(P-TS-74) Passenger Lymphocyte Syndrome and Hemolysis Following Liver Transplant

Passenger lymphocyte syndrome (PLS) is a potential complication of solid organ transplant. Donor B lymphocytes present within the transplanted organ may be exposed to antigens on the recipient’s red blood cells (RBC) resulting in stimulation of antibody production post-transplant. PLS is most often caused by a minor ABO mismatch between the donor and recipient, but cases of hemolysis due to non-ABO RBC alloantibodies have also been described. Here we present a rare PLS case with severe hemolysis due to anti-D and anti-C after a liver transplant.

Study

Design/Methods:

The recipient was a 56-year-old O+ male that underwent cadaveric liver transplantation from an O- donor. Prior to the transplant, the recipient’s antibody screen and DAT were negative. During the transplant, the recipient received 21 units of O+ RBC. Three days post-op the recipient’s antibody screen and DAT had turned positive. The type, screen, and antibody identification were performed by gel-based methodology. DAT testing was done by tube method using polyspecific (anti-IgG and C3d), monospecific anti-IgG, and monospecific anti-C3d. An acid elution was tested with screening and panel cells using tube method. DNA testing using molecular methods was performed for the RHD and RHCE genes at a reference laboratory.

Results/Findings:

Anti-D and anti-C were identified in the recipient’s plasma and eluate. DNA analysis of the RHD and RHCE genes of the recipient revealed RHD/RHD RHCE*Ce/Ce with no variants (indicating that the recipient would not develop alloanti-D or alloanti-C). Eight days post-op the recipient’s hemoglobin dropped from 8.8 g/dL to 6.2 g/dL with no signs of bleeding. Haptoglobin and indirect bilirubin tested on post-op day 9 resulted as < 20 mg/dL and 3.4 mg/dL, respectively, suggesting hemolysis. Retrospective review of the liver donor history revealed that the donor had known anti-D and anti-C alloantibodies.

The recipient was transfused with 15 units of D- and C- RBC over 12.5 weeks and received 3 doses of intravenous immunoglobulin (IVIG). Rituximab therapy was considered but deferred due to infection concerns. Anti-D and anti-C were still detectable in the recipient’s plasma even after the recipient was no longer transfusion dependent.

Conclusions:

PLS is a potential cause for post-transplant hemolysis and should be considered when blood bank testing reveals new antibodies directed to recipient RBC antigens post organ transplantation. A history of RBC alloantibodies in organ donors is a noteworthy finding and should be communicated to the transplant team and the blood bank caring for the transplant recipient.