期刊
CELL TRANSPLANTATION
卷 17, 期 12, 页码 1403-1414出版社
COGNIZANT COMMUNICATION CORP
DOI: 10.3727/096368908787648083
关键词
Engraftment; Factor VII deficiency; Crigler-Najjar syndrome; Ornithine transcarbamylase deficiency; Progressive familial intrahepatic cholestasis type 2 (PFIC-2)
There are limited data regarding donor hepatocyte engraftment into recipient liver after human hepatocyte transplantation (HHTx). We reviewed the explant livers of seven children with metabolic disorders [ornithine-transcarbamylase deficiency (one), coagulation factor VII deficiency (three), Crigler-Najjar syndrome (one), progressive familial intrahepatic cholestasis type 2 (PFIC-2) deficiency (two)] who received allograft hepatocytes by intrarportal infusion with improvement in phenotype, although all later underwent liver transplantation (LT). Immunohistochemistry for bile salt export protein (BSEP) in the PFIC-2 patients and genetic typing following laser capture microdissection (LCM) of liver cells in the others were used to identify donor hepatocytes in recipient explant livers. Explant livers usually showed a preserved lobular architecture. In one patient, hepatocytes were identified inside portal vein thrombi. No donor hepatocytes in liver cell plates were identified immunohistochemically or by genetic typing. HHTx was generally followed by partial recovery of metabolic function; the procedure was well tolerated: any increase in portal vein pressure was transient. Hepatocytes were identified in portal vein thrombi. even months after portal vein infusion. Further studies are needed to monitor donor hepatocytes in vivo, to quantify better the efficacy of the procedure and to find ways of improving engraftment and function.
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