Cited by 122Systemic Lupus Erythematosus ResearchBlood Coagulation and Thrombosis MechanismsHeparin-Induced Thrombocytopenia and Thrombosis

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Correlation between antiphospholipid antibodies that recognize domain I of β2-glycoprotein I and a reduction in the anticoagulant activity of annexin A5

de Laat, Bas, Wu, Xiao-Xuan, van Lummel, Menno, Derksen, Ronald H. W. M., de Groot, Philip G., Rand, Jacob H.·2007·Blood

DOI 10.1182/blood-2006-07-030148

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Abstract

The paradoxical correlation between thrombosis and the lupus anticoagulant (LAC) effect is an enigmatic feature of the antiphospholipid (aPL) syndrome. The Dutch authors previously reported that thrombosis-related anti–β2-glycoprotein I (β2GPI) antibodies recognize domain I and cause LAC. The American authors reported that aPLs disrupt an anticoagulant annexin A5 (AnxA5) crystal shield. We investigated whether antidomain I antibodies correlate with disruption of AnxA5-anticoagulant activity. We studied a well-characterized group of 33 patients including subgroups with β2GPI-dependent LAC that recognize domain I (n = 11), with β2GPI-independent LAC (n = 12), and lacking LAC (n = 10). The effects on AnxA5-anticoagulant activity were determined with an AnxA5 resistance assay that measures coagulation times with and without AnxA5. Patients with β2GPI-dependent LAC (group A, all with thrombosis) had significantly lower AnxA5-anticoagulant ratios than those with β2GPI-independent LAC (group B, thrombosis n = 4; 157.8% versus 235.6%, P < .001) and those without LAC (group C, thrombosis n = 2; 157.8% versus 232.5%, P < .001). There was no difference in the ratios between groups B and C (P = .92). Plasmas with β2GPI-dependent LAC that recognize domain I displayed significantly increased AnxA5 resistance, suggesting that specifically anti-β2GPI antibodies compete with AnxA5 for anionic phospholipids. These results are consistent with a model in which aPL antibodies may promote thrombosis by interfering with the anticoagulant activity of AnxA5.

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Authors: de Laat, B., Wu, X.-X., van Lummel, M., Derksen, R. H. W. M., de Groot, P. G., & Rand, J. H.
Affiliations: University Medical Center Utrecht (NL)
Albert Einstein College of Medicine (US)
ORCID: de Laat, Bas
Wu, Xiao-Xuan
de Groot, Philip G.
Rand, Jacob H.
Venue: Blood
Publisher: American Society of Hematology
Published: 2006-10-19
Volume: 109
Issue: 4
Pages: 1490-1494
ISSN: 0006-4971 (ISSN-L)
1528-0020
DOI: 10.1182/blood-2006-07-030148
OpenAlex: W2047089135
Cited by: 122
References: 32
Citations by year: 2026: 2 · 2025: 2 · 2024: 5 · 2023: 2 · 2022: 1 · 2021: 6 · 2020: 8 · 2019: 7 · 2018: 7 · 2017: 6 · 2016: 12 · 2015: 1 · 2014: 8 · 2013: 9 · 2012: 9
FWCI: 3.96
Type: journal article
Language: en
Open access: closed
Locations: Blood (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
Health Sciences › Medicine › Hematology › Heparin-Induced Thrombocytopenia and Thrombosis
Keywords: antiphospholipid syndrome, lupus anticoagulant, beta2-glycoprotein I, annexin V, anticoagulant activity, thrombosis, anionic phospholipids
MeSH terms: Adult, Epitopes, Binding Sites, Blood Coagulation, Female, Humans, Male, Thrombosis, Case-Control Studies, Lupus Coagulation Inhibitor, Antibodies, Antiphospholipid, Annexin A5, Thrombophilia, beta 2-Glycoprotein I

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Correlation between antiphospholipid antibodies that recognize domain I of β2-glycoprotein I and a reduction in the anticoagulant activity of annexin A5

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