Complement blockade with eculizumab to treat acute symptomatic humoral rejection after heart transplantation.

Fiche du document

Type de document
Périmètre
Langue
Identifiants
Relations

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1111/xen.12726

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/35001433

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1399-3089

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_81DB4AE7643B2

Licences

info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/




Citer ce document

P. Yerly et al., « Complement blockade with eculizumab to treat acute symptomatic humoral rejection after heart transplantation. », Serveur académique Lausannois, ID : 10.1111/xen.12726


Métriques


Partage / Export

Résumé 0

Antibody-mediated rejection (AMR) is a major barrier preventing successful discordant organ xenotransplantation, but it also occurs in allotransplantation due to anti-HLA antibodies. Symptomatic acute AMR is rare after heart allograft but carries a high risk of mortality, especially >1 year after transplant. As complement activation may play a major role in mediating tissue injury in acute AMR, drugs blocking the terminal complement cascade like eculizumab may be useful, particularly since "standards of care" like plasmapheresis are not based on strong evidence. Eculizumab was successfully used to treat early acute kidney AMR, a typical condition of "active AMR," but showed mitigated results in late AMR, where "chronic active" lesions are more prevalent. Here, we report the case of a heart recipient who presented with acute heart failure due to late acute AMR with eight de novo donor-specific anti-HLA antibodies (DSA), and who fully recovered allograft function and completely cleared DSA following plasmapheresis-free upfront eculizumab administration in addition to thymoglobulin, intravenous immunoglobulins (IVIG), and rituximab. Several clinical (acute onset, abrupt and severe loss of graft function), biological (sudden high-level production of DSA), and pathological features (microvascular injury, C4d deposits) of this cardiac recipient are shared with early kidney AMR and may indicate a strong role of complement in the pathogenesis of acute graft injury that may respond to drugs like eculizumab. Terminal complement blockade should be further explored to treat acute AMR in recipients of heart allografts and possibly also in recipients of discordant xenografts in the future.

document thumbnail

Par les mêmes auteurs

Sur les mêmes sujets

Exporter en