Antibody‐mediated rejection after ABO‐incompatible pediatric living donor liver transplantation for propionic acidemia: A case report. (20th July 2016)

• Record Type: Journal Article
• Authors: Honda, Masaki; Sakamoto, Seisuke; Sakamoto, Rieko; Matsumoto, Shirou; Irie, Tomoaki; Uchida, Koushi; Shimata, Keita; Kawabata, Seiichi; Isono, Kaori; Hayashida, Shintaro; Yamamoto, Hidekazu; Endo, Fumio; Inomata, Yukihiro
• Is Part Of: Pediatric transplantation. Volume 20:Number 6(2016:Sep.)
• Page Start: 840
• Page End: 845
• Publication Date: 2016-07-20
• Subjects: antibody‐mediated rejection -- propionic acidemia -- rituximab -- streptococcal infection; Transplantation of organs, tissues, etc. in children -- Periodicals; 617.95408305
• DOI: 10.1111/petr.12722
• Languages: English
• ISSNs: 1397-3142

Abstract

Abstract: We herein present the case of a four‐yr‐old boy with PA who developed AMR after ABO‐incompatible LDLT despite undergoing B cell desensitization using rituximab. Although the CD19+ lymphocyte count decreased to 0.1% nine days after the administration of rituximab, he developed a high fever which was accompanied by arthralgia due to a streptococcal infection 13 days after rituximab prophylaxis. After the clearance of the infection, he underwent ABO‐incompatible LDLT 36 days after the administration of rituximab. The CD19+ lymphocyte count just prior to LDLT was 1.2%. He developed AMR five days after LDLT, and the antidonor‐type IgM and IgG antibody titers increased to 1:1024 and 1:1024, respectively. He was treated by plasma exchange, IVIG, steroid pulse therapy, and rituximab re‐administration; however, his liver dysfunction continued. Despite intensive treatment, he died due to complicated abdominal hernia, acute renal failure, and ARDS. This case suggests that a streptococcal infection may induce the activation of innate immune responses; thus, additional desensitization therapy should be considered prior to ABO‐incompatible LDLT if B cell reactivation is suspected.