Immunologic strategies and outcomes in ABO-incompatible living donor liver transplantation

Abstract

In the past, adult ABO incompatible living donor liver transplantation (ABO-I LDLT) had poor graft survival and low patient survival due to hyperacute rejection and a high risk of vascular biliary complication, and it was considered a contraindication. 1-4 Susceptibility to rejection, including severe hepatic necrosis and diffuse intravascular coagulation disorder within the graft, appears to be due to the blood group antigen expressed in the vascular endothelium and bile ducts after transplantation. 5,6 Various desensitization strategies have been introduced to overcome the barrier of ABO incompatibility. 7-9 However, desensitization protocols differ at each center, and the necessity of local infusion, splenectomy, intravenous immunoglobulin (IVIG), and plasmapheresis is controversial. After the rituximab era, the outcome of ABO-I LDLT has been reported in many studies to be comparable to ABO compatible living donor liver transplantation (ABO-C LDLT). 10-13 Many centers are now trying to simplify protocols. 14-20 We review the past and current immune strategies for desensitization and to provide outcomes and ABO incompatibility-related complications in ABO-I LDLT.

Impact of Graft Weight Change During Perfusion on Hepatocellular Carcinoma Recurrence After Living Donor Liver Transplantation

“…Methylprednisolone therapy was initiated on the operation day at a dose of 500 mg/day and then tapered to 4–8 mg/day within 1–2 months postoperatively. In case of ABO-incompatible LDLT, rituximab prophylaxis and frequent total plasma exchange were conducted for desensitization ( 6 ). When HCC recurs, tacrolimus trough level was lowered compared to patients without HCC recurrence and everolimus was added.…”

Characteristics of Immunoglobulin M Type Antibodies of Different Origins from the Immunologic and Clinical Viewpoints and Their Application in Controlling Antibody-Mediated Allograft Rejection

“…Contrarily, other reports indicated that ABO-incompatible transplants do not require specialized immunosuppressive therapy. In one study, the survival rates of the transplanted graft and the recipient were comparable with either those in ABO-compatible-matched controls or patients with low baseline antiblood group antibody titers [ 14 ], whereas a second study recorded a graft survival rate of 100% at 36 months after transplantation [ 15 ].…”

“…Additionally, antibodies against ABO blood group antigens, which are representative of IgM and IgG antibodies, induce the development of AMR, causing transplanted graft failure in ABO-incompatible liver transplant recipients [ 13 , 14 , 15 ].…”

“…Concerning the association of the type of transplanted organs with AMR development, AMR has not been overcome in ABO-incompatible liver transplantation from brain-dead donors, but it is mostly controlled in ABO-incompatible liver transplantation from living donors, and in ABO-incompatible kidney transplantation, through improvements in immunosuppression protocols [ 13 , 14 , 16 , 17 , 18 , 19 , 20 , 21 , 22 ].…”

Fatal intracardiac and pulmonary arterial thromboembolic damage following ABO-incompatible living donor liver transplantation for autoimmune hepatitis

“…[ 4 ] With improvements in desensitization management, including plasmapheresis and immunosuppression regimens, the graft survival rate in ABOi LDLT has improved greatly. [ 5 ] Desensitization measures include splenectomy, given the spleens function in the production and storage of antibodies, B cells and plasma cells as well as in blood filtration, phagocytosis, red blood cell destruction, antigen uptake and hemopoiesis. However, splenectomy increases the risk of complications, including infection, portal vein thrombosis and bleeding.…”