Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis – a shared mechanism of NETosis

Anti-platelet factor 4 (PF4) immunothrombosis is characterized by thrombocytopenia, thrombosis and enhanced NETosis and has been described in the absence of prior heparin exposure. This case report describes a patient with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) who, w...

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Main Authors: Lital Remez-Gabay, Olga Vdovich, Luiza Akria, Etty Kruzel-Davila
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-04-01
Series:Frontiers in Immunology
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Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2025.1567999/full
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author Lital Remez-Gabay
Lital Remez-Gabay
Olga Vdovich
Olga Vdovich
Luiza Akria
Luiza Akria
Etty Kruzel-Davila
Etty Kruzel-Davila
Etty Kruzel-Davila
author_facet Lital Remez-Gabay
Lital Remez-Gabay
Olga Vdovich
Olga Vdovich
Luiza Akria
Luiza Akria
Etty Kruzel-Davila
Etty Kruzel-Davila
Etty Kruzel-Davila
author_sort Lital Remez-Gabay
collection DOAJ
description Anti-platelet factor 4 (PF4) immunothrombosis is characterized by thrombocytopenia, thrombosis and enhanced NETosis and has been described in the absence of prior heparin exposure. This case report describes a patient with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) who, while under immunosuppression, developed anti-PF4-mediated immunothrombosis, with NETosis significantly elevated compared to baseline markers observed during AAV. Treatment with intravenous immunoglobulin (IVIG) led to resolution of the syndrome, marked by a reduction in NETosis markers, restoration of platelet counts, and alleviation of the hypercoagulable state. We review the epidemiology, pathogenesis, clinical manifestations, and management strategies of thrombotic anti-PF4 immune disorders, highlighting the roles of AAV and dysregulated NETosis as key triggers. Early recognition of anti-PF4-mediated immunothrombosis without prior heparin exposure is critical, as prompt treatment with IVIG and direct thrombin inhibitors can significantly improve outcomes. This case underscores the interplay between NETosis, ANCA vasculitis, and thrombotic anti-PF4 immune disorders, emphasizing the therapeutic potential of IVIG in mitigating NETosis-related complications.
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publisher Frontiers Media S.A.
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spelling doaj-art-0cc29d3c245f433585791ff4e3a824f22025-08-20T03:09:07ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-04-011610.3389/fimmu.2025.15679991567999Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis – a shared mechanism of NETosisLital Remez-Gabay0Lital Remez-Gabay1Olga Vdovich2Olga Vdovich3Luiza Akria4Luiza Akria5Etty Kruzel-Davila6Etty Kruzel-Davila7Etty Kruzel-Davila8Nephrology Laboratory, Research Institute, Galilee Medical Center, Nahariya, IsraelNephrology Department, Galilee Medical Center, Nahariya, IsraelNephrology Department, Galilee Medical Center, Nahariya, IsraelAzrieli Faculty of Medicine, Bar-Ilan University, Zefat, IsraelAzrieli Faculty of Medicine, Bar-Ilan University, Zefat, IsraelHematology Unit, Galilee Medical Center, Nahariya, IsraelNephrology Laboratory, Research Institute, Galilee Medical Center, Nahariya, IsraelNephrology Department, Galilee Medical Center, Nahariya, IsraelAzrieli Faculty of Medicine, Bar-Ilan University, Zefat, IsraelAnti-platelet factor 4 (PF4) immunothrombosis is characterized by thrombocytopenia, thrombosis and enhanced NETosis and has been described in the absence of prior heparin exposure. This case report describes a patient with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) who, while under immunosuppression, developed anti-PF4-mediated immunothrombosis, with NETosis significantly elevated compared to baseline markers observed during AAV. Treatment with intravenous immunoglobulin (IVIG) led to resolution of the syndrome, marked by a reduction in NETosis markers, restoration of platelet counts, and alleviation of the hypercoagulable state. We review the epidemiology, pathogenesis, clinical manifestations, and management strategies of thrombotic anti-PF4 immune disorders, highlighting the roles of AAV and dysregulated NETosis as key triggers. Early recognition of anti-PF4-mediated immunothrombosis without prior heparin exposure is critical, as prompt treatment with IVIG and direct thrombin inhibitors can significantly improve outcomes. This case underscores the interplay between NETosis, ANCA vasculitis, and thrombotic anti-PF4 immune disorders, emphasizing the therapeutic potential of IVIG in mitigating NETosis-related complications.https://www.frontiersin.org/articles/10.3389/fimmu.2025.1567999/fullanti-PF4 immunothrombosisNEtosisANCAIVIgcase report
spellingShingle Lital Remez-Gabay
Lital Remez-Gabay
Olga Vdovich
Olga Vdovich
Luiza Akria
Luiza Akria
Etty Kruzel-Davila
Etty Kruzel-Davila
Etty Kruzel-Davila
Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis – a shared mechanism of NETosis
Frontiers in Immunology
anti-PF4 immunothrombosis
NEtosis
ANCA
IVIg
case report
title Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis – a shared mechanism of NETosis
title_full Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis – a shared mechanism of NETosis
title_fullStr Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis – a shared mechanism of NETosis
title_full_unstemmed Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis – a shared mechanism of NETosis
title_short Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis – a shared mechanism of NETosis
title_sort case report anti platelet factor 4 mediated immunothrombosis in a patient with anca vasculitis a shared mechanism of netosis
topic anti-PF4 immunothrombosis
NEtosis
ANCA
IVIg
case report
url https://www.frontiersin.org/articles/10.3389/fimmu.2025.1567999/full
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