Epstein-Barr virus as a trigger for autoimmune hepatitis in susceptible individuals

Vento, Sandro; Guella, Lorenza; Mirandola, F.; Cainelli, Francesca; Perri, Giovanni Di; Solbiati, M; Concia, Ercole; Ferraro, Teresa

doi:10.1016/s0140-6736(95)91438-2

Cited by 181 publications

(128 citation statements)

References 7 publications

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“…In this context, several viruses have been identified as triggers of AIH in the nontransplanted population. [13][14][15][16][17] Likewise, the apparent paradox of developing AD in the context of immunocompromised patients can contribute to the low clinical suspicion of this entity. However, it is well known that some immunodeficiency conditions are associated with AD.…”

Section: Discussionmentioning

confidence: 99%

Response to steroids inde novoautoimmune 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%

Response to steroids inde novoautoimmune hepatitis after liver transplantation

et al. 2002

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“…An association with measles virus was first proposed in 1987 after identification of persistent measles virus genome in lymphocytes and high antibody titers in 12 of 18 patients with AIH [8] . Vento et al [9] reported the development of AIH in healthy relatives of patients with AIH that was associated with cases of infectious mononucleosis due to Epstein-Barr virus (EBV) infection. In these cases, the development and persistence of autoantibodies to the asialoglycoprotein receptor were documented, and it was proposed that cross reactivity between asialoglycoprotein and EBV antibodies caused an autoimmune reaction.…”

Section: Peer-reviewmentioning

confidence: 99%

Direct acting antiviral therapy is curative for chronic hepatitis C/autoimmune hepatitis overlap syndrome

Sahebjam

Hajdu

Nortey

et al. 2016

WJH

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Autoimmune phenomena are common in patients with chronic hepatitis C. Management of chronic hepatitis C/ autoimmune hepatitis syndrome has until recently been problematic due to the adverse effects of interferon on autoimmune processes and immunosuppression on viral replication. In this report we describe 3 patients with chronic hepatitis C/autoimmune hepatitis overlap syndrome who responded rapidly to direct acting antiviral therapy. The resolution of the autoimmune process supports a direct viral role in its pathophysiology.

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“…23,24 We had no evidence for hepatitis A and Epstein-Barr virus infection as a triggering agent in our patients. The role of drugs is also well known as a possible trigger of AIH.…”

Section: Discussionmentioning

confidence: 81%

Development of autoimmune hepatitis in patients with typical primary biliary cirrhosis

et al. 2006

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Primary biliary cirrhosis (PBC)-autoimmune hepatitis (AIH) overlap syndrome is a clinical entity characterized by the occurence of both conditions at the same time in the same patient. In addition to PBC-AIH overlap syndrome, transitions from one autoimmune disease to another have been reported, but no systematic series have been published. We report a series of 12 patients with consecutive occurrence of PBC and AIH (i.e., PBC followed by AIH). Among 282 PBC patients, 39 were identified who fulfilled criteria for probable or definitive AIH. AIH developed in 12 patients (4.3%). The baseline characteristics of the patients were similar to those of patients with classical PBC. Time elapsed between the diagnosis of PBC and the diagnosis of AIH varied from 6 months to 13 years. Patients with multiple flares of hepatitis at the time of diagnosis of AIH had cirrhosis on liver biopsy. Ten patients were given prednisone ؎ azathioprine; short-term as well as sustained remissions were obtained in 8 of these, while two had multiple relapses and eventually died 8 and 7 years after diagnosis of AIH. In conclusion, the development of superimposed AIH could not be predicted from baseline characteristics and initial response to UDCA therapy. If not detected early, superimposed AIH can result in rapid progression toward cirrhosis and liver failure in PBC patients. (HEPATOLOGY 2006;44:85-90.)

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Epstein-Barr virus as a trigger for autoimmune hepatitis in susceptible individuals

Cited by 181 publications

References 7 publications

Response to steroids inde novoautoimmune hepatitis after liver transplantation

Response to steroids inde novoautoimmune hepatitis after liver transplantation

Direct acting antiviral therapy is curative for chronic hepatitis C/autoimmune hepatitis overlap syndrome

Development of autoimmune hepatitis in patients with typical primary biliary cirrhosis

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