, and its risk factors.…”

mentioning

confidence: 99%

“…8 However, findings in various centers have been discrepant regarding the prevalence of recurrence, its consequences, and its risk factors. The importance of HLA-DR3 mismatching between donor and recipient 3,5,6,11,12,13 and the impact of corticosteroid withdrawal on the recurrence of autoimmune hepatitis 5,9,14,18 are now disputed. Optimal results after transplantation require clarification of factors contributing to recurrence and better understanding of the frequency and consequences of recurrent disease.…”

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confidence: 99%

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Recurrent autoimmune hepatitis after orthotopic liver transplantation

González-Koch¹,

Czaja²,

Carpenter³

et al. 2001

Liver Transpl

182

156

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To determine the frequency, risk factors, and consequences of recurrent autoimmune hepatitis after liver transplantation, 41 patients with type 1 disease were monitored after surgery in accordance with a surveillance protocol. Tacrolimus or cyclosporine plus prednisone were administered to each patient, and liver biopsy examinations were performed at least annually according to protocol. Corticosteroid therapy was ultimately discontinued in only 2 patients. Recurrent disease was defined as the presence of lymphoplasmacytic infiltrates in liver tissue in the absence of other causes of allograft dysfunction. Autoimmune hepatitis recurred in 7 patients (17%), and the mean time to recurrence was 4.6 ؎ 1 years. Recurrence was asymptomatic in 4 of 7 patients and detected only by surveillance liver biopsy assessment in 2 patients. Histological changes were mild, and there was no progression to cirrhosis during 4.9 ؎ 0.9 years of observation. Five-year patient (86% v 82%; P ‫؍‬ .9) and graft (86% v 67%; P ‫؍‬ .5) survival rates were not statistically different between patients with and without recurrent disease. HLA-DR3 or HLA-DR4 occurred more commonly in patients with than without recurrence (100% v 40%; P ‫؍‬ .008) and healthy subjects (100% v 49%; P ‫؍‬ .01). Recurrent disease was unrelated to donor HLA status. In conclusion, recurrence after transplantation for type 1 autoimmune hepatitis is common. Its mild manifestations and favorable prognosis may reflect early detection by a surveillance protocol and/or continuous corticosteroid treatment. L iver transplantation is effective in the treatment of decompensated autoimmune hepatitis. Five-year patient and graft survival rates range from 83% to 92%, 1,2 and the actuarial 10-year survival rate after transplantation is 75%. 3,4 Furthermore, autoantibodies and hypergammaglobulinemia disappear in most patients within 2 years. 1,2 Despite these successes, recurrent disease is possible, 2,3,5-13 and recent reports have indicated that it may lead to cirrhosis and graft failure. 2,8,12 Furthermore, the immunoreactive propensity of the recipient may contribute to greater frequencies of acute rejection, steroid-resistant rejection, and chronic rejection, especially if corticosteroids are withdrawn in the posttransplantation period. [12][13][14][15] The reasons for recurrent disease are unclear, but associations have been made with corticosteroid withdrawal, 5,9,11,16 implantation of an HLA-DR3-negative liver into a HLA-DR3-positive recipient, 5,6,17 immunosuppressive regimens based on tacrolimus, 8,10,12 and pediatric propensities for aggressive disease. 8 However, findings in various centers have been discrepant regarding the prevalence of recurrence, its consequences, and its risk factors. The importance of HLA-DR3 mismatching between donor and recipient 3,5,6,11,12,13 and the impact of corticosteroid withdrawal on the recurrence of autoimmune hepatitis 5,9,14,18 are now disputed. Optimal results after transplantation require clarification of factors contributing to recurre...

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