Nonhemolytic passenger lymphocyte syndrome

Sandler, S. Gerald; Han, Suhua; Langeberg, Albert; Matsumoto, Cal; Fishbein, Thomas M.

doi:10.1111/trf.14383

Cited by 12 publications

(4 citation statements)

References 33 publications

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“…The incidence of biochemically evident passenger lymphocyte syndrome in liver transplantation is reported to be up to 40%; however, less than 30% of these cases will demonstrate clinically significant haemolysis requiring intervention 7–9. Less than 20 published studies have reported passenger lymphocyte syndrome following liver transplantation 4 5 8 10–26. Most cases were in the setting of minor ABO mismatch followed by Rh incompatibility.…”

Section: Discussionmentioning

confidence: 99%

Passenger lymphocyte syndrome following minor ABO-mismatched liver transplantation

Mathavan,

Krekora,

Kleehammer

et al. 2024

BMJ Case Rep

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Passenger lymphocyte syndrome is an immunologic disorder observed in solid organ and haematopoietic stem cell transplantation in which B lymphocytes within a donor graft are transferred to the recipient and subsequently produce circulating antibodies against host red blood cell antigens. The syndrome is most likely to occur in minor ABO blood group mismatched or Rh incompatible transplantation. Although generally mild and self-limited, the resulting haemolytic burden has the potential to increase the risk of infection, graft failure and death. The phenomenon is observed in the transplantation of any solid organ with lymphoid tissue, including the liver. We present a structured case report of passenger lymphocyte syndrome following minor ABO-mismatched liver transplantation, which was initially complicated by blood loss anaemia early in the postoperative period. By reviewing the limited literature of this disorder following liver transplantation, we emphasise common clinical findings and treatment strategies as well as introduce chimerism analysis to confirm resolution.

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Section: Discussionmentioning

confidence: 99%

Passenger lymphocyte syndrome following minor ABO-mismatched liver transplantation

Mathavan,

Krekora,

Kleehammer

et al. 2024

BMJ Case Rep

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“…In the clinic, the transfusion of incompatible RBCs causes specific alloantibodies, thereby leading to intravascular or extravascular haemolysis, which leads to the aggravation of anaemia symptoms and threatens the lives of patients [61][62][63]. Preventing or minimizing alloimmunization will improve the efficacy of erythrocyte transfusion and avoid adverse transfusion reactions [64][65][66]. DCs or their precursors have the ability to distinguish between self and allogeneic non-self as they would between self and microbial non-self -a phenomenon referred to as 'innate allorecognition' [67].…”

Section: Discussionmentioning

confidence: 99%

Anti-JMH alloantibody in inherited JMH-negative patients leads to immunogenic destruction of JMH-positive RBCs

Zhang

Wei

Chen

et al. 2021

Clinical and Experimental Immunology

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The clinical significance of the specific anti-John Milton Hagen (JMH) alloantibody in inherited JMH-negative patients remains unclear. During clinical blood transfusion, it is often classified as an anti-JMH autoantibody in acquired JMH-negative patients, which might further lead to the occurrence of haemolysis events. In this study, we found that the proportion of inherited JMH-negative people in the Guangzhou population was 0.41%, based on the study of 243 blood samples by flow cytometry. Gene sequencing analysis revealed two novel variants located in exon 11 (c.1348G>A, p.Ala449Thr) and exon 14 (c.1989G>T, p.Leu663Phe). Specific antigen presentation showed that JMH-positive RBCs (red blood cells) could be internalized by SEMA7A −/− dendritic cells (DCs) and that SEMA7A −/− DCs activated by the semaphorin 7a (Sema7a) protein or JMH-positive erythrocytes further induced activation of CD4 + T cells to secrete interferon (IFN)-γ. Transfusion of JMH-positive RBCs could lead to the production of the specific anti-JMH alloantibody in Sema7a knock-out (KO) C57 mice. After erythrocyte sensitization, complement C3 was specifically fixed, causing the destruction of JMH-positive erythrocytes. The anti-JMH alloantibody caused immunological destruction of JMH-positive erythrocytes and promoted the clearance of JMH-positive RBCs. We should be cautious when making conclusions about the clinical significance of the anti-JMH alloantibody.

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“…Es gibt Hinweise in der Literatur, dass Lymphozyten aus dem Transplantat auch Antikörper gegen Blutgruppenmerkmale bilden können, die beim Empfänger nicht vorhanden sind. Die Autoren sprechen da von einem "nicht hämolytischen PLS", das lediglich von immunologischem Interesse ist, aber praktisch keine klinische Bedeutung aufweist [30].…”

Section: Immunhämatologische Komplikationen Bei Ab0-minor-inkompatibiunclassified

Transfusionsmedizinische Versorgung von Patienten nach allogener Blutstammzelltransplantation

Hölig

Rosner

2019

TumorDiagn u Ther

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ZusammenfassungIm Rahmen einer allogenen Blutstammzelltransplantation kommt es häufig zu immunhämatologischen Phänomenen, die im Rahmen der Diagnostik und der supportiven Hämotherapie berücksichtigt werden müssen. Durch Diskrepanzen der AB0-Merkmale von Spender und Empfänger können verschiedene Komplikationen auftreten. Die wesentlichsten sind ein verzögertes Engraftment der Erythropoese nach major-inkompatibler Transplantation (sogenannte Pure-red-Cell-Aplasie, PRCA) und die verzögerte Hämolyse durch Aktivierung von minor-inkompatiblen Lymphozyten im Transplantat, das sogenannte Passenger-Lymphocyte-Syndrom (PLS). Durch ein gezieltes immunhämatologisches Monitoring der Patienten können diese Phänomene zeitgerecht erkannt und adäquat therapiert werden. Ein Wechsel im Bereich des Rhesusantigens D ist ebenfalls bei der Hämotherapie allogen transplantierter Patienten zu berücksichtigen, verursacht allerdings nur selten Komplikationen. Hinsichtlich der Thrombozytenversorgung sollte rechtzeitig vor Konditionierungsbeginn eine gezielte Diagnostik von Immunisierungen gegen HLA- (humane Leukozyten-Antigene) und Plättchen-spezifische Antigene erfolgen, um die Thrombozytenversorgung mit ausgewählten Spendern in der Aplasiephase zuverlässig gewährleisten zu können. Bei sehr breit und hochtitrig immunisierten Patienten kann eine Immunsuppression mit Rituximab und Immunadsorption vor Transplantation die Inkremente nach Thrombozytensubstitution verbessern und im Falle von einem HLA-Mismatch des Transplantats auch das Engraftment unterstützen.

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Nonhemolytic passenger lymphocyte syndrome

Cited by 12 publications

References 33 publications

Passenger lymphocyte syndrome following minor ABO-mismatched liver transplantation

Passenger lymphocyte syndrome following minor ABO-mismatched liver transplantation

Anti-JMH alloantibody in inherited JMH-negative patients leads to immunogenic destruction of JMH-positive RBCs

Transfusionsmedizinische Versorgung von Patienten nach allogener Blutstammzelltransplantation

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