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Cited by 35Systemic Lupus Erythematosus ResearchBlood Coagulation and Thrombosis MechanismsVasculitis and related conditions

From antibody to clinical phenotype, the black box of the antiphospholipid syndrome: Pathogenic mechanisms of the antiphospholipid syndrome

Du, Vivian X., Kelchtermans, Hilde, de Groot, Philip G., de Laat, Bas·2013·Thrombosis Research
DOI 10.1016/j.thromres.2013.07.023
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Abstract

The antiphospholipid syndrome (APS) is diagnosed by the combination of vascular thrombosis and/or pregnancy morbidity and the detection of antiphospholipid antibodies (aPLs) in plasma. In the last few years, a great effort has been made to unravel the mechanism by which aPLs cause thrombosis and a vast amount of mechanisms have been proposed. aPLs were proposed to induce a prothrombotic state by influencing the cellular blood compartment, the plasma compartment, the vascular wall and even metabolic pathways beyond the hemostatic system. However, due to the diversity in the mechanisms and the differences in the methodology, the focus of the mechanistical studies in this field seems to be largely diffused. It is hard to imagine that aPLs can exert such a diversity of effects, resulting in either thrombosis and/or pregnancy morbidity and the relationship between aPLs and the clinical manifestations remains to be a mysterious "black box". In an attempt to get insight in what takes place inside the black box, we have analyzed 126 mechanistical studies on aPLs and discussed differences in the type of antibodies that were used, the involvement of beta2-glycoprotein I (β2GPI), and the criteria used to diagnose APS patients.

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Crossref · 10.1016/j.thromres.2013.07.023

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  • In vitro, interference by aPL autoantibodies with the clotting cascade is reflected in prolongation of phospholipid-dependent clotting assays, such as the activated partial thromboplastin time (aPTT).

    “In vitro, the interference by these autoantibodies with the clotting cascade is reflected in the prolongation of phospholipid-dependent clotting assays, such as the activated partial thromboplastin time (aPTT) [2].”

    From Cardiovascular risk factors are major determinants of thrombotic risk in patients with the lupus anticoagulant (2017) · cites this paper as [2]

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Authors
Du, V. X., Kelchtermans, H., de Groot, P. G., & de Laat, B.
Affiliations
  • University Medical Center Utrecht (NL)
  • Maastricht University Medical Centre (NL)
Corresponding author
Kelchtermans, Hilde
ORCID
Kelchtermans, Hilde
Venue
Thrombosis Research
Publisher
Elsevier BV
Published
2013-09
Volume
132
Issue
3
Pages
319-326
ISSN
0049-3848 (ISSN-L)
DOI
10.1016/j.thromres.2013.07.023
OpenAlex
W1976928839
Cited by
35
References
87
Citations by year
2024: 1 · 2023: 1 · 2022: 2 · 2021: 1 · 2019: 6 · 2018: 3 · 2017: 3 · 2016: 5 · 2015: 7 · 2014: 6
FWCI
0.95
Type
journal article
Language
en
Open access
closed
Locations
  • Thrombosis Research (publishedVersion)
  • PubMed (publishedVersion)
  • Research Publications (Maastricht University) (publishedVersion)
  • Research Publications (Maastricht University) (submittedVersion)
Topics
  • Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
  • Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Vasculitis and related conditions
Keywords
antiphospholipid syndrome, antiphospholipid antibodies, pathophysiological mechanisms, thrombosis, pregnancy morbidity, beta2-glycoprotein I, hypercoagulability, vascular thrombosis, clinical phenotype
MeSH terms
Animals, Female, Humans, Phenotype, Pregnancy, Pregnancy Complications, Thrombosis, Antiphospholipid Syndrome, Antibodies, Antiphospholipid

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