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Updated: Sep 14, 2025

Porcine Liver Transplantation Without Veno-Venous Bypass As an Extended Criteria Donor Model
Published on: August 17, 2022
Living donor liver transplantation using ABO-incompatible grafts for chronic and acute liver failure
Toru Ikegami1, Masashi Tsunematsu2, Kenei Furukawa2
1Division of Hepatobiliary and Pancreas Surgery, Department of Surgery, The Jikei University School of Medicine, Tokyo, 105-8461, Japan. toruikegamijikei@jikei.ac.jp.
The introduction of rituximab, an anti-CD20 antibody, has changed the treatment strategies and outcomes for ABO-incompatible living donor liver transplantation (ABOi-LDLT) dramatically. Rituximab targets the CD20-positive B-cells that would differentiate into plasma cells, producing antibodies against A or B antigen-expressing cells and causing microvascular multiple thrombosis and graft necrosis or diffuse bile-duct necrosis. Now, the universal desensitization of the ABOi combination between the donor and recipient is performed by rituximab, and ABOi-LDLT has become the treatment of choice for end-stage liver disease. However, because rituximab takes 1-3 weeks to mediate its effects, complicated strategies are necessary to perform ABOi-LDLT for acute liver failure. For example, high-dose intravenous immunoglobulin (IVIG) or bortezomib may be used to alleviate the elevation of isoagglutinin titers. The diagnosis and treatment of antibody-mediated rejection (AMR) remain challenging. Treatment options include plasma exchange, high-dose IVIG, and bortezomib, but the optimal strategies have not been identified. In this review, we discuss standard ABOi-LDLT for chronic liver disease, ABOi-LDLT for acute liver failure, and the diagnosis and treatment of AMR.
The introduction of rituximab, an anti-CD20 antibody, has changed the treatment strategies and outcomes for ABO-incompatible living donor liver transplantation (ABOi-LDLT) dramatically. Rituximab targets the CD20-positive B-cells that would differentiate into plasma cells, producing antibodies against A or B antigen-expressing cells and causing microvascular multiple thrombosis and graft necrosis or diffuse bile-duct necrosis. Now, the universal desensitization of the ABOi combination between the donor and recipient is performed by rituximab, and ABOi-LDLT has become the treatment of choice for end-stage liver disease. However, because rituximab takes 1-3 weeks to mediate its effects, complicated strategies are necessary to perform ABOi-LDLT for acute liver failure. For example, high-dose intravenous immunoglobulin (IVIG) or bortezomib may be used to alleviate the elevation of isoagglutinin titers. The diagnosis and treatment of antibody-mediated rejection (AMR) remain challenging. Treatment options include plasma exchange, high-dose IVIG, and bortezomib, but the optimal strategies have not been identified. In this review, we discuss standard ABOi-LDLT for chronic liver disease, ABOi-LDLT for acute liver failure, and the diagnosis and treatment of AMR.
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