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Antibody-Mediated Thrombotic Diseases
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Antibody-Mediated Thrombotic Diseases

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Hematology".

Deadline for manuscript submissions: 10 July 2024 | Viewed by 9093

Special Issue Editors

Prof. Dr. Tamam Bakchoul

E-Mail Website
Guest Editor
1. Institute for Clinical and Experimental Transfusion Medicine (IKET), University Hospital of Tuebingen, Tuebingen, Germany
2. Centre for Clinical Transfusion Medicine, University Hospital of Tuebingen, Tuebingen, Germany
Interests: platelet; thrombocytopenia; hematology; coagulation disorders; thrombosis; transfusion medicine
Dr. Günalp Uzun

E-Mail Website
Guest Editor
Centre for Clinical Transfusion Medicine, University Hospital of Tuebingen, 72076 Tuebingen, Germany
Interests: vaccine-induced thrombotic thrombocytopenia; immune thrombocytopenia; platelet immunology; diagnosis of platelet disorders

Special Issue Information

Dear colleagues,

In recent years, our knowledge of the interplay between adaptive immunity and hemostasis has increased considerably. One aspect of this connection is the antibody-mediated activation of the coagulation system. Antibody-mediated thrombotic diseases include thrombotic thrombocytopenic purpura (TTP), heparin-induced thrombocytopenia (HIT), and antiphospholipid syndrome (APS). Antibody-mediated platelet activation also plays a role in COVID-19-induced coagulatopathy, in which thrombotic complications are an important prognostic factor. Recently, vaccine-induced immune thrombotic thrombocytopenia (VITT), a prothrombotic side effect of adenoviral vector-based COVID-19 vaccines, was added to this list of conditions with antibody-mediated thrombosis. Remarkable progress has been made recently in the diagnosis and treatment of thrombotic diseases. Platelet count and thrombosis are important clinical signs. It is critical to identify the cause responsible for thrombocytopenia, but this often proves difficult due to the complex comorbidities. Anticoagulation is the mainstay of treatment for thrombotic diseases, and novel therapeutics targeting the underlying mechanisms of platelet activation and thrombus formation are under investigation.

This Special Issue aims to show the latest achievements in the field of antibody-mediated thrombotic diseases, including, but not restricted to, clinical presentations, pathophysiological studies, current treatment progress, and future therapeutic perspectives, in order to obtain a comprehensive view of the state of the art of new trends in this area.

Prof. Dr. Tamam Bakchoul
Dr. Günalp Uzun
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • thrombotic diseases
  • thrombotic thrombocytopenic purpura
  • TTP
  • heparin-induced thrombocytopenia
  • HIT
  • vaccine-induced immune thrombotic thrombocytopenia
  • VITT
  • antiphopholipid syndrome
  • APS

Published Papers (4 papers)

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Research

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11 pages, 975 KiB  
Article
A Long-Term Follow-Up Study in Immune-Mediated Thrombotic Thrombocytopenic Purpura: What Are the Outcomes?
by Maria Addolorata Bonifacio, Daniele Roselli, Claudia Pia Schifone, Alessandra Ricco, Angelantonio Vitucci, Lara Aprile, Maria Addolorata Mariggiò and Prudenza Ranieri
J. Clin. Med. 2023, 12(23), 7305; https://doi.org/10.3390/jcm12237305 - 25 Nov 2023
Viewed by 809
Abstract
Endothelium damage triggers the multimeric protein von Willebrand factor (VWF) release and subsequent binding to platelets, which are recruited at sites of vascular injury. A complex and fragile equilibrium between circulating levels of von Willebrand factor and its metalloprotease, ADAMTS13, is responsible for [...] Read more.
Endothelium damage triggers the multimeric protein von Willebrand factor (VWF) release and subsequent binding to platelets, which are recruited at sites of vascular injury. A complex and fragile equilibrium between circulating levels of von Willebrand factor and its metalloprotease, ADAMTS13, is responsible for the hemostatic balance. However, the presence of autoantibodies targeting ADAMTS13 results in an increase in von Willebrand factor, mainly in its ultra-large multimers. The latter lead to platelet aggregation, the formation of thrombi and microangiopathic hemolytic anemia. This pathologic condition, known as immune-mediated thrombotic thrombocytopenic purpura (iTTP), occurs with high morbidity and a high rate of relapses. In this work, the long-term follow-up of 40 patients with iTTP is reported. We assessed ADAMTS13 activity, plasmatic VWF levels and the ADAMTS13/VWF ratio, comparing iTTP relapsing patients with remitting ones. A decrease in the ADAMTS13/VWF ratio, along with a reduced ADAMTS13 activity, could serve as predictive and sensitive biomarkers of incoming relapses. Full article
(This article belongs to the Special Issue Antibody-Mediated Thrombotic Diseases)
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Review

