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liver allograft

Monday 7 June 2004

Liver transplantation has become a routine, life-saving therapy for children with end-stage liver disease. Current long-term survival rates are over 80%.

However, chronic graft injuries, manifesting with elevated serum liver enzymes and histological abnormalities, are being recognized more frequently as a long-term problem.

Chronic rejection usually presents with foam cell arteriopathy, loss of bile ducts in at least 50% of portal tracts, significant initial elevation of serum aspartate aminotransferase (AST), and slowly increasing bilirubin throughout its evolution.

A less frequent form of chronic rejection is directed against pericentral hepatocytes, manifesting as a chronic inflammatory infiltrate, cellular collapse, and ultimate fibrosis.

Both humoral immunity and cellular immunity are believed to be responsible for this process, and endothelial and biliary epithelial cells are the target.

The spectrum of diseases encountered in post-transplant liver pathology biopsies is broad. They belong to one of three categories:
- (1) new-onset/de novo post-transplant abnormalities (early and late)
- (2) rejection
- (3) recurrence of original disease.

Early new-onset conditions are mostly related to surgical complications, donor factors and ischaemia to the graft. These include reperfusion/preservation injury, lipopeliosis, small-for-size-syndrome, biliary sludge syndrome and hepatic artery thrombosis.

The various forms of rejection (cellular, chronic, antibody-mediated, and late atypical rejection) are detailed.

Most chronic liver diseases can and do recur in the graft. They may display features that overlap with de novo conditions (eg, primary sclerosing cholangitis versus chronic rejection).

As with most cases of allograft biopsy interpretation, accurate diagnosis rests with careful correlation of histological features with clinical, imaging and laboratory findings, and often comparison with previous sequential and follow-up biopsies.

Late-onset new diseases include biliary strictures, idiopathic chronic hepatitis and de novo autoimmune hepatitis, among others.

De novo autoimmune hepatitis (AIH) or hepatocytic rejection

De novo autoimmune hepatitis (AIH) is a special type of graft dysfunction, . This term refers to a progressive posttransplant disease associated with chronic active hepatitis at liver biopsy, elevated serum liver enzymes, increased serum immunoglobulin G (IgG) concentrations, and the presence of non-organ-specific autoantibodies. Its incidence in pediatric patients is between 2.3% and 5.2%, and its incidence is even lower in adult orthotopic liver transplantation (OLT) recipients. The etiology and pathogenesis of this chronic disease are not known, but molecular mimicry and autoimmunity have been hypothesized. Others have tried to classify it as a form of late graft dysfunction in the context of chronic rejection.

Links

- Liver allograft pathology at TPIS, University of Pittsburgh.

References

- Liver allograft pathology: approach to interpretation of needle biopsies with clinicopathological correlation. Adeyi O, Fischer SE, Guindi M. J Clin Pathol. 2010 Jan;63(1):47-74. PMID: #19847014# (Free)


- Liver allograft pathology at TPIS, University of Pittsburgh.

- Transplant Pathology at the Univ. of Pittsburgh