ArticleCase reports in transplantation2026
Passenger Lymphocyte Syndrome With Multiple Allo- and Autoantibodies Following Liver Transplantation: A Case Report.
Article in Case reports in transplantation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Passenger Lymphocyte Syndrome With Multiple Allo- and Autoantibodies Following Liver Transplantation: A Case Report.Case reports in transplantation · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Passenger lymphocyte syndrome (PLS) is a rare immune-mediated haemolytic complication of solid organ transplantation caused by donor-derived lymphocytes producing antibodies against recipient red blood cell (RBC) antigens. Multiple alloantibodies and concomitant autoantibody formation are uncommon, particularly in ABO-identical liver transplantation. Case Presentation: A 56-year-old male underwent ABO-identical but D- and Kell-non-identical liver transplantation. Approximately, 3 weeks posttransplantation, haemoglobin decreased to 81 g/L, and indirect antiglobulin testing identified anti-D and anti-E antibodies, while direct antiglobulin testing confirmed IgG-coated RBCs. Subsequently, anti-K alloantibodies and transient pan-reactive IgG autoantibodies were detected, resulting in positive crossmatches and complicated transfusion support. Because most transfused RBC units before antibody detection were D+, E+ and K+, anti-E was interpreted as probable recipient-derived transfusion-associated alloimmunisation, whereas anti-D and anti-K were consistent with donor-derived PLS. Transfusion support was subsequently restricted to D-, E- and K- RBC units. The patient remained clinically stable despite haemoglobin decline with serologic evidence of immune-mediated RBC sensitization consistent with PLS. During 4 years of follow-up, anti-D and anti-K antibodies disappeared, while only weak residual anti-E reactivity persisted. Discussion: The simultaneous occurrence of donor-derived alloantibodies, probable recipient-derived alloimmunisation and transient pan-reactive autoantibodies suggests broader posttransplant humoral immune activation than typically observed in classical PLS. Although clinically significant autoimmune haemolytic anaemia did not develop, the coexistence of multiple antibody specificities substantially complicated serologic interpretation and transfusion management. Conclusion: This case highlights complex posttransplant humoral immune dysregulation involving donor-derived alloantibodies, probable recipient alloimmunisation and transient autoantibody formation after ABO-identical liver transplantation. The coexistence of multiple antibodies significantly complicated serologic testing and transfusion support.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.