Jump to: Research

14 pages, 308 KiB  
Review
Vaccine-Induced Immune Thrombotic Thrombocytopenia: Clinicopathologic Features and New Perspectives on Anti-PF4 Antibody-Mediated Disorders
by Yi Zhang, Anna-Lise Bissola, Jared Treverton, Michael Hack, Mark Lychacz, Sarah Kwok, Addi Arnold and Ishac Nazy
J. Clin. Med. 2024, 13(4), 1012; https://doi.org/10.3390/jcm13041012 - 09 Feb 2024
Cited by 1 | Viewed by 1084
Abstract
Introduction: Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare yet severe adverse complication first identified during the global vaccination effort against SARS-CoV-2 infection, predominantly observed following administration of the ChAdOx1-S (Oxford-AstraZeneca) and Ad26.CoV2.S (Johnson & Johnson/Janssen) adenoviral vector-based vaccines. Unlike other anti-platelet factor [...] Read more.
Introduction: Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare yet severe adverse complication first identified during the global vaccination effort against SARS-CoV-2 infection, predominantly observed following administration of the ChAdOx1-S (Oxford-AstraZeneca) and Ad26.CoV2.S (Johnson & Johnson/Janssen) adenoviral vector-based vaccines. Unlike other anti-platelet factor 4 (PF4) antibody-mediated disorders, such as heparin-induced thrombocytopenia (HIT), VITT arises with the development of platelet-activating anti-PF4 antibodies 4–42 days post-vaccination, typically featuring thrombocytopenia and thrombosis at unusual sites. Aim: To explore the unique properties, pathogenic mechanisms, and long-term persistence of VITT antibodies in patients, in comparison with other anti-PF4 antibody-mediated disorders. Discussion: This review highlights the complexity of VITT as it differs in antibody behavior and clinical presentation from other anti-PF4-mediated disorders, including the high incidence rate of cerebral venous sinus thrombosis (CVST) and the persistence of anti-PF4 antibodies, necessitating a re-evaluation of long-term patient care strategies. The nature of VITT antibodies and the underlying mechanisms triggering their production remain largely unknown. Conclusion: The rise in awareness and subsequent prompt recognition of VITT is paramount in reducing mortality. As vaccination campaigns continue, understanding the role of adenoviral vector-based vaccines in VITT antibody production is crucial, not only for its immediate clinical implications, but also for developing safer vaccines in the future. Full article
(This article belongs to the Special Issue Antibody-Mediated Thrombotic Diseases)
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33 pages, 5438 KiB  
Review
Autoimmune Heparin-Induced Thrombocytopenia
by Theodore E. Warkentin
J. Clin. Med. 2023, 12(21), 6921; https://doi.org/10.3390/jcm12216921 - 03 Nov 2023
Cited by 4 | Viewed by 4578
Abstract
Autoimmune thrombocytopenia (aHIT) is a severe subtype of heparin-induced thrombocytopenia (HIT) with atypical clinical features caused by highly pathological IgG antibodies (“aHIT antibodies”) that activate platelets even in the absence of heparin. The clinical features of aHIT include: the onset or worsening of [...] Read more.
