Serongative Acute Hepatic Failure-associated Aplastic Anemia in Pediatric Liver Transplantation.
10.4285/jkstn.2011.25.4.276
- Author:
Eon Chul HAN
1
;
Nam Joon YI
;
Geun HONG
;
Min Su PARK
;
Young Rok CHOI
;
Heyoung KIM
;
Kwang Woong LEE
;
In Ho KIM
;
Yoon Jun KIM
;
Jae Sung KO
;
Kyung Duk PARK
;
Hoan Jong LEE
;
Eun Hwa CHOI
;
Jeong Kee SEO
;
Kyoung Bun LEE
;
Kyung Suk SUH
Author Information
1. Department of Surgery, Seoul National University College of Medicine, Seoul, Korea. gsleenj@hanmail.net
- Publication Type:Case Report
- Keywords:
Liver transplantation;
Aplastic anemia;
Bone marrow transplantation;
Pediatric liver transplantation;
Fulminant hepatic failure
- MeSH:
Adolescent;
Anemia, Aplastic;
Bone Marrow Transplantation;
Emergencies;
Fever;
Hepatitis;
Humans;
Hyperbilirubinemia;
Jaundice;
Lethargy;
Liver;
Liver Failure, Acute;
Liver Transplantation;
Living Donors;
Neutropenia;
Preschool Child;
Thrombocytopenia;
Transplants;
Young Adult
- From:The Journal of the Korean Society for Transplantation
2011;25(4):276-281
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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.
