Alteration of MRP2 expression and the graft outcome after liver transplantation

PURPOSE: Multidrug resistance-associated protein (MRP) 2 is a glutathione conjugate in the canalicular membrane of hepatocytes. Early graft damage after liver transplantation (LT) can result in alteration of MRP2 expression. The purpose of this study was to evaluate the relationship between the pattern of MRP2 alteration and graft outcome. METHODS: Forty-one paraffin-embedded liver graft tissues obtained by protocol biopsy within 2 months after LT; these were stained using monoclonal antibodies of MRP2. We selected 15 live donor biopsy samples as a control, that showed homogenous canalicular staining for MRP2. The pattern of canalicular MRP2 staining of graft was classified into 3 types: homogenous (type C0), focal (type C1), and no (type C2,) staining of the canaliculi. RESULTS: In total, 17.1% graft tissues were type C0, 36.6% were type C1, and 46.3% were type C2. The median operation time was longer in patients with type C2 (562.6 minutes) than in patients with type C0 (393.8 minutes) (P = 0.038). The rates of posttransplant complications were higher in patients with type C2 (100%) than in patients with type C0 (42.9%) and C1 (73.3%) (P < 0.001). CONCLUSION: MRP2 expression pattern was altered in 82.9% after LT. The pattern of MRP2 alteration was associated with longer operation time and higher rates of post-LT complications.

Serongative Acute Hepatic Failure-associated Aplastic Anemia in Pediatric Liver Transplantation / 대한이식학회지

Aplastic anemia (AA) is a rare complication of liver transplantation. The causes of AA have not yet been identified, and optimal treatment for AA after liver transplantation has not been firmly established. We experienced two cases of AA accompanied with fulminant hepatitis among 157 pediatric recipients (1.3%) and among 17 recipients of Korean Network of Organ Sharing (KONOS) status 1 (11.8%). The patients were a 16-year-old girl and a 3-year-old boy who had jaundice and lethargy due to non-A, non-B, non-C fulminant hepatitis. The girl underwent split liver transplantation involving the liver of a 24-year-old man, and the boy underwent an emergency living donor liver transplantation with a liver obtained from his 16-year-old cousin. Each transplantation procedure was uneventful. However, both patients were diagnosed with AA caused by thrombocytopenia and neutropenia at 140 and 26 days, respectively, after liver transplantation. The girl recovered completely after undergoing bone marrow transplantation and was followed up for 70 months. However, the boy was conservatively treated because of the development of hyperbilirubinemia and pyrexia. He died of multi-organ failure 74 days after liver transplantation. AA is not a rare complication of pediatric liver transplantation for fulminant hepatic failure. Therefore, AA must be suspected in pediatric cases of cytopenia even after liver transplantation. Our findings indicate bone marrow transplantation is the treatment of choice for AA even in cases where AA develops after liver transplantation.

Serongative Acute Hepatic Failure-associated Aplastic Anemia in Pediatric Liver Transplantation / 대한이식학회지

Aplastic anemia (AA) is a rare complication of liver transplantation. The causes of AA have not yet been identified, and optimal treatment for AA after liver transplantation has not been firmly established. We experienced two cases of AA accompanied with fulminant hepatitis among 157 pediatric recipients (1.3%) and among 17 recipients of Korean Network of Organ Sharing (KONOS) status 1 (11.8%). The patients were a 16-year-old girl and a 3-year-old boy who had jaundice and lethargy due to non-A, non-B, non-C fulminant hepatitis. The girl underwent split liver transplantation involving the liver of a 24-year-old man, and the boy underwent an emergency living donor liver transplantation with a liver obtained from his 16-year-old cousin. Each transplantation procedure was uneventful. However, both patients were diagnosed with AA caused by thrombocytopenia and neutropenia at 140 and 26 days, respectively, after liver transplantation. The girl recovered completely after undergoing bone marrow transplantation and was followed up for 70 months. However, the boy was conservatively treated because of the development of hyperbilirubinemia and pyrexia. He died of multi-organ failure 74 days after liver transplantation. AA is not a rare complication of pediatric liver transplantation for fulminant hepatic failure. Therefore, AA must be suspected in pediatric cases of cytopenia even after liver transplantation. Our findings indicate bone marrow transplantation is the treatment of choice for AA even in cases where AA develops after liver transplantation.