Chronic allograft dysfunction: Diagnosis and management. Is it always progressive?

Neuberger, James

doi:10.1002/lt.20603

Cited by 26 publications

(17 citation statements)

References 27 publications

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“…In some centers, up to 40% of adult patients subjected to biopsy more than 12 months after transplantation have unexplained chronic hepatitis. 76 A similar prevalence has been observed in the pediatric population, in which recurrent native disease is less of a problem; the frequency of "idiopathic" chronic hepatitis was 20% at 1 year of age, rising to 60% at 10 years of age. 77 Cases presenting as central perivenulitis probably represent centrilobular-based acute rejection, or AIH if autoantibodies are also present, 57 because allograft dysfunction usually responds to increased immunosuppression.…”

Section: Recurrent Diseases and New-onset Diseasessupporting

confidence: 56%

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: Recurrent Diseases and New-onset Diseasessupporting

confidence: 56%

Liver biopsy interpretation for causes of late liver allograft dysfunction

2006

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“…Other terms used in this context include ''portal/parenchymal mononuclear inflammation'' [132], ''portal lymphocytic inflammation'' [133], ''non-specific inflammation'' [134], ''graft inflammation'' [14], ''interface hepatitis'' [135], and ''non-specific hepatitis'' [10]. Overall, it has been estimated that features compatible with a diagnosis of IPTH can be observed in 10-50% of patients undergoing protocol biopsy >1 year post-transplant [16] and up to 60% of [12], making this the commonest overall diagnosis in annual review biopsies from adults [136] and children [12] in some centres. The prevalence increases with time -ranging from 20% to 30% during the first 3 years post-transplant to more than 60% at 10 years [12,14,135,137].…”

Section: Idiopathic Post-transplant Hepatitis (Ipth)mentioning

confidence: 95%

What is the long-term outcome of the liver allograft?

Hübscher

2011

Journal of Hepatology

122

127

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With improved long-term survival following liver transplantation (LT), issues relating to the assessment of the liver allograft in long-term survivors are becoming increasingly relevant. Histological abnormalities are commonly present in late post-transplant biopsies, including protocol biopsies from patients who appear to be well with good graft function. Recurrent disease is the commonest recognised cause of abnormal graft histology, but may be modified by the effects of immunosuppression or interactions with other graft complications, resulting in complex or atypical changes. Other abnormalities seen in late post-transplant biopsies include rejection (which often has different appearances to those seen in the post-transplant period), de novo disease, "idiopathic" post-transplant hepatitis (IPTH) and nodular regenerative hyperplasia. In many cases graft dysfunction has more than one cause and liver biopsy may help to identify the predominant cause of graft damage. Problems exist with the terminology used to describe less well understood patterns of graft injury, but there is emerging evidence to suggest that late rejection, de novo autoimmune hepatitis and IPTH may all be part of an overlapping spectrum of immune-mediated injury occurring in the late post-transplant liver allograft. Careful clinico-pathological correlation is very important and the wording of the biopsy report should take into account therapeutic implications, particularly whether changes in immunosuppression may be indicated. This article will provide an overview of the main histological changes occurring in long-term survivors post-LT, focusing on areas where the assessment of late post-transplant biopsies is most relevant clinically.

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“…Furthermore, IPTH is often subclinical, being more apparent in centres, which perform protocol biopsies, because abnormalities in liver enzymes may be minimal or absent [38,[40][41][42]. Overall, inflammatory changes that could be classified as IPTH have been observed in 10-50% of patients undergoing protocol biopsy >1 year post-transplant [41] and more than 60% of children biopsied >10 years post-transplant [38], making this the commonest diagnosis in annual review biopsies in some centres [43]. In protocol biopsy series, IPTH is documented in 10-30% of adults [40, 44,45] and in 22-64% of children [38] compared with 2-11% of children and adults [39, 46,47] in indication biopsy series, supporting the concept of this often being subclinical.…”

Section: Idiopathic Post-transplant Hepatitismentioning

confidence: 99%