The immunoreactive patient: Rejection and autoimmune disease

O’Grady, John

doi:10.1002/lt.22413

Cited by 19 publications

(11 citation statements)

References 38 publications

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“…In many cases, mild to moderated rejection can be treated with increasing the levels of CNI alone. 77 As compared to Cyclosporine, use of Tacrolimus has been shown to reduce the incidence of both acute cellular rejection and steroid resistant rejection. 78 Chronic rejection is characterized by progressive bile duct loss (defined as ductopenia in at-least 50% of portal tracts) and by arteriopathy with foamy cell infiltration (may not be picked up by liver biopsy).…”

Section: Immunosuppression and CMV Infectionmentioning

confidence: 99%

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Current Status of Immunosuppression in Liver Transplantation

Choudhary

Saigal

Shukla

et al. 2013

Journal of Clinical and Experimental Hepatology

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With advancements in immunosuppressive strategies and availability of better immunosuppressive agents, survival rate following liver transplantation has improved significantly in the recent times. Besides improvements in surgical techniques, the most important factor that has contributed to this better outcome is the progress made in the field of immunosuppression. Over the last several years, the trend has changed to tailored immunosuppression with the aim of achieving optimal graft function while avoiding its undesirable side effects. Induction agents are no longer used routinely and the aim is to provide minimal immunosuppression in the maintenance phase. The present review discusses the various types of immunosuppressive agents, their mechanism of action, clinical utility, advantages and disadvantages, and their side effects in short and long-term. It also discusses about tailoring immunosuppression in presence of various situations such as renal dysfunction, metabolic syndrome, hepatitis C recurrence, cytomegalovirus infections and so on. The issue of chronic kidney disease and the available renal sparing immunosuppressive strategies has been particularly stressed upon. Finally, it discusses about the practical aspects of various immunosuppression regimens including drug monitoring. ( J CLIN EXP HEPATOL 2013;3:150-158)

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Section: Immunosuppression and CMV Infectionmentioning

confidence: 99%

“…As pathogenesis of chronic ductopenic rejection is complex, it responds uncommonly to increase in immunosuppression. 77 …”

Section: Immunosuppression and CMV Infectionmentioning

confidence: 99%

Current Status of Immunosuppression in Liver Transplantation

Choudhary

Saigal

Shukla

et al. 2013

Journal of Clinical and Experimental Hepatology

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“…Several studies have shown an association between PCH (de novo AIH) and antiviral therapy for recurrent hepatitis C after liver transplantation . In these studies, most of the patients developed PCH during antiviral therapy, and a few cases of PCH after the termination of antiviral therapy have been reported.…”

Section: Discussionmentioning

confidence: 99%

“…P LASMA CELL HEPATITIS (PCH), termed de novo autoimmune hepatitis (AIH), is an idiopathic disorder with the histological characteristics of AIH, showing interface hepatitis with a predominantly lymphoplasmacytic necroinflammatory infiltrate with or without lobular involvement and bridging necrosis in patients after undergoing liver transplantation for indications besides AIH. [1][2][3][4] Interestingly, an increasing number of PCH cases have been reported in liver transplant recipients infected with hepatitis C virus (HCV), including patients treated with interferon and ribavirin for recurrent hepatitis C. [2][3][4][5][6][7][8] However, it is unclear whether PCH is induced by interferon itself because the frequency of this disorder is low in a limited number of reports. Moreover, the histological features of PCH could not be completely distinguished from interface hepatitis because of HCV.…”

Section: Introductionmentioning

confidence: 99%

Plasma cell hepatitis induced by the termination of antiviral therapy for recurrent hepatitis C after living donor liver transplantation

Ueda

Yoshizawa

Ogura

et al. 2013

Hepatology Research

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Plasma cell hepatitis (PCH) is an idiopathic disorder characterized by plasma cell infiltration in the allografts of patients who have undergone liver transplantation. Although an increasing number of cases of PCH have been reported in liver transplant recipients with hepatitis C recurrence treated with interferon, it is unclear whether PCH is induced by interferon itself. Here, we describe the cases of two patients who developed PCH just after the termination of antiviral therapy for recurrent hepatitis C after living donor liver transplantation. Liver dysfunction appeared at 1 month in one patient and 2 months in the other patient after pegylated interferon plus ribavirin therapy, and liver histology showed interface hepatitis with plasma cell-rich lymphoid aggregates. Both patients recovered after steroid therapy and achieved sustained virological response. These cases suggest that PCH could be induced by the alteration of the immune condition resulting from the termination of antiviral therapy. PCH should be considered when the transaminase levels increase after antiviral therapy, and it should be carefully distinguished from hepatitis C relapse.

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“…The pathogenesis of CR is not completely understood, although its association with donor-specific human leukocyte antigen antibodies was recently reported (16). Additional immunosuppressive therapy is unlikely to be beneficial for CR patients, particularly those with late disease in which bile duct loss affects more than 50% of the portal tracts, and retransplantation is required (15).…”

mentioning

confidence: 98%