Marked hyperbilirubinemia caused by acute cellular rejection combined with preservation injury in an infant undergoing living-related liver transplantation.

Abstract: Acute cellular rejection (ACR) and preservation injury (PI) are major complications occurring early after liver transplantation (LTx) and sometimes lead to severe graft dysfunction. We herein report an infant who developed marked hyperbilirubinemia as a result of combined ACR and PI in addition to ischemic damage from bleeding, but recovered without re-LTx. In a 1-yr-old-girl undergoing living-related LTx, liver biopsy (LBx) on post-operative day 7 showed ballooning of the hepatocytes, i.e. microvesicular steatosis (30%) and occasional centrolobular necrosis, consistent with mild-to-moderate PI and ACR with a rejection activity index (RAI) of 2.0. Because drainage of an intra-abdominal abscess was performed and a systemic infection was considered severe, the tacrolimus level was decreased and steroids were discontinued. The total bilirubin level started to rise, thereafter, reaching a maximum of 47.6 mg/dL at 1 month after LTx. LBx showed an RAI of 6.0 and steatosis of 10%. With good response to an increase of tacrolimus level and administration of steroid, the total bilirubin level gradually decreased, finally reaching the normal range in 3 months, and LBx showed no steatosis or finding of ACR. From this experience, ACR, if combined with mild-to-moderate PI or other ischemic damage, may lead to severe clinical manifestations after LTx, which, however, could remit with conservative therapy and without re-LTx. [ABSTRACT FROM AUTHOR]