As more individuals are living for longer periods post liver transplantation the likelihood of encountering a liver allograft biopsy in clinical practice increases. Rejection is not the only complication to affect the allograft, others include technical (related to creating anastomoses or to thrombosis), manifestations of immunosuppression (including EBV driven PTLD, especially in childhood) and recurrent disease. Complications are not mutually exclusive. Access to the patients history and knowledge of previous biopsies is essential especially in cases where damage may be multifactorial. Most allograft biopsies will be taken for a clinical indication but in some centres, usually paediatric, planned or protocol biopsies are performed on clinically well patients in order to monitor the graft and optimise long term outcomes.
Rejection changes are helpfully described and updated by the Banff liver group. Rather than ‘acute cellular rejection’ current guidelines recommend classification in terms of T cell or antibody mediated (AMR) mechanisms and plasma cell rich rejection. Histological assessment is focussed on the intensity and composition of portal infiltrates, presence of endothelitis and damage to or loss of bile ducts. Interface hepatitis should be noted. It is important to remember that rejection changes can be manifest around central veins. Recognising microvasculitis and C4d immunohistochemistry are helpful for suggesting the possibility of AMR and prompting the measurement of donor specific antibodies in serum. Guidelines are offered for the assessment of the severity of these processes which can occur together. Appropriate classification gives a better chance for effective treatment. Of particular importance in younger recipients, but not exclusive to them, more subtle lesions, perhaps vascular (in the spectrum of nodular regenerative hyperplasia NRH for example), which may influence long term graft allograft function can be identified. Pathologists have a role in identifying patients in whom immunosuppression might safely be reduced, avoiding significant complications.

Bone marrow transplantation is a commonly performed technique for a wide range of haematological disorders. Bone marrow transplant recipients may develop liver dysfunction following transplant. A common cause for this is acute graft-versus-host disease. Affected patients often show evidence of graft-versus-host disease at other sites e.g., the skin or luminal gastrointestinal tract. This condition is mediated by donor T-cells. Acute graft-versus-host disease usually develops within 100 days of transplantation, although late onset acute graft-versus-host disease is described. Within the liver, acute graft-versus-host disease is characterised by a light mononuclear inflammatory infiltrate within portal tracts together with reactive changes within biliary epithelium, with intraepithelial lymphocytosis sometimes seen. Cholestasis is not uncommonly present. Focal parenchymal necro-inflammation, more extensive lobular inflammation and hepatocyte necrosis can be seen, although these features are usually associated with the characteristic portal tract changes. Chronic graft-versus-host disease is characterised by bile duct loss and portal tract fibrosis. Hepatic iron overload is a common finding after bone marrow transplantation, since these patients have often received multiple blood transfusions. Other possible reasons for liver dysfunction in this setting include drug reactions, hepatic veno-occlusive disease and infections. The latter include new infections e.g., cytomegalovirus and recurrence of a pre-existing infection e.g., viral hepatitis. It is also possible that pre-existing liver disease, unrelated to the haematological disorder or the transplant procedure, may be identified on liver biopsy.