Evidence map›Paper›PMID 42529585›Full record

ArticleCase reports in transplantation2026

Passenger Lymphocyte Syndrome With Multiple Allo- and Autoantibodies Following Liver Transplantation: A Case Report.

Ivica Marić, Tobia Gomilšek, Klara Železnik

Abstract read
In one paragraph

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.

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1citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Ivica MarićSlovenian Institute for Transfusion Medicine, Ljubljana, Slovenia.ORCID https://orcid.org/0009-0004-9377-0211
Tobia GomilšekFaculty of Medicine, University of Ljubljana, Ljubljana, Slovenia, uni-lj.si.
Klara ŽeleznikSlovenian Institute for Transfusion Medicine, Ljubljana, Slovenia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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

PMID42529585
PMCPMC13418208

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