Autoimmune thrombocytopenia (aHIT) is a severe subtype of heparin-induced thrombocytopenia (HIT) with atypical clinical features caused by highly pathological IgG antibodies (“aHIT antibodies”) that activate platelets even in the absence of heparin. The clinical features of aHIT include: the onset or worsening of thrombocytopenia despite stopping heparin (“delayed-onset HIT”), thrombocytopenia persistence despite stopping heparin (“persisting” or “refractory HIT”), or triggered by small amounts of heparin (heparin “flush” HIT), most cases of fondaparinux-induced HIT, and patients with unusually severe HIT (e.g., multi-site or microvascular thrombosis, overt disseminated intravascular coagulation [DIC]). Special treatment approaches are required. For example, unlike classic HIT, heparin cessation does not result in de-escalation of antibody-induced hemostasis activation, and thus high-dose intravenous immunoglobulin (IVIG) may be indicated to interrupt aHIT-induced platelet activation; therapeutic plasma exchange may be required if high-dose IVIG is ineffective. Also, aHIT patients are at risk for treatment failure with (activated partial thromboplastin time [APTT]-adjusted) direct thrombin inhibitor (DTI) therapy (argatroban, bivalirudin), either because of APTT confounding (where aHIT-associated DIC and resulting APTT prolongation lead to systematic underdosing/interruption of DTI therapy) or because DTI inhibits thrombin-induced protein C activation. Most HIT laboratories do not test for aHIT antibodies, contributing to aHIT under-recognition. Full article
(This article belongs to the Special Issue Antibody-Mediated Thrombotic Diseases)
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20 pages, 6124 KiB  
Review
Vaccine-Induced Immune Thrombocytopenia and Thrombosis (VITT)—Insights from Clinical Cases, In Vitro Studies and Murine Models
by Venkata A. S. Dabbiru, Luisa Müller, Linda Schönborn and Andreas Greinacher
J. Clin. Med. 2023, 12(19), 6126; https://doi.org/10.3390/jcm12196126 - 22 Sep 2023
Viewed by 2026
Abstract
An effective worldwide vaccination campaign started and is still being carried out in the face of the coronavirus disease 2019 (COVID-19) pandemic. While vaccines are great tools to confront the pandemic, predominantly adenoviral vector-based vaccines can cause a rare severe adverse effect, termed [...] Read more.
An effective worldwide vaccination campaign started and is still being carried out in the face of the coronavirus disease 2019 (COVID-19) pandemic. While vaccines are great tools to confront the pandemic, predominantly adenoviral vector-based vaccines can cause a rare severe adverse effect, termed vaccine-induced immune thrombocytopenia and thrombosis (VITT), in about 1 in 100,000 vaccinated individuals. VITT is diagnosed 5–30 days post-vaccination and clinically characterized by thrombocytopenia, strongly elevated D-dimer levels, platelet-activating anti-platelet factor 4 (PF4) antibodies and thrombosis, especially at atypical sites such as the cerebral venous sinus and/or splanchnic veins. There are striking similarities between heparin-induced thrombocytopenia (HIT) and VITT. Both are caused by anti-PF4 antibodies, causing platelet and leukocyte activation which results in massive thrombo-inflammation. However, it is still to be determined why PF4 becomes immunogenic in VITT and which constituent of the vaccine triggers the immune response. As VITT-like syndromes are increasingly reported in patients shortly after viral infections, direct virus-PF4 interactions might be most relevant. Here we summarize the current information and hypotheses on the pathogenesis of VITT and address in vivo models, especially murine models for further studies on VITT. Full article
(This article belongs to the Special Issue Antibody-Mediated Thrombotic Diseases)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

1. Clinical Aspects and Treatment of Heparin Induced Thrombocytopenia

2. Antiphospholipid Syndrome

3. Pathophysiology of Heparin induced thrombocytopenia

4. Laboratory diagnosis of the Antiphospholipid Syndrome – clinical utility and current challenges

 

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