ABSTRACT
The Banff Working Group on Liver Allograft Pathology reviewed and discussed literature evidence regarding antibody-mediated liver allograft rejection at the 11th (Paris, France, June 5-10, 2011), 12th (Comandatuba, Brazil, August 19-23, 2013), and 13th (Vancouver, British Columbia, Canada, October 5-10, 2015) meetings of the Banff Conference on Allograft Pathology. Discussion continued online. The primary goal was to introduce guidelines and consensus criteria for the diagnosis of liver allograft antibody-mediated rejection and provide a comprehensive update of all Banff Schema recommendations. Included are new recommendations for complement component 4d tissue staining and interpretation, staging liver allograft fibrosis, and findings related to immunosuppression minimization. In an effort to create a single reference document, previous unchanged criteria are also included.
Subject(s)
Graft Rejection/etiology , Graft Rejection/pathology , Isoantibodies/immunology , Liver Transplantation/adverse effects , Allografts , Humans , Research ReportABSTRACT
OBJECTIVE: To describe fulminant hepatic failure (FHF) in children in the United States with clinical and histopathologic features distinctly different from those typical of FHF. PATIENTS: Seven young children were seen in early 1994 with encephalopathy, coagulopathy, and elevated aminotransferase levels. Liver failure was preceded by a prodromal viral illness that resulted in a period of fasting without dehydration. Unlike the majority of children with FHF, these patients had serum bilirubin levels < 171 mumol/L (10 mg/dl). All children had received therapeutic doses of acetaminophen during the prodromal illness. HISTOPATHOLOGIC FINDINGS: Histologic findings included zonal necrosis of hepatocytes in a centrilobular distribution, which is characteristic of toxic liver injury but is atypical for viral hepatitis and sporadic non-A non-B hepatitis. OUTCOME: Six patients recovered spontaneously, and one died of complications of liver failure and fungal sepsis. The cause of this disorder remains unknown, but we postulate a viral or environmental insult that preferentially damages zone 3 hepatocytes. The potential for this injury may have been augmented by ingestion of therapeutic doses of acetaminophen while patients were in a fasted state. The prognosis was good compared with typical FHF in children and correlated with the degree of liver necrosis on histologic examination.