Cited by 118Systemic Lupus Erythematosus ResearchBlood Coagulation and Thrombosis MechanismsSystemic Sclerosis and Related Diseases

Hydroxychloroquine as an anti-thrombotic in antiphospholipid syndrome

Belizna, Cristina·2015·Autoimmunity Reviews

Abstract

Elective therapeutic approaches are required since recurrent thrombosis remains a major challenge in the management of antiphospholipid syndrome (APS) despite an efficient anticoagulation. Several data suggest that hydroxychloroquine (HCQ) could play a role in the prevention of thrombosis. The goal of this review is to point out the different aspects that could suggest the usefulness and the efficacy of HCQ for the prevention of thrombosis relapse in APS. By Medline research we collected important data dealing with potential anti-thrombotic effects of HCQ. The mechanisms of action of HCQ, and clinical and experimental data in systemic lupus erythematosus (SLE) and APS are discussed. As HCQ reduces the risk of thrombosis in both SLE patients and animal models of APS (1-7), and possibly decreases the titre of aPL [8], its beneficial role as a potential antithrombotic could be suggested.

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Crossref · 10.1016/j.autrev.2014.12.006

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  • Experimental studies show that hydroxychloroquine interferes with the binding of antiphospholipid antibody-β2-glycoprotein I complexes to phospholipid surfaces, reverses antiphospholipid antibody-induced thrombogenicity, reduces platelet activation, downregulates endothelial tissue factor expression, modulates complement activation and improves endothelial function.

    “Experimental studies have shown that HCQ interferes with the binding of aPL–β2-glycoprotein I complexes to phospholipid surfaces, reverses aPL-induced thrombogenicity, reduces platelet activation, downregulates endothelial tissue factor expression, modulates complement activation and improves endothelial function [3–5].”
  • Hydroxychloroquine reduces platelet activation, downregulates endothelial tissue factor expression, modulates complement activation and improves endothelial function, collectively targeting multiple thrombo-inflammatory pathways central to APS pathophysiology.

    “In addition, HCQ reduces platelet activation, downregulates endothelial tissue factor expression, modulates complement activation and improves endothelial function, collectively targeting multiple thrombo-inflammatory pathways central to APS pathophysiology [3, 5].”

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Authors
Belizna, C.
Affiliations
Inserm (FR)
Corresponding author
Belizna, Cristina
Venue
Autoimmunity Reviews
Publisher
Elsevier BV
Published
2015-04
Volume
14
Issue
4
Pages
358-362
ISSN
1568-9972 (ISSN-L)
OpenAlex
W2068265433
Cited by
118
References
74
Citations by year
2026: 5 · 2025: 7 · 2024: 8 · 2023: 8 · 2022: 8 · 2021: 10 · 2020: 16 · 2019: 16 · 2018: 17 · 2017: 7 · 2016: 10 · 2015: 6
FWCI
1.26
Type
journal article
Language
en
Open access
closed
Locations
  • Autoimmunity Reviews (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
  • Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Systemic Sclerosis and Related Diseases
Keywords
hydroxychloroquine, antiphospholipid syndrome, thromboprophylaxis, recurrent thrombosis, systemic lupus erythematosus, antiphospholipid antibodies, anti-thrombotic effects, mechanism of action
MeSH terms
Animals, Blood Platelets, Erythrocytes, Humans, Hydroxychloroquine, Lupus Erythematosus, Systemic, Thrombosis, Antiphospholipid Syndrome, Antibodies, Antiphospholipid